|Classification and external resources|
Post-concussion syndrome, also known as postconcussive syndrome or PCS, is a set of symptoms that may continue for weeks, months, or a year or more after a concussion – a minor form of traumatic brain injury (TBI). The rates of PCS vary, but most studies report that about 15% of individuals with a history of a single concussion develop persistent symptoms associated with the injury. A diagnosis may be made when symptoms resulting from concussion last for more than three months after the injury. Loss of consciousness is not required for a diagnosis of concussion or post-concussion syndrome.
The condition is associated with a wide range of symptoms: physical, such as headache; cognitive, such as difficulty concentrating; and emotional and behavioral, such as irritability. Many of the symptoms associated with PCS are common or may be exacerbated by other disorders, so there is considerable risk of misdiagnosis. Headaches that occur after a concussion may feel like migraine headaches or tension-type headaches. Most headaches are tension-type headaches, which may be associated with a neck injury that occurred at the same time of the head injury.
Though there is no treatment for PCS, symptoms can be treated; medications and physical and behavioral therapy may be used, and individuals can be educated about symptoms and provided with the expectation of recovery. The majority of PCS cases resolve after a period of time.
It is not known what causes PCS to occur and persist, or why some people who suffer a minor traumatic brain injury later 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, being female, and older age all increase the chances that someone will suffer PCS. Physiological and psychological factors present before, during, and after the injury are all thought to be involved in the development of PCS.
Some experts believe post-concussion symptoms are caused by structural damage to the brain or disruption of neurotransmitter systems, resulting from the impact that caused the concussion. Others believe that post-concussion symptoms are related to common psychological factors. Most common symptoms like headache, dizziness, and sleep problems are similar to those often experienced by individuals diagnosed with depression, anxiety, or post traumatic stress disorder. In many cases, both physiological effects of brain trauma and emotional reactions to these events play a role in the development of symptoms.
- 1 Signs and symptoms
- 2 Causes
- 3 Diagnosis
- 4 Treatment
- 5 Prognosis
- 6 Epidemiology
- 7 History
- 8 Controversy
- 9 See also
- 10 References
Signs and symptoms
In the past, the term PCS was also used to refer to immediate physical symptoms or post-concussive symptoms following a minor TBI or concussion. The severity of these symptoms typically decreases rapidly. In addition, the nature of the symptoms may change over time: acute symptoms are most commonly of a physical nature, while persisting symptoms tend to be predominantly psychological. Symptoms such as noise sensitivity, problems with concentration and memory, irritability, depression, and anxiety may be called 'late symptoms' because they generally do not occur immediately after the injury, but rather in the days or weeks after the injury. Nausea and drowsiness commonly occur acutely following concussion. Headache and dizziness occur immediately after the injury, but also can be long lasting.
A common condition associated with PCS is headache. While most people have headaches of the same type they experienced before the injury, people diagnosed with PCS often report more frequent or longer-lasting headaches. Between 30% and 90% of people treated for PCS report having more frequent headaches and between 8% and 32% still report them a year after the injury.
Dizziness is another common symptom reported in about half of people diagnosed 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, which can contribute to subsequent injuries and higher rates of mortality due to falls.
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% report blurred vision. People may also have double vision or ringing in the ears, also called tinnitus. PCS may cause insomnia, fatigue, or other problems with sleep.
Psychological and behavioral
Psychological conditions, which are present in about half of people with PCS, may include irritability, anxiety, depression, and a change in personality. Other emotional and behavioral symptoms include restlessness, aggression, and mood swings. Some common symptoms, such as apathy, insomnia, irritability, or lack of motivation, may result from other co-occurring conditions, such as depression.
Higher mental functions
Common symptoms associated with a diagnosis of PCS are related to cognition, attention, and memory, especially short-term memory, which can also worsen other problems such as forgetting appointments or difficulties at work. In one study, one in four people diagnosed with PCS continued to report memory problems a year after the injury, but most experts agree that cognitive symptoms clear within six months to a year after injury in the vast majority of individuals.
The question of the cause or causes of PCS has been heavily debated for many years and remain controversial. It is not known to exactly what degree the symptoms are due to physiological changes or to other factors, such as pre-existing psychiatric disorders or factors related to secondary gain or disability compensation. The subjectivity of the complaints complicates assessment and makes it difficult to determine whether symptoms are being exaggerated or feigned.
