|Classification and external resources|
Post-concussion syndrome, also known as postconcussive syndrome or PCS, and historically called shell shock, is a set of symptoms that may continue for weeks, months, or occasionally a year or more after a concussion – a mild form of traumatic brain injury (TBI). 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.
Signs and symptoms 
The abbreviation 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 two to four weeks after concussion and can be long lasting. Also, headache and dizziness occur immediately after the injury and can be long lasting.
The main PCS symptom is headache. While most people have headaches of the same type they experienced before the injury, people with PCS often report more frequent or longer-lasting headaches. Between 30 and 90% of people treated for PCS report having more headaches than they did before the injury, and between 8 and 32% still report them a year after the injury.
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.
Psychological and behavioral 
Psychological symptoms, 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, mood swings, anger, decreased libido, impulsiveness, loss of social judgment, and lack of ability to tolerate stress or alcohol. People with PCS may also display a lack of emotion, or emotional lability. Another common symptom—apathy, or lack of motivation—may result directly from the syndrome or be secondary to depression.
Higher mental functions 
Cognitive or mental symptoms can include confusion or impaired cognition, problems with attention, impaired judgment, and amnesia or other problems with memory, especially short-term memory. Problems with memory and attention are the longest-lasting cognitive symptoms; one in four people with PCS still suffer from memory problems a year after the injury. PCS may cause slowed information processing and reactions to stimuli or difficulty with abstract thinking or problem solving. People may also experience a decrease in abilities related to work performance or social interaction. While cognitive symptoms usually resolve within a few months of injury, physical and emotional symptoms can last longer. Most cognitive symptoms clear within half a year of the injury, and the longest-lasting ones, such as memory, attention and language problems, usually resolve within a year.
The question of the cause or causes of PCS and PPCS has been heavily debated for many years. It is not known to exactly what degree the symptoms are due to organic factors, such as microscopic damage to the brain, and to other factors, such as psychological ones. The subjectivity of the complaints complicates assessment and makes it difficult to determine whether symptoms are being exaggerated or feigned.
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.
It has been convincingly shown 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 PPCS. In one study, levels of daily stress were found to be correlated to PCS symptoms in both mildly brain injured subjects and controls, but in another, stress was not significantly related to symptoms. Iatrogenic effects (those caused by the medical intervention) may also occur, for example when people focus and dwell on the idea that their brains may be damaged, or when they are led to expect symptoms to occur. Expectation of symptoms may also lead head-injured people 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 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.
Differential diagnosis 
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.
Management of post-concussion syndrome typically involves rest and potentially psychotherapy to address emotional difficulties. Specific symptoms may also be addressed; for example, people can take pain relievers for headaches and medicine to relieve depression, dizziness, or nausea. 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 especially for PCS, if necessary 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, headache medications may 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 excellent, with total resolution of symptoms in the large majority of cases. For most 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 most cases are completely resolved within that time. 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 symptom-free within three months. It is frequently stated in the literature and considered to be common knowledge that 10–20% of people with PCS have not recovered by a year after the injury, but this may be an overestimate because it is based on studies of people admitted to a hospital, the methodologies of which have been criticized. In a small minority of people, symptoms may persist for years or be permanent; however, it has not been conclusively shown that permanent neurological symptoms ever result from an uncomplicated concussion. 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.
Risk factors 
Factors that predict that a person will suffer PPCS (persistent PCS) include low socioeconomic status, previous MTBI, a serious associated injury, headaches, an ongoing court case, and female gender. Being older than 40 and being female are related to both PCS and PPCS. Women are more likely than men to suffer PCS, and likely to suffer it more severely. In addition, the development of PPCS may be predicted by having a history of alcohol abuse, low cognitive abilities before the injury, a personality disorder or a medical or psychiatric illness. PCS is more prevalent in people who had psychiatric symptoms 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; 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.
The symptoms that occur after a concussion have been known for hundreds of years. The idea that this set of symptoms forms a distinct entity began to attain wide 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 was started in 1866 when Erichsen published a paper about persisting symptoms after sustaining mild head trauma. He suggested that the condition was due to injury by "molecular disarrangement" to the spine, and 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 showing no evidence of a head wound. The illness was called shell shock, and a psychological explanation was eventually favoured. The current concept of PCS had replaced ideas of hysteria as the cause of post-concussion symptoms by 1934. 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 "accident neurosis" to refer to symptoms of PCS and asserted that the condition only ever occurs in situations where people stand to be compensated for the injury, but this contention was widely challenged. The real causes of the condition remain unclear.
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).
Headaches is one of the criteria for PCS, but it is notably controversial where these headaches come from. Couch, Lipton, Stewart & 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 examining headaches with 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. Further, the headaches may be better accounted for by medical causes, such as whiplash, which is often mistook for PCS. An additional possibility is that Post-traumatic Stress Disorder can better account for PCS, not just because of the headaches, but for emotional regulation as well.
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. 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).
- Jones E, Fear NT, Wessely S (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.
- 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.
- 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.
- 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 mild traumatic brain injury". Brain and Cognition 60 (2): 209–11. PMID 16646125.
- Legome E. 2006. Postconcussive syndrome. eMedicine.com. Accessed January 1, 2007.
- 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.
- Evans RW (2004). "Post-traumatic headaches". Neurological Clinics 22 (1): 237–249. doi:10.1016/S0733-8619(03)00097-5. PMID 15062537.
- 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.
- 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.
- Cobb S, Battin B (2004). "Second-impact syndrome". The Journal of School Nursing 20 (5): 262–7. doi:10.1177/10598405040200050401. PMID 15469376.
- 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.
- 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.
- 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.
- Yeates KO, Taylor HG (2005). "Neurobehavioural outcomes of mild head injury in children and adolescents". Pediatric Rehabilitation 8 (1): 5–16. PMID 15799131.
- Merck manuals online medical library. 2003. Concussion. Accessed May 11, 2008.
- Evans RW (1992). "The postconcussion syndrome and the sequelae of mild head injury". Neurologic Clinics 10 (4): 815–47. PMID 1435659.
- Olver J (2005). "Traumatic brain injury—the need for support and follow up". Australian Family Physician 34 (4): 269–71. PMID 15861750.
- 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.
- 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.
- 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.[dead link]
- 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 (2011 Oct). "The pathophysiology of concussion". PM & R : the journal of injury, function, and rehabilitation 3 (10 Suppl 2): S359–68. doi:10.1016/j.pmrj.2011.07.018. PMID 22035678.
- Wetjen, NM; Pichelmann, MA; Atkinson, JL (2010 Oct). "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 (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 (inactive 2010-03-18). 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 (1989). "Historical notes on the postconcussion syndrome". Mild Head Injury. Oxford [Oxfordshire]: Oxford University Press. pp. 3–5. ISBN 0-19-505301-X. Unknown parameter
- 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 (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 (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 (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 (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 (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 (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.