Concussion

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Concussion
Deceleration can exert rotational forces in the brain, especially the midbrain and diencephalon.
ICD-10 S06.0
ICD-9 850
MedlinePlus 000799
eMedicine aaem/123  sports/27
MeSH D001924

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Overview

Concussion, from the Latin concutere ("to shake violently"),[1] is the most common and least serious type of traumatic brain injury. The terms mild brain injury, mild traumatic brain injury (MTBI), mild head injury (MHI), and minor head trauma and concussion may be used interchangeably,[2][3] although the latter is often treated as a narrower category.[4] The term 'concussion', has been used for centuries and is still commonly used in sports medicine, while 'MTBI' is a technical term used more commonly nowadays in general medical contexts. Frequently defined as a head injury with a transient loss of brain function, concussion can cause a variety of physical, cognitive, and emotional symptoms.

Concussion can be diagnosed and assigned a level of severity based largely on symptoms. Treatment involves monitoring and rest. Symptoms usually go away entirely within three weeks, though they may persist, or complications may occur.[5] Repeated concussions can cause cumulative brain damage such as dementia pugilistica or severe complications such as second-impact syndrome.

Due to factors such as widely varying definitions and possible underreporting of concussion, the rate at which it occurs annually is not known; however it may be more than 6 per 1000 people.[6] Common causes include sports injuries, bicycle accidents, auto accidents, and falls; the latter two are the most frequent causes among adults.[7] Concussion may be caused by a blow to the head, or by acceleration or deceleration forces without a direct impact. The forces involved disrupt cellular processes in the brain for days or weeks.

It is not known whether the concussed brain is structurally damaged the way it is in other types of brain injury (albeit to a lesser extent) or whether concussion mainly entails a loss of function with physiological but not structural changes.[8] Cellular damage has reportedly been found in concussed brains, but it may have been due to artifacts from the studies.[9] A debate about whether structural damage exists in concussion has raged for centuries and is ongoing.

Definitions

No single definition of concussion, mild head injury,[10] or mild traumatic brain injury is universally accepted, though a variety of definitions have been offered.[11] In 2001, the first International Symposium on Concussion in Sport was organized by the International Olympic Committee Medical Commission and other sports federations.[12] A group of experts called the Concussion in Sport Group met there and defined concussion as "a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces."[13] They agreed that concussion typically involves temporary impairment of neurological function which quickly resolves by itself, and that neuroimaging normally shows no gross structural changes to the brain as the result of the condition.[5]

According to the classic definition, no structural brain damage occurs in concussion;[14] it is a functional state, meaning that symptoms are caused primarily by temporary biochemical changes in neurons, taking place for example at their cell membranes and synapses.[5] However, in recent years researchers have included injuries in which structural damage does occur under the rubric of concussion. According to the National Institute for Health and Clinical Excellence definition, concussion may involve a physiological or physical disruption in the brain's synapses.[15]

Definitions of mild traumatic brain injury (MTBI) have been inconsistent since the 1970s, but the World Health Organization's International Statistical Classification of Diseases and Related Health Problems (ICD-10) described MTBI-related conditions in 1992, providing a consistent, authoritative definition across specialties.[3] In 1993, the American Congress of Rehabilitation Medicine defined MTBI as 30 minutes or fewer of loss of consciousness (LOC), 24 hours or fewer of post-traumatic amnesia (PTA), and a Glasgow Coma Scale (GCS) score of at least 13.[16] In 1994, the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders defined MTBI using PTA and LOC.[3] Other definitions of MTBI incorporate focal neurological deficit and altered mental status, in addition to PTA and GCS.[11]

Concussion falls under the classification of mild TBI.[17] It is not clear whether concussion is implied in mild brain injury or mild head injury.[18] "MTBI" and "concussion" are often treated as synonyms in medical literature.[16] However, other injuries such as intracranial hemorrhages (e.g. intra-axial hematoma, epidural hematoma, and subdural hematoma) are not necessarily precluded in MTBI[5] or mild head injury,[19][20] but they are in concussion.[21] MTBI associated with abnormal neuroimaging may be considered "complicated MTBI".[22] "Concussion" can be considered to imply a state in which brain function is temporarily impaired and "MTBI" to imply a pathophysiological state, but in practice few researchers and clinicians distinguish between the terms.[5] Descriptions of the condition, including the severity and the area of the brain affected, are now used more often than "concussion" in clinical neurology.[23]

Although the term "concussion" is still used in sports literature as interchangeable with "MHI" or "MTBI", the general clinical medical literature now uses "MTBI" instead.[24]

Controversy exists about whether the definition of concussion should include only those injuries in which loss of consciousness occurs.[1] Historically, concussion by definition involved a loss of consciousness, but the definition has changed over time to include a change in consciousness, such as amnesia.[25] The best-known concussion grading scales count head injuries in which loss of consciousness does not occur to be mild concussions and those in which it does to be more severe.[26]

Causes

The leading causes of MTBI in adults are falls and vehicle accidents, and other causes include sports injuries, assaults, industrial and work-related injuries, and injuries that occur in the home.[11] Among children aged 5 to 14, sports and bicycle accidents cause the greatest number of concussions.[7] Soldiers are at elevated risk for concussion from causes such as bomb blasts, with as many as 15% of U.S. infantry soldiers who return from the Iraq War meeting the criteria for MTBI.[27]