While the causes of symptoms occurring immediately after a concussion are likely to be physiological, it is less evident that persistent post-concussive symptoms have an entirely organic basis, and nonorganic factors are likely to be involved in symptoms that last longer than three months. PCS may also be exacerbated by psychosocial factors, chronic pain, or an interaction of some or all of these. The majority of experts believe that PCS results from a mix of factors, including preexisting psychological factors and those directly relating to the physical injury.
Conventional neuroimaging studies of the brain following a concussion are typically normal. However, studies have found some subtle physiological changes associated with PCS using more novel imaging modalities. Studies using positron emission tomography have linked PCS to a reduction in glucose use by the brain. Changes in cerebral blood flow have also been observed 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 although they were not examining PCS specifically. Not all people with PCS 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, or post-traumatic stress disorder (PTSD). Proponents of the view that PCS has a physiological basis point to findings that children demonstrate deficits on standardized tests of cognitive function following a mild TBI. A few studies have shown that people with PCS score lower than controls on neuropsychological tests that measure attention, verbal learning, reasoning, and information processing, but issues related to effort and secondary gain can not be ruled out as contributing to these differences. Recovery as measured by scores on cognitive tests frequently do not correlate with resolution of symptoms; individuals diagnosed with PCS may still report subjective symptoms after their performance on tests of cognitive functioning have returned to normal. Another study found that although children with PCS 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.
It has been argued that psychological factors play an important role in the presence of post-concussion symptoms. The development of PCS may be due to a combination of factors such as adjustment to effects of the injury, preexisting vulnerabilities, and brain dysfunction. Setbacks related to the injury, for example problems at work or with physical or social functioning, may act as stressors that interact with preexisting factors such as personality and mental conditions to cause and perpetuate PCS. In one study, levels of daily stress were found to be correlated to PCS symptoms in both concussed subjects and controls, but in another, stress was not significantly related to symptoms.
Iatrogenic effects (those caused by the medical intervention) may also occur when individuals are provided with misleading or incorrect information related to recovery of symptoms. This information may cause people to focus and dwell on the idea that their brains are permanently damaged,. It appears that even the expectation of symptoms may contribute to the development of PCS by causing individuals with MTBI to focus on symptoms and therefore perceive them to be more intense, to attribute symptoms that occur for other reasons to the injury, and to underestimate the rate of symptoms before the injury.
anxiety, or depression
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 has had a head injury "usually sufficiently severe to result in loss of consciousness" and then 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 is 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 have 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 hormones that are deficient.
Management of post-concussion syndrome typically involves treatments addressing specific symptoms; for example, people can take pain relievers for headaches and medicine to relieve depression or insomnia. Rest is advised, but is only somewhat effective. Physical and behavioral therapy may also be prescribed for problems such as loss of balance and difficulties with attention, respectively.
Though no pharmacological treatments exist for PCS, doctors may prescribe medications used for symptoms that also occur in other conditions; for example, antidepressants are used for the depression that frequently follows MTBI. Side effects of medications may affect people suffering the consequences of MTBI more severely than they do others, and thus it is recommended that medications be avoided if possible; there may be a benefit to avoiding narcotic medications. In addition, some pain medications prescribed for headaches can cause rebound headaches when they are discontinued.
Psychological treatment, to which about 40% of PCS patients are referred for consultation, has been shown to reduce problems. Ongoing disabilities may be treated with therapy to improve function at work, or in social or other contexts. Therapy aims to aid in the gradual return to work and other preinjury activities, as symptoms permit. A protocol for PCS treatment has been designed based on the principles behind Cognitive behavioral therapy (CBT), a psychotherapy aimed at influencing disturbed emotions by improving thoughts and behaviors. CBT may help prevent persistence of iatrogenic symptoms – those that occur because health care providers create the expectation that they will. A risk exists that the "power of suggestion" may worsen symptoms and cause long-term disabilities; therefore, when counseling is indicated, the therapist must take a psychological origin of symptoms into account and not assume that all symptoms are a direct result of neurological damage from the injury.
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.
Education about symptoms and their usual time course is a part of psychological therapy, and is most effective when provided soon after the injury. Since stress exacerbates post-concussion symptoms, and vice versa, an important part of treatment is reassurance that PCS symptoms are normal, and education about how to deal with impairments. One study found that PCS patients who were coached to return to activities gradually, told what symptoms to expect, and trained how to manage them had a reduction in symptoms compared to a control group of uninjured people. Early education has been found to reduce symptoms in children as well.