The relative contribution of causes of mild head injury differs by region, gender, and age.[5] For example, in Scotland and Sweden, falls account for the greatest percentage of MHIs, while in the U.S. and Australia, transportation is the largest cause.[5]

Mechanism

Rotational force is key in concussion. Punches in boxing deliver more rotational force to the head than impacts in sports such as football, and boxing carries a higher risk of concussion than football.[28]

The brain is surrounded by cerebrospinal fluid, one of the functions of which is to protect it from light trauma, but more severe impacts or the forces associated with rapid acceleration and deceleration may not be absorbed by this cushion.[8] Concussion may be caused by impact forces, in which the head strikes or is struck by something, or impulsive forces, in which the head moves without itself being subject to blunt trauma (for example, when the chest hits something and the head snaps forward).[4]

Forces may cause linear, rotational, or angular movement of the brain, or a combination of these types of motion.[4] In rotational movement, the head turns around its center of gravity, and in angular movement it turns on an axis other than its center of gravity.[4] The amount of rotational force is thought to be the major type of force to cause concussion[29] and the largest component in its severity.[5] Studies with athletes have shown that the amount of force and the location of the impact are not necessarily correlated to the severity of the concussion or its symptoms, and have called into question the threshold for concussion previously thought to exist at around 70-75g.[30][31]

The parts of the brain most affected by rotational forces are the midbrain and diencephalon.[1][7] It is thought that the forces from the injury disrupt the normal cellular activities in the reticular activating system located in these areas, and that this disruption produces the loss of consciousness often seen in concussion.[7] Other areas of the brain that may be affected include the upper part of the brain stem, the fornix, the corpus callosum, the temporal lobe, and the frontal lobe.[32]

Pathophysiology

In both animals and humans, MTBI can alter the brain's physiology for hours to weeks, setting into motion a variety of pathological events.[33] Though these events are thought to interfere with neuronal and brain function, the metabolic processes that follow concussion are reversed in a large majority of affected brain cells; however a few cells may die after the injury.[22]

Included in the cascade of events unleashed in the brain by concussion is impaired neurotransmission, loss of regulation of ions, deregulation of energy use and cellular metabolism, and a reduction in cerebral blood flow.[22] Excitatory neurotransmitters, chemicals such as glutamate that serve to stimulate nerve cells, are released in excessive amounts as the result of the injury.[34] The resulting cellular excitation causes neurons to fire excessively.[35] This creates an imbalance of ions such as potassium and calcium across the cell membranes of neurons (a process like excitotoxicity).[22] Since the neuron firing involves a net influx of positively charged ions into the cell, the ionic imbalance causes cells to have a more positive membrane potential (i.e. it leads to neuronal depolarization). This depolarization in turn causes ion pumps that serve to restore resting potential within cells to work more than they normally do.[22] This increased need for energy leads cells to require greater-than-usual amounts of glucose, which is made into ATP, an important source of energy for cells.[22] The brain may stay in this state of hypermetabolism for days or weeks.[36] At the same time, cerebral blood flow is relatively reduced for unknown reasons,[37] though the reduction in blood flow is not as severe as it is in ischemia.[22] Thus cells get less glucose than they normally do, which causes an "energy crisis".[37]

Concurrently with these processes, the activity of mitochondria may be reduced, which causes cells to rely on anaerobic metabolism to produce energy, which increases levels of the byproduct lactate.[22]

For a period of minutes to days after a concussion, the brain is especially vulnerable to changes in intracranial pressure, blood flow, and anoxia.[37] According to studies performed on animals, large numbers of neurons can die during this period in response to slight, normally innocuous changes in blood flow.[37]

Concussion involves diffuse brain injury (as opposed to focal brain injury), meaning that the dysfunction occurs over a widespread area of the brain rather than in a particular spot.[38] Concussion is thought to be a milder type of diffuse axonal injury because axons may be injured to a minor extent due to stretching.[4] Animal studies in which primates were concussed have revealed damage to brain tissues such as small petechial hemorrhages and axonal injury.[39] Axonal damage has been found in the brains of concussion sufferers who died from other causes, but inadequate blood flow to the brain due to other injuries may have contributed to the damage.[9]

Signs and symptoms

Common symptoms in MTBI include headache and difficulty concentrating.[16]

Concussion can be associated with a variety of symptoms, which typically occur rapidly after the injury.[12] Early symptoms usually subside within days or weeks.[9] The number and type of symptoms a person suffers varies widely.[11]

Physical

Headache is the most common MTBI symptom.[16] Other symptoms include dizziness, vomiting, nausea, lack of motor coordination, difficulty balancing,[16] or other problems with movement or sensation. Visual symptoms include light sensitivity,[37] seeing bright lights,[40] blurred vision,[9] and double vision.[41] Tinnitus, or a ringing in the ears, is also commonly reported.[9] In one in about seventy concussions, concussive convulsions occur, but these are not actual post-traumatic epilepsy, which is a symptom of more serious injury.[42] Concussive convulsions are thought to result from temporary loss of brain function rather than from structural damage and are usually associated with a good outcome.[43]

Cognitive and emotional

Cognitive symptoms include confusion, disorientation, and difficulty focusing attention. Loss of consciousness may occur but is not necessarily correlated with the severity of the concussion if it is brief.[13] Post-traumatic amnesia, in which the person cannot remember events leading up to the injury or after it, or both, is a hallmark of concussion.[16] Confusion, another concussion hallmark, may be present immediately or may develop over several minutes.[16] A patient may, for example, repeatedly ask the same questions,[44] be slow to respond to questions or directions, have a vacant stare, or have slurred[16] or incoherent speech.[45] Other MTBI symptoms include changes in sleeping patterns[9] and difficulty with reasoning,[41] concentrating, and performing everyday activities.[16]

Affective results of concussion include crankiness, loss of interest in favorite activities or items,[46] tearfulness,[4] and displays of emotion that are inappropriate to the situation.[45] Common symptoms in concussed children include restlessness, lethargy, and irritability.[36]

Diagnosis

Diagnosis of MTBI is based on physical and neurological exams, duration of unconsciousness (usually less than 30 minutes) and post-traumatic amnesia (PTA; usually less than 24 hours), and the Glasgow Coma Scale (MTBI sufferers have scores of 13 to 15).[47] Neuropsychological tests exist to measure cognitive function.[9] The tests may be administered hours, days, or weeks after the injury, or at different times to determine whether there is a trend in the patient's condition.[48] Athletes may be tested before a sports season begins to provide a baseline comparison in the event of an injury.[49]

Unequal pupil size is a sign of a brain injury more serious than concussion.

Health care providers examine head trauma survivors to ensure that the injury is not a more severe medical emergency such as an intracranial hemorrhage. Indications that screening for more serious injury is needed include worsening of symptoms such as headache, persistent vomiting,[50] increasing disorientation or a deteriorating level of consciousness,[51] seizures, and unequal pupil size.[52] Patients with such symptoms, or who are at higher risk for a more serious brain injury, are given MRIs or CT scans to detect brain lesions and are observed by medical staff.

Health care providers make the decision about whether to give a CT scan using the Glasgow Coma Scale.[7] In addition, they may be more likely to perform a CT scan on people who would be difficult to observe after discharge or those who are intoxicated, at risk for bleeding, older than 60,[7] or younger than 16. Most concussions cannot be detected with MRI or CT scans.[29] However, changes have been reported to show up on MRI and SPECT imaging in concussed people with normal CT scans, and post-concussion syndrome may be associated with abnormalities visible on SPECT and PET scans.[22] Mild head injury may or may not produce abnormal EEG readings.[53]

Concussion may be under-diagnosed. The lack of the highly noticeable signs and symptoms that are frequently present in other forms of head injury could lead clinicians to miss the injury, and athletes may cover up their injuries in order to be allowed to remain in the competition.[24] A retrospective survey in 2005 found that more than 88% of concussions go unrecognized.[54]

Diagnosis of concussion can be complicated because it shares symptoms with other conditions. For example, post-concussion symptoms such as cognitive problems may be misattributed to brain injury when they are in fact due to post-traumatic stress disorder (PTSD).[55]

Grading systems

Main article: Concussion grading systems

At least 41 systems exist to measure the severity, or grade, of a mild head injury,[5] and there is little agreement among professionals about which is the best.[40] Several of the systems use loss of consciousness and amnesia as the primary determinants of the severity of the concussion.[40]

The decision about when to allow athletes to return to contact sports is frequently based on the grade of concussion. Injured athletes are prohibited from returning to play before they are symptom-free during rest and exertion and their neuropsychological tests are normal again, in order to avoid a risk of cumulative effects.

Three grading systems are followed most widely: one was developed by Robert Cantu, one by the Colorado Medical Society, and a third by the American Academy of Neurology.[26] Each divides concussion into three grades, as summarized in the following table:[40]

Comparison of concussion grading scales
  Grade I Grade II Grade III
Cantu guidelines Post-traumatic amnesia <30 minutes, no loss of consciousness Loss of consciousness <5 minutes or amnesia lasting 30 minutes–24 hours Loss of consciousness >5 minutes or amnesia >24 hours
Colorado Medical Society guidelines Confusion, no loss of consciousness Confusion, post-traumatic amnesia, no loss of consciousness Any loss of consciousness
American Academy of Neurology guidelines Confusion, symptoms last <15 minutes, no loss of consciousness Symptoms last >15 minutes, no loss of consciousness Loss of consciousness (IIIa, coma lasts seconds, IIIb for minutes)

Prevention

Prevention of MTBI involves taking general measures to prevent traumatic brain injury, such as wearing seat belts and using airbags in cars.[16] Older people are encouraged to try to prevent falls, for example by keeping floors free of clutter and wearing thin, flat, shoes with hard soles that do not interfere with balance.[46]

Use of protective equipment such as headgear has been found to reduce the number of concussions in athletes.[28] Improvements in the design of protective athletic gear such as helmets may decrease the number and severity of such injuries.[56] Changes to the rules or the practices of enforcing existing rules in sports, such as those against "head-down tackling", or "spearing", which is associated with a high injury rate, may also prevent concussions.[28]