Neurotherapy is an operant conditioning test where patients are given conditional audio/visual rewards after producing particular types of brainwave activity. Recent neurotherapy improvements in QEEG can identify the specific brainwave patterns that need to be corrected. Studies have shown that neurotherapy is effective in the treatment of post-concussion syndrome and other disorders with similar symptoms.
The prognosis for PCS is generally considered positive, with total resolution of symptoms in many, but not all, cases. For 50% of people, post-concussion symptoms go away within a few days to several weeks after the original injury occurs. In others, symptoms may remain for three to six months, but evidence indicates that many cases are completely resolved within 6 months. The majority of symptoms are largely gone in about half of people with concussion one month after the injury, and about two thirds of people with minor head trauma are nearly symptom-free within three months. Persistent, often severe headaches are the longest lingering symptom in most cases and are the most likely symptom to never fully resolve. It is frequently stated in the literature and considered to be common knowledge that 15–30% of people with PCS have not recovered by a year after the injury, but this estimate is imprecise because it is based on studies of people admitted to a hospital, the methodologies of which have been criticized. In approximately 15% of people, symptoms may persist for years or be permanent. If symptoms are not resolved by one year, they are likely to be permanent, though improvements may occur after even two or three years, or may suddenly occur after a long time without much improvement. Older people and those who have previously suffered another head injury are likely to take longer to recover.
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 who 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 slight risk of developing the serious 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 and Gridiron football players, are at risk for chronic traumatic encephalopathy (or the related variant dementia pugilistica), a severe, chronic disorder involving a decline in mental and physical abilities.
It is not known exactly how common PCS is. Estimates of the prevalence at 3 months post-injury are between 24 and 84%, a variation possibly caused by different populations or study methodologies. The estimated incidence of PPCS is around 10% of MTBI cases. Since PCS by definition only exists in people who have suffered a head injury, demographics and risk factors are similar to those for head injury; for example, young adults are at higher risk than others for receiving head injury, and, consequently, of developing PCS.
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.
A wide range of factors have been identified as being predictive of PCS, including low socioeconomic status, previous MTBI, a serious associated injury, headaches, an ongoing court case, and female gender. Being older than 40 and being female have also been identified as being predictive of a diagnosis of PCS, and women tend to experience more severe symptoms. In addition, the development of PCS can be predicted by having a history of alcohol abuse, low cognitive abilities before the injury, a personality disorder, or a medical illness not related to the injury. PCS is also more prevalent in people with a history of psychiatric conditions such as clinical depression or anxiety before the injury.
Mild brain injury-related factors that increase the risk for persisting post-concussion symptoms include an injury associated with acute headache, dizziness, or nausea; an acute Glasgow Coma Score of 13 or 14; and suffering another head injury before recovering from the first. The risk for developing PCS also appears to be increased in people who have traumatic memories of the injury or expect to be disabled by the injury.
The symptoms that occur after a concussion have been described in various reports and writings for hundreds of years. The idea that this set of symptoms forms a distinct entity began to attain greater recognition in the latter part of the 19th century. John Erichsen, a surgeon from London, played an important role in developing the study of PCS. The controversy surrounding the cause of PCS began in 1866 when Erichsen published a paper about persisting symptoms after sustaining mild head trauma. He suggested that the condition was due to "molecular disarrangement" to the spine. The condition was originally called "railroad spine" because most of the injuries studied had happened to railroad workers. While some of his contemporaries agreed that the syndrome had an organic basis, others attributed the symptoms to psychological factors or to outright feigning. In 1879, the idea that a physical problem was responsible for the symptoms was challenged by Rigler, who suggested that the cause of the persisting symptoms was actually "compensation neurosis": the railroad's practice of compensating workers who had been injured was bringing about the complaints. Later, the idea that hysteria was responsible for the symptoms after a mild head injury was suggested by Charcot. Controversy about the syndrome continued through the 20th century. During World War I many soldiers suffered from puzzling symptoms after being close to a detonation but without any evidence of a head wound. The illness was called shell shock, and a psychological explanation was eventually favoured. By 1934 the current concept of PCS had replaced ideas of hysteria as the cause of post-concussion symptoms. British authorities banned the term shell shock during World War II to avoid an epidemic of cases, and the term posttrauma concussion state was coined in 1939 to describe "disturbance of consciousness with no immediate or obvious pathologic change in the brain". The term postconcussion syndrome was in use by 1941.