Treatment

Usually concussion symptoms go away without treatment,[57] and no specific treatment exists.[58] About one percent of people who receive treatment for MTBI need surgery for a brain lesion.[47] Traditionally, concussion sufferers are prescribed rest,[58] including plenty of sleep at night plus rest during the day.[52] Health care providers recommend a gradual return to normal activities at a pace that does not cause symptoms to worsen.[52] Education about symptoms, how to manage them, and their normal time course can lead to an improved outcome.[11]

Medications may be prescribed to treat symptoms such as sleep problems and depression.[11] Analgesics such as ibuprofen can be taken for the headaches that frequently occur after concussion.[5] Concussed individuals are advised not to drink alcohol or take drugs that have not been approved by a doctor, as they could impede healing.[52]

Observation to monitor for worsening condition is an important part of treatment.[59] Health care providers recommend that those suffering from concussion return for further medical care and evaluation 24 to 72 hours after the concussive event if the symptoms worsen. Athletes, especially intercollegiate or professional athletes, are typically followed closely by team trainers during this period. But others may not have access to this level of health care and may be sent home with no medical person monitoring them unless the situation gets worse. Patients may be released from the hospital to the care of a trusted person with orders to return if they display worsening symptoms[7] or those which might indicate an emergent condition, like unconsciousness or altered mental status; convulsions; severe, persistent headache; extremity weakness; vomiting; or new bleeding or deafness in either or both ears.[60] Repeated observation for the first 24 hours after concussion is recommended; however it is not known whether it is necessary to wake the patient up every few hours.[7]

Prognosis and lasting effects

MTBI has a mortality rate of almost zero.[47] The symptoms of most concussions resolve within weeks, but problems may persist.[5] It is not common for problems to be permanent, and outcome is usually excellent.[22] People over age 55 may take longer to heal from MTBI or may heal incompletely.[61] Similarly, factors such as a previous head injury or a coexisting medical condition have been found to predict longer-lasting post-concussion symptoms.[39] Other factors that may lengthen recovery time after MTBI include psychological problems such as substance abuse or clinical depression, poor health before the injury or additional injuries sustained during it, and life stress.[22] Longer periods of amnesia or loss of consciousness immediately after the injury may indicate longer recovery times from residual symptoms.[62] For unknown reasons, having had one concussion significantly increases a person's risk of having another.[48] The prognosis may differ between concussed adults and children.[48] Little research has been done on concussion in the pediatric population, but concern exists that severe concussions could interfere with brain development in children.[48]

Post-concussion syndrome

Main article: Post-concussion syndrome

In post-concussion syndrome, symptoms do not resolve for weeks, months, or years after a concussion, and may occasionally be permanent.[63] Symptoms may include headaches, dizziness, fatigue, anxiety, memory and attention problems, sleep problems, and irritability.[64] There is no scientifically established treatment, and rest, a recommended recovery technique, has limited effectiveness.[58] Symptoms usually go away on their own within months.[21] The question of whether the syndrome is due to structural damage or other factors such as psychological ones, or a combination of these, has long been the subject of debate.[55]

Cumulative effects

Cumulative effects of concussions are poorly understood. The severity of concussions and their symptoms may worsen with successive injuries, even if a subsequent injury occurs months or years after an initial one.[65] Symptoms may be more severe and changes in neurophysiology can occur with the third and subsequent concussions.[48] Studies have had conflicting findings on whether athletes have longer recovery times after repeat concussions and whether cumulative effects such as impairment in cognition and memory occur.[28]

Cumulative effects may include psychiatric disorders and loss of long-term memory. For example, the risk of developing clinical depression has been found to be significantly greater for retired football players with a history of three or more concussions than for those with no concussion history.[66] Three or more concussions is also associated with a five-fold greater chance of developing Alzheimer's disease earlier and a three-fold greater chance of developing memory deficits.[66]

Dementia pugilistica

Main article: Dementia pugilistica

Chronic encephalopathy is an example of the cumulative damage that can occur as the result of multiple concussions or less severe blows to the head. The condition called dementia pugilistica, or "punch drunk" syndrome, which is associated with boxers, can result in cognitive and physical deficits such as parkinsonism, speech and memory problems, slowed mental processing, tremor, and inappropriate behavior.[67] It shares features with Alzheimer's disease.[68]

Second-impact syndrome

Main article: Second-impact syndrome

Second-impact syndrome, in which the brain swells dangerously after a minor blow, may occur in very rare cases. The condition may develop in people who receive a second blow days or weeks after an initial concussion, before its symptoms have gone away.[37] No one is certain of the cause of this often fatal complication, but it is commonly thought that the swelling occurs because the brain's arterioles lose the ability to regulate their diameter, causing a loss of control over cerebral blood flow.[48] As the brain swells, intracranial pressure rapidly rises.[50] The brain can herniate, and the brain stem can fail within five minutes.[37] Except in boxing, all cases have occurred in athletes under age 20.[34] Due to the very small number of documented cases, the diagnosis is controversial, and doubt exists about its validity.[69]

Epidemiology

Annual incidence of MTBI by age group in Canada[70]