In 1961, H. Miller first used the term "accident neurosis" to refer to the syndrome which is now called PCS and asserted that the condition only occurs in situations where people stand to be compensated for the injury. The real causes of the condition remain unclear.
Though no universally accepted definition of postconcussive syndrome exists, most of the literature defines the syndrome as the development of at least 3 of the following symptoms: headache, dizziness, fatigue, irritability, impaired memory and concentration, insomnia, and lowered tolerance for noise and light., One complication in diagnosis 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 64% of people with TBI, 11% of those with brain injuries, and 7% of those with other injuries met the DSM-IV criteria for post-concussion syndrome. Many of these PCS sufferers were misdiagnosed as having other unrelated conditions due to commonality of symptoms. (see diagnosis, below).
Headache is one of the criteria for PCS, but it is notably undetermined where the headache comes from. Couch, Lipton, Stewart and Scher (2007) argue that headaches, one of the hallmarks of PCS, occur in a variety of injuries to the head and neck. Further, Lew et al. (2006)  reviewed ample studies comparing headaches to post-traumatic headaches and found that there is wide heterogeneity in the source and causes of headaches. They point out that the International Headache Society lists 14 known causes of headaches, as well. Furthermore, the headaches may be better accounted for by mechanical causes, such as whiplash, which is often mistaken for PCS. An additional possibility is that Post-traumatic Stress Disorder can account for some cases diagnosed as PCS, but for emotional regulation as well.
Depression, post-traumatic stress disorder, and chronic pain share 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. Additionally, it has been found that neuroendocrinology may account for depressive symptoms and stress management due to irregularities in cortisol regulation, and thyroid hormone regulation. Lastly, there is evidence that major depression following TBI is quite common, but may be better accounted for with a diagnosis of dysexecutive syndrome 
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).
- Daniel Amen, post-concussion expert for the National Football League
- Rao V, Lyketsos C (2000). "Neuropsychiatric sequelae of traumatic brain injury". Psychosomatics 41 (2): 95–103. doi:10.1176/appi.psy.41.2.95. PMID 10749946.
- Mittenberg W, Strauman S (2000). "Diagnosis of mild head injury and the postconcussion syndrome". Journal of Head Trauma Rehabilitation 15 (2): 783–791. doi:10.1097/00001199-200004000-00003. PMID 10739967.
- McHugh T, Laforce R, Gallagher P, Quinn S, Diggle P, Buchanan L (2006). "Natural history of the long-term cognitive, affective, and physical sequelae of a minor traumatic brain injury". Brain and Cognition 60 (2): 209–11. doi:10.1016/j.bandc.2004.09.018. PMID 16646125.
- Bigler ED (2008). "Neuropsychology and clinical neuroscience of persistent post-concussive syndrome". Journal of the International Neuropsychological Society 14 (1): 1–22. doi:10.1017/S135561770808017X. PMID 18078527.
- Iverson GL, Lange RT (2003). "Examination of "postconcussion-like" symptoms in a healthy sample". Applied Neuropsychology 10 (3): 137–144. doi:10.1207/S15324826AN1003_02. PMID 12890639.
- King NS (1996). "Emotional, neuropsychological, and organic factors: Their use in the prediction of persisting postconcussion symptoms after moderate and mild head injuries". Journal of Neurology, Neurosurgery, and Psychiatry 61 (1): 75–81. doi:10.1136/jnnp.61.1.75. PMC 486463. PMID 8676166.
- Ryan LM, Warden DL (2003). "Post concussion syndrome". International Review of Psychiatry 15 (4): 310–6. doi:10.1080/09540260310001606692. PMID 15276952.
- Kushner D (1998). "Mild traumatic brain injury: Toward understanding manifestations and treatment". Archives of Internal Medicine 158 (15): 1617–24. doi:10.1001/archinte.158.15.1617. PMID 9701095.
- Weight DG (1998). "Minor head trauma". Psychiatric Clinics of North America 21 (3): 609–624. doi:10.1016/S0193-953X(05)70026-5. PMID 9774799.
- Anderson T, Heitger M, Macleod AD (2006). "Concussion and mild head injury". Practical Neurology 6 (6): 342–357. doi:10.1136/jnnp.2006.106583.