Most cases of traumatic brain injury are concussions. A World Health Organization (WHO) study estimated that between 70 and 90% of head injuries that receive treatment are mild.[6] However, due to underreporting and to the widely varying definitions of concussion and MTBI, it is difficult to estimate how common the condition is.[3] Estimates of the incidence of concussion may be artificially low, for example due to underreporting. At least 25% of MTBI sufferers fail to get assessed by a medical professional.[22] The WHO group reviewed studies on the epidemiology of MTBI and found a hospital treatment rate of 1–3 per 1000 people, but since not all concussions are treated in hospitals, they estimated that the rate per year in the general population is over 6 per 1000 people.[6]

Young children have the highest concussion rate among all age groups.[7] A Canadian study found that the yearly incidence of MTBI is lower in older age groups (graph at right).[70] Studies suggest males suffer MTBI at about twice the rate of their female counterparts.[6] However, female athletes may be at a higher risk for suffering concussion than their male counterparts.[71]

Up to five percent of sports injuries are concussions.[34] The U.S. Centers for Disease Control and Prevention estimates that 300,000 sports-related concussions occur yearly in the U.S., but that number includes only athletes who lost consciousness.[72] Since loss of consciousness is thought to occur in less than 10% of concussions,[73] the CDC estimate is likely lower than the real number.[72] Sports in which concussion is particularly common include football and boxing (a boxer aims to "knock out", i.e. give a mild traumatic brain injury to, the opponent). The injury is so common in the latter that several medical groups have called for a ban on the sport, including the American Academy of Neurology, the World Medical Association, and the medical associations of the UK, the U.S., Australia, and Canada.[74]

Due to the lack of a consistent definition, the economic costs of MTBI are not known, but they are estimated to be very high.[75] These high costs are due in part to the large percentage of hospital admissions for head injury that are due to mild head trauma,[18] but indirect costs such as lost work time and early retirement account for the bulk of the costs.[75] These direct and indirect costs cause the expense of mild brain trauma to rival that of moderate and severe head injuries.[76]

Histopathology: Cerebral contusion

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History and controversy

The Hippocratic Corpus mentioned concussion.[62]

The Hippocratic Corpus, collection of medical works from ancient Greece, mentions concussion, later translated to commotio cerebri, and discusses loss of speech, hearing and sight that can result from "commotion of the brain".[62] This idea of disruption of mental function by 'shaking of the brain' remained the widely accepted understanding of concussion until the 19th century.[62] The Persian physician Muhammad ibn Zakarīya Rāzi was the first to write about concussion as distinct from other types of head injury in the 10th century AD.[77] He may have been the first to use the term "cerebral concussion", and his definition of the condition, a transient loss of function with no physical damage, set the stage for the medical understanding of the condition for centuries.[4] In the 13th century, the physician Lanfranc of Milan's Chiurgia Magna described concussion as brain "commotion", also recognizing a difference between concussion and other types of traumatic brain injury (though many of his contemporaries did not), and discussing the transience of post-concussion symptoms as a result of temporary loss of function from the injury.[77] In the 14th century, the surgeon Guy de Chauliac pointed out the relatively good prognosis of concussion as compared to more severe types of head trauma such as skull fractures and penetrating head trauma.[77] In the 16th century, the term "concussion" came into use, and symptoms such as confusion, lethargy, and memory problems were described.[77] The 16th century physician Ambroise Paré used the term commotio cerebri,[4] as well as "shaking of the brain", "commotion", and "concussion".[62]

Guillaume Dupuytren distinguished between concussion and unconsciousness associated with brain contusion.[62]

Until the 17th century, concussion was usually described by its clinical features, but after the invention of the microscope, more physicians began exploring underlying physical and structural mechanisms.[77] However, the prevailing view in the 17th century was that the injury did not result from physical damage, and this view continued to be widely held throughout the 18th century.[77] The word "concussion" was used at the time to describe the state of unconsciousness and other functional problems that resulted from the impact, rather than a physiological condition.[77]

In 1839, Guillaume Dupuytren described brain contusions, which involve many small hemorrhages, as contusio cerebri and showed the difference between unconsciousness associated with damage to the brain parenchyma and that due to concussion, without such injury.[62] In 1941, animal experiments showed that no macroscopic damage occurs in concussion.[62][78]

The debate over whether concussion is a functional or structural phenomenon is ongoing.[77] Structural damage has been found in the mildly traumatically injured brains of animals, but it is not clear whether these changes would be applicable to humans.[1] Such changes in brain structure could be responsible for certain symptoms such as visual disturbances, but other sets of symptoms, especially those of a psychological nature, are more likely to be caused by reversible pathophysiological changes in cellular function that occur after concussion, such as alterations in neurons' biochemistry.[5] These reversible changes could also explain why dysfunction is frequently temporary.[77] A task force of head injury experts called the Concussion In Sport Group met in 2001 and decided that "concussion may result in neuropathological changes but the acute clinical symptoms largely reflect a functional disturbance rather than structural injury."[12]