- Hall RC, Hall RC, Chapman MJ (2005). "Definition, diagnosis, and forensic implications of postconcussional syndrome". Psychosomatics 46 (3): 195–202. doi:10.1176/appi.psy.46.3.195. PMID 15883140.
- Maskell F, Chiarelli P, Isles R (2006). "Brain Injury": 293–305.
- Barth JT, Ruff R, Espe-Pfeifer P (2006). "Mild traumatic brain injury: Definitions". In Nicholson, Keith; Young, Gerald; Andrew K. Kane. Psychological Knowledge in Court: PTSD, Pain and TBI. Berlin: Springer. pp. 271–7. ISBN 0-387-25609-1.
- Margulies S (September 2000). "The postconcussion syndrome after mild head trauma: Is brain damage overdiagnosed? Part 1". Journal of Clinical Neuroscience 7 (5): 400–8. doi:10.1054/jocn.1999.0681. PMID 10942660.
- King NS. 2003. Post-concussion syndrome: clarity amid the controversy?. Accessed January 1, 2007.
- Shaw NA (2002). "The neurophysiology of concussion". Progress in Neurobiology 67 (4): 281–344. doi:10.1016/S0301-0082(02)00018-7. PMID 12207973.
- Jagoda A, Riggio S (2000). "Mild traumatic brain injury and the postconcussive syndrome". Emergency Medicine Clinics of North America 18 (2): 355–363. doi:10.1016/S0733-8627(05)70130-9. PMID 10798893.
- Evans RW (1992). "The postconcussion syndrome and the sequelae of mild head injury". Neurologic Clinics 10 (4): 815–47. PMID 1435659.
- Cobb S, Battin B (2004). "Second-impact syndrome". The Journal of School Nursing 20 (5): 262–7. doi:10.1177/10598405040200050401. PMID 15469376.
- Olver J (2005). "Traumatic brain injury—the need for support and follow up". Australian Family Physician 34 (4): 269–71. PMID 15861750.
- Merck manuals online medical library. 2003. Concussion. Accessed May 11, 2008.
- Goodyear B, Umetsu D (2002). "Selected issues in forensic neuropsychology". In Van Dorsten B. Forensic Psychology: From Classroom to Courtroom. New York: Kluwer Academic/Plenum. pp. 289–290. ISBN 0-306-47270-8.
- Jacobson RR (August 1995). "The post-concussional syndrome: physiogenesis, psychogenesis and malingering. An integrative model". Journal of Psychosomatic Research 39 (6): 675–693. doi:10.1016/0022-3999(95)00006-5. PMID 8568727.
- Iverson GL (2005). "Outcome from mild traumatic brain injury". Current Opinion in Psychiatry 18 (3): 301–317. doi:10.1097/01.yco.0000165601.29047.ae. PMID 16639155.
- Jorge RE (2005). "Neuropsychiatric consequences of traumatic brain injury: A review of recent findings". Current Opinion in Psychiatry 18 (3): 289–299. doi:10.1097/01.yco.0000165600.90928.92. PMID 16639154.
- Yeates KO, Taylor HG (2005). "Neurobehavioural outcomes of mild head injury in children and adolescents". Pediatric Rehabilitation 8 (1): 5–16. doi:10.1080/13638490400011199. PMID 15799131.
- Bryant RA (2008). "Disentangling mild traumatic brain injury and stress reactions". New England Journal of Medicine 358 (5): 525–7. doi:10.1056/NEJMe078235. PMID 18234757.
- Lee LK (2007). "Controversies in the sequelae of pediatric mild traumatic brain injury". Pediatric Emergency Care 23 (8): 580–3. doi:10.1097/PEC.0b013e31813444ea. PMID 17726422.
- Boake C, McCauley SR, Levin HS, Pedroza C, Contant CF, Song JX, et al. (2005). "Diagnostic criteria for postconcussional syndrome after mild to moderate traumatic brain injury". Journal of Neuropsychiatry and Clinical Neurosciences 17 (3): 350–6. doi:10.1176/appi.neuropsych.17.3.350. PMID 16179657.
- ICD-10, International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10) Version for 2010, F07.2 Postconcussional syndrome, World Health Organization.
- Sivák S, Kurca E, Jancovic D, Petriscák S, Kucera P (2005). "[Contemporary view on mild brain injuries in adult population]" (PDF). Cas. Lek. Cesk. (in Slovak) 144 (7): 445–50; discussion 451–4. PMID 16161536.
- Mittenberg W, Canyock EM, Condit D, Patton C (2001). "Treatment of post-concussion syndrome following mild head injury". Journal of Clinical and Experimental Neuropsychology 23 (6): 829–836. doi:10.1076/jcen.23.6.829.1022. PMID 11910547.
- Legome E. 2006. Postconcussive syndrome. eMedicine.com. Accessed January 1, 2007.
- Bazarian JJ, Atabaki S (August 2001). "Predicting postconcussion syndrome after minor traumatic brain injury". Academic Emergency Medicine 8 (8): 788–795. doi:10.1111/j.1553-2712.2001.tb00208.x. PMID 11483453.
- Hulshoff Pol HE, Hijman R, Baaré WF, van Eekelen S, van Ree JM (August 2000). "Odor discrimination and task duration in young and older adults". Chemical Senses 25 (4): 461–464. doi:10.1093/chemse/25.4.461. PMID 10944510.
- Iverson GL, Zasler ND, Lange RT (2006). "Post-concussive disorder". In Zasler ND, Katz DI, Zafonte RD. Brain Injury Medicine: Principles and Practice. Demos Medical Publishing. pp. 374–385. ISBN 1-888799-93-5. Retrieved 2008-06-05.
- Rees PM (2003). "Contemporary issues in mild traumatic brain injury". Archives of Physical Medicine and Rehabilitation 84 (12): 1885–94. doi:10.1016/j.apmr.2003.03.001. PMID 14669199.
- Schapiro S, Mandel S, Sataloff RT (1993). Minor Head Trauma: Assessment, Management, and Rehabilitation. Berlin: Springer-Verlag. p. 152. ISBN 0-387-97943-3.
- Willer B, Leddy JJ (September 2006). "Management of concussion and post-concussion syndrome". Current Treatment Options in Neurology 8 (5): 415–426. doi:10.1007/s11940-006-0031-9. PMID 16901381.
- Schnadower D, Vazquez H, Lee J, Dayan P, Roskind CG (2007). "Controversies in the evaluation and management of minor blunt head trauma in children". Current Opinion in Pediatrics 19 (3): 258–264. doi:10.1097/MOP.0b013e3281084e85. PMID 17505183.
- McAllister TW, Arciniegas D (2002). "Evaluation and treatment of postconcussive symptoms". NeuroRehabilitation 17 (4): 265–83. PMID 12547976.
- Ropper AH, Gorson KC (2007). "Clinical practice. Concussion". New England Journal of Medicine 356 (2): 166–172. doi:10.1056/NEJMcp064645. PMID 17215534.
- Gualtieri CT (1999). "The pharmacologic treatment of mild brain injury". In Varney NR, Roberts RJ. The Evaluation and Treatment of Mild Traumatic Brain Injury. Hillsdale, N.J.: Lawrence Erlbaum Associates. pp. 411–2. ISBN 0-8058-2394-8.
- Alexander MP (1995). "Mild traumatic brain injury: Pathophysiology, natural history, and clinical management". Neurology 45 (7): 1253–60. doi:10.1212/WNL.45.7.1253. PMID 7617178.
- Duff J (2004). "The Usefulness of Quantitative EEG(QEEG) and Neurotherapy in the Assessment and Treatment of Post-concussion Syndrome". Clinical EEG and Neuroscience 35 (4).
- McCrea 2008, pp. 163–4
- Komaroff A, Harvard University Harvard Business School (1999). The Harvard Medical School Family Health Guide. New York: Simon & Schuster. p. 359. ISBN 0-684-84703-5.
- Signoretti, S; Lazzarino, G; Tavazzi, B; Vagnozzi, R (October 2011). "The pathophysiology of concussion". PM&R 3 (10 Suppl 2): S359–68. doi:10.1016/j.pmrj.2011.07.018. PMID 22035678.
- Wetjen, NM; Pichelmann, MA; Atkinson, JL (October 2010). "Second impact syndrome: concussion and second injury brain complications". Journal of the American College of Surgeons 211 (4): 553–7. doi:10.1016/j.jamcollsurg.2010.05.020. PMID 20822744.
although the syndrome might be uncommon
- Saulle M, Greenwald BD (2012). "Chronic traumatic encephalopathy: a review". Rehabil Res Pract 2012: 816069. doi:10.1155/2012/816069. PMC 3337491. PMID 22567320.
- Necajauskaite O, Endziniene M, Jureniene K (2005). "The prevalence, course and clinical features of post-concussion syndrome in children". Medicina (Kaunas) 41 (6): 457–64. PMID 15998982.
- Lovell MR, Fazio V; Fazio (February 2008). "Concussion management in the child and adolescent athlete". Current Sports Medicine Reports 7 (1): 12–5. doi:10.1097/01.CSMR.0000308671.45558.e2. PMID 18296938.
- Traumatic Brain Injury: Hope Through Research. NINDS. Publication date February 2002. NIH Publication No. 02-2478. Prepared by: Office of Communications and Public Liaison, National Institute of Neurological Disorders and Stroke, National Institutes of Health
- Benton AL, Levin HS, Eisenberg HM (1989). "Historical notes on the postconcussion syndrome". Mild Head Injury. Oxford [Oxfordshire]: Oxford University Press. pp. 3–5. ISBN 0-19-505301-X.
- Evans RW (2004). "Post-traumatic headaches". Neurological Clinics 22 (1): 237–249. doi:10.1016/S0733-8619(03)00097-5. PMID 15062537.
- Jones E, Fear NT, Wessely S; Fear; Wessely (November 2007). "Shell shock and mild traumatic brain injury: A historical review". The American Journal of Psychiatry 164 (11): 1641–5. doi:10.1176/appi.ajp.2007.07071180. PMID 17974926.
- McCrea, MA (2008). Mild Traumatic Brain Injury and Postconcussion Syndrome: The New Evidence Base for Diagnosis and Treatment. Oxford [Oxfordshire]: Oxford University Press. p. 157. ISBN 0-19-532829-9.
- Couch JR, Lipton RB, Stewart WF, Scher AI; Lipton; Stewart; Scher (September 2007). "Head or neck injury increases the risk of chronic daily headache: a population-based study". Neurology 69 (11): 1169–77. doi:10.1212/01.wnl.0000276985.07981.0a. PMID 17846416.
- Lew HL, Lin PH, Fuh JL, Wang SJ, Clark DJ, Walker WC; Lin; Fuh; Wang; Clark; Walker (July 2006). "Characteristics and treatment of headache after traumatic brain injury: a focused review". Am J Phys Med Rehabil 85 (7): 619–27. doi:10.1097/01.phm.0000223235.09931.c0. PMID 16788394.
- Kasch H, Bach FW, Jensen TS; Bach; Jensen (June 2001). "Handicap after acute whiplash injury: a 1-year prospective study of risk factors". Neurology 56 (12): 1637–43. doi:10.1212/WNL.56.12.1637. PMID 11425927.
- Hickling EJ, Blanchard EB, Silverman DJ, Schwarz SP; Blanchard; Silverman; Schwarz (March 1992). "Motor vehicle accidents, headaches and post-traumatic stress disorder: assessment findings in a consecutive series". Headache 32 (3): 147–51. doi:10.1111/j.1526-4610.1992.hed3203147.x. PMID 1563947.
- Jorge R, Robinson RG; Robinson (November 2003). "Mood disorders following traumatic brain injury". Int Rev Psychiatry 15 (4): 317–27. doi:10.1080/09540260310001606700. PMID 15276953.
- Abreu, B.C.; Zgaljardic, D.; Borod, J.C.; Seale, G.; Temple, R.O.; Ostir, G.V.; Ottenbacher, K.J. (2009). "Emotional Regulation, Processing, and Recovery After Acquired Brain Injury". In Matuska, K.; Christiansen, C.H.; Polatajko, H.; Davis, J.A. Life Balance: Multidisciplinary Theories and Research. Thorofare NJ: SLACK/AOTA Press. pp. 223–240. ISBN 1556429061.
- Jorge RE, Robinson RG, Moser D, Tateno A, Crespo-Facorro B, Arndt S; Robinson; Moser; Tateno; Crespo-Facorro; Arndt (January 2004). "Major depression following traumatic brain injury". Arch. Gen. Psychiatry 61 (1): 42–50. doi:10.1001/archpsyc.61.1.42. PMID 14706943.
- Smith DH (2006). "Postconcussional symptoms not a syndrome". Psychosomatics 47 (3): 271–2. doi:10.1176/appi.psy.47.3.271. PMID 16684949.