References

  1. ↑ 1.0 1.1 1.2 1.3 Pearce JM (2007). "Observations on concussion. A review". European Neurology. 59 (3–4): 113–119. doi:10.1159/000111872. PMID 18057896.
  2. ↑ National Center for Injury Prevention and Control (2003). "Report to congress on mild traumatic brain injury in the United States: Steps to prevent a serious public health problem" (PDF). Atlanta, GA: Centers for Disease Control and Prevention. Retrieved 2008-01-19.
  3. ↑ 3.0 3.1 3.2 3.3 Petchprapai N, Winkelman C (2007). "Mild traumatic brain injury: determinants and subsequent quality of life. A review of the literature". Journal of Neuroscience Nursing. 39 (5): 260–272. PMID 17966292.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 Sivák Š, Kurča E, Jančovič D, Petriščák Š, Kučera P (2005). "An outline of the current concepts of mild brain injury with emphasis on the adult population" (PDF). Časopis Lėkařů Českých. 144 (7): 445–450.
  5. ↑ 5.00 5.01 5.02 5.03 5.04 5.05 5.06 5.07 5.08 5.09 5.10 5.11 Anderson T, Heitger M, Macleod AD (2006). "Concussion and mild head injury (requires free registration)". Practical Neurology. 6: 342–357. doi:10.1136/jnnp.2006.106583. External link in |title= (help)
  6. ↑ 6.0 6.1 6.2 6.3 Cassidy JD, Carroll LJ, Peloso PM, Borg J, von Holst H, Holm L; et al. (2004). "Incidence, risk factors and prevention of mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury". Journal of Rehabilitation Medicine. 36 (Supplement 43): 28–60. PMID 15083870.
  7. ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 Ropper AH, Gorson KC (2007). "Clinical practice. Concussion". New England Journal of Medicine. 356 (2): 166–172. doi:10.1056/NEJMcp064645. PMID 17215534.
  8. ↑ 8.0 8.1 Shaw NA (2002). "The neurophysiology of concussion". Progress in Neurobiology. 67 (4): 281–344. doi:10.1016/S0301-0082(02)00018-7. PMID 12207973.
  9. ↑ 9.0 9.1 9.2 9.3 9.4 9.5 9.6 Rees PM (2003). "Contemporary issues in mild traumatic brain injury". Archives of Physical Medicine and Rehabilitation. 84 (12): 1885–1894. PMID 14669199.
  10. ↑ Satz P, Zaucha K, McCleary C, Light R, Asarnow R, Becker D (1997). "Mild head injury in children and adolescents: A review of studies (1970–1995)". Psychological Bulletin. 122 (2): 107–131. PMID 9283296.
  11. ↑ 11.0 11.1 11.2 11.3 11.4 11.5 Comper P, Bisschop SM, Carnide N, Tricco A (2005). "A systematic review of treatments for mild traumatic brain injury". Brain Injury. 19 (11): 863–880. doi:10.1080-0269050400025042 Check |doi= value (help). ISSN 0269-9052. PMID 16296570.
  12. ↑ 12.0 12.1 12.2 Aubry M, Cantu R, Dvorak J, Graf-Baumann T, Johnston K, Kelly J, Lovell M, McCrory P, Meeuwisse W, Schamasch P; Concussion in Sport Group. (2002). "Summary and agreement statement of the first international conference on concussion in sport, Vienna 2001. Recommendations for the improvement of safety and health of athletes who may suffer concussive injuries (requires free registration)". British Journal of Sports Medicine. 36 (1): 6–10. PMID 11867482. External link in |title= (help)
  13. ↑ 13.0 13.1 Cantu RC (2006). "An overview of concussion consensus statements since 2000" (PDF). Neurosurgical Focus. 21 (4:E3): 1–6.
  14. ↑ Parkinson D (1999). "Concussion confusion". Critical Reviews in Neurosurgery. 9 (6): 335–339. doi:10.1007/s003290050153. ISSN 1433-0377.
  15. ↑ "Head Injury: Triage, Assessment, Investigation and Early Management of Head Injury in Infants, Children and Adults" (PDF). National Institute for Health and Clinical Excellence. September 2007. ISBN 0-9549760-5-3. Retrieved 2008-01-26.
  16. ↑ 16.0 16.1 16.2 16.3 16.4 16.5 16.6 16.7 16.8 16.9 Kushner D (1998). "Mild Traumatic brain injury: Toward understanding manifestations and treatment". Archives of Internal Medicine. 158 (15): 1617–1624. PMID 9701095.
  17. ↑ Lee LK (2007). "Controversies in the sequelae of pediatric mild traumatic brain injury". Pediatric Emergency Care. 23 (8): 580–583. doi:10.1097/PEC.0b013e31813444ea. PMID 17726422.
  18. ↑ 18.0 18.1 Benton AL, Levin HS, Eisenberg HM (1989). Mild Head Injury. Oxford [Oxfordshire]: Oxford University Press. pp. v. ISBN 0-19-505301-X.
  19. ↑ van der Naalt J (2001). "Prediction of outcome in mild to moderate head injury: A review". Journal of Clinical and Experimental Neuropsychology. 23 (6): 837–851. doi:10.1076/jcen.23.6.837.1018. PMID 11910548.
  20. ↑ Savitsky EA, Votey SR (2000). "Current controversies in the management of minor pediatric head injuries". American Journal of Emergency Medicine. 18 (1): 96–101. doi:10.1016/S0735-6757(00)90060-3. PMID 10674544.
  21. ↑ 21.0 21.1 Parikh S, Koch M, Narayan RK (2007). "Traumatic brain injury". International Anesthesiology Clinics. 45 (3): 119–135. doi:10.1097/AIA.0b013e318078cfe7. PMID 17622833.
  22. ↑ 22.00 22.01 22.02 22.03 22.04 22.05 22.06 22.07 22.08 22.09 22.10 22.11 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.
  23. ↑ Larner AJ, Barker RJ, Scolding N, Rowe D (2005). The A-Z of Neurological Practice: a Guide to Clinical Neurology. Cambridge, UK: Cambridge University Press. p. 199. ISBN 0521629608.
  24. ↑ 24.0 24.1 Barth JT, Varney NR, Ruchinskas RA, Francis JP (1999). "Mild head injury: The new frontier in sports medicine". In Varney NR, Roberts RJ. The Evaluation and Treatment of Mild Traumatic Brain Injury. Hillsdale, New Jersey: Lawrence Erlbaum Associates. pp. 85–86. ISBN 0-8058-2394-8. Retrieved 2008-03-06.
  25. ↑ Ruff RM, Grant I (1999). "Postconcussional disorder: Background to DSM-IV and future considerations". In Varney NR, Roberts RJ. The Evaluation and Treatment of Mild Traumatic Brain Injury. Hillsdale, New Jersey: Lawrence Erlbaum Associates. p. 320. ISBN 0-8058-2394-8.
  26. ↑ 26.0 26.1 Cobb S, Battin B (2004). "Second-impact syndrome". The Journal of School Nursing. 20 (5): 262–267. PMID 15469376.
  27. ↑ Hoge CW, McGurk D, Thomas DL, Cox AL, Engel CC, Castro CA (2008). "Mild traumatic brain injury in U.S. soldiers returning from Iraq". The New England Journal of Medicine. 358 (5): 453–463. PMID 18234750.
  28. ↑ 28.0 28.1 28.2 28.3 Pellman EJ, Viano DC (2006). "Concussion in professional football: Summary of the research conducted by the National Football League's Committee on Mild Traumatic Brain Injury" (PDF). Neurosurgical Focus. 21 (4): E12. PMID 17112190.
  29. ↑ 29.0 29.1 Poirier MP (2003). "Concussions: Assessment, management, and recommendations for return to activity (abstract)". Clinical Pediatric Emergency Medicine. 4 (3): 179–185. doi:10.1016/S1522-8401(03)00061-2. External link in |title= (help)
  30. ↑ Guskiewicz KM, Mihalik JP, Shankar V; et al. (2007). "Measurement of head impacts in collegiate football players: Relationship between head impact biomechanics and acute clinical outcome after concussion". Neurosurgery. 61 (6): 1244–1252, discussion 1252–1253. PMID 18162904.
  31. ↑ Gever D (December 7, 2007). "Any football helmet hit can cause potential concussion". MedPage Today, LLC. Retrieved 2008-02-27.
  32. ↑ 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.
  33. ↑ McAllister TW, Sparling MB, Flashman LA, Saykin AJ (2001). "Neuroimaging findings in mild traumatic brain injury". Journal of Clinical and Experimental Neuropsychology. 23 (6): 775–791. doi:10.1076/jcen.23.6.775.1026. PMID 11910544.
  34. ↑ 34.0 34.1 34.2 Herring SA, Bergfeld JA, Boland A, Boyajian-O'Neil LA, Cantu RC, Hershman E; et al. (2005). "Concussion (mild traumatic brain injury) and the team physician: A consensus statement" (PDF). Medicine and Science in Sports and Exercise. American College of Sports Medicine, American Academy of Family Physicians, American Academy of Orthopaedic Surgeons, American Medical Society for Sports Medicine, American Orthopaedic Society for Sports Medicine, American Osteopathic Academy of Sports Medicine: 2012–2016. doi:10.1249/01.mss.0000186726.18341.70.
  35. ↑ Giza CC, Hovda DA (2001). "The neurometabolic cascade of concussion". Journal of Athletic Training. 36 (3): 228–235. PMID 12937489.
  36. ↑ 36.0 36.1 Heegaard W, Biros M (2007). "Traumatic brain injury". Emergency Medicine Clinics of North America. 25 (3): 655–678, viii. doi:10.1016/j.emc.2007.07.001. PMID 17826211.
  37. ↑ 37.0 37.1 37.2 37.3 37.4 37.5 37.6 Bowen AP (2003). "Second impact syndrome: A rare, catastrophic, preventable complication of concussion in young athletes". Journal of Emergency Nursing. 29 (3): 287–289. doi:10.1067/men.2003.90. PMID 12776088.
  38. ↑ Hardman JM, Manoukian A (2002). "Pathology of head trauma". Neuroimaging Clinics of North America. 12 (2): 175–187, vii. doi:10.1016/S1052-5149(02)00009-6. PMID 12391630.
  39. ↑ 39.0 39.1 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.
  40. ↑ 40.0 40.1 40.2 40.3 Cantu RC (2001). "Posttraumatic retrograde and anterograde amnesia: Pathophysiology and implications in grading and safe return to play". Journal of Athletic Training. 36 (3): 244–248. PMID 12937491.
  41. ↑ 41.0 41.1 Erlanger DM, Kutner KC, Barth JT, Barnes R (1999). "Neuropsychology of sports-related head enjury: Dementia pugilistica to post concussion syndrome". The Clinical Neuropsychologist. 13 (2): 193–209. doi:10.1076/clin.13.2.193.1963. PMID 10949160.
  42. ↑ McCrory PR, Berkovic SF (1998). "Concussive convulsions. Incidence in sport and treatment recommendations". Sports Medicine. 25 (2): 131–136. PMID 9519401.
  43. ↑ Perron AD, Brady WJ, Huff JS (2001). "Concussive convulsions: Emergency department assessment and management of a frequently misunderstood entity". Academic Emergency Medicine. 8 (3): 296–298. PMID 11229957.
  44. ↑ Quality Standards Subcommittee of the American Academy of Neurology (1997). "Practice Parameter: The Management of Concussion in Sports (Summary Statement)" (PDF). American Academy of Neurology. pp. 1–7. Retrieved 2008-03-05.
  45. ↑ 45.0 45.1 Anderson MK, Hall SJ, Martin M (2004). Foundations of Athletic Training: Prevention, Assessment, and Management. Lippincott Williams & Wilkins. ISBN 0781750016. Retrieved 2008-01-09. Unknown parameter |Pages= ignored (|pages= suggested) (help)
  46. ↑ 46.0 46.1 Mayo Clinic Staff (2007). "Concussion". Mayo Clinic. Retrieved 2008-01-10.
  47. ↑ 47.0 47.1 47.2 Borg J, Holm L, Cassidy JD; et al. (2004). "Diagnostic procedures in mild traumatic brain injury: Results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury". Journal of Rehabilitation Medicine. 36 (Supplement 43): 61–75. doi:10.1080/16501960410023822. PMID 15083871.
  48. ↑ 48.0 48.1 48.2 48.3 48.4 48.5 Moser RS, Iverson GL, Echemendia RJ, Lovell MR, Schatz P, Webbe FM; et al. (2007). "Neuropsychological evaluation in the diagnosis and management of sports-related concussion". Archives of Clinical Neuropsychology. 22 (8): 909–916. PMID 17988831.
  49. ↑ Maroon JC, Lovell MR, Norwig J, Podell K, Powell JW, Hartl R (2000). "Cerebral concussion in athletes: Evaluation and neuropsychological testing". Neurosurgery. 47 (3): 659–669, discussion 669–672. PMID 10981754.
  50. ↑ 50.0 50.1 Cook RS, Schweer L, Shebesta KF, Hartjes K, Falcone RA (2006). "Mild traumatic brain injury in children: Just another bump on the head?". Journal of Trauma Nursing. 13 (2): 58–65. PMID 16884134.
  51. ↑ Kay A, Teasdale G (2001). "Head injury in the United Kingdom". World Journal of Surgery. 25 (9): 1210–1220. doi:10.1007/s00268-001-0084-6. PMID 11571960.
  52. ↑ 52.0 52.1 52.2 52.3 "Facts About Concussion and Brain Injury". Centers for Disease Control and Prevention. 2006. Retrieved 2008-01-13.
  53. ↑ Binder LM (1986). "Persisting symptoms after mild head injury: A review of the postconcussive syndrome". Journal of Clinical and Experimental Neuropsychology. 8 (4): 323–346. doi:10.1080/01688638608401325. PMID 3091631.
  54. ↑ Delaney JS, Abuzeyad F, Correa JA, Foxford R (2005). "Recognition and characteristics of concussions in the emergency department population". Journal of Emergency Medicine. 29 (2): 189–197. doi:10.1016/j.jemermed.2005.01.020. PMID 16029831.
  55. ↑ 55.0 55.1 Bryant RA (2008). "Disentangling mild traumatic brain injury and stress reactions". New England Journal of Medicine. 358 (5): 525–527. doi:10.1056/NEJMe078235. PMID 18234757.
  56. ↑ Levy ML, Ozgur BM, Berry C, Aryan HE, Apuzzo ML (2004). "Birth and evolution of the football helmet". Neurosurgery. 55 (3): 656–661, discussion 661–662. PMID 15335433.
  57. ↑ Komaroff A (1999). The Harvard Medical School Family Health Guide. New York: Simon & Schuster. p. 359. ISBN 0-684-84703-5.
  58. ↑ 58.0 58.1 58.2 Willer B, Leddy JJ (2006). "Management of concussion and post-concussion syndrome". Current Treatment Options in Neurology. 8 (5): 415–426. doi:10.1007/s11940-006-0031-9. ISSN 1534-3138. PMID 16901381.
  59. ↑ Anderson MK (2003). Fundamentals of Sports Injury Management. Hagerstown, MD: Lippincott Williams & Wilkins. p. 79. ISBN 0-7817-3272-7. Retrieved 2008-03-06.
  60. ↑ "Information About NICE Clinical Guideline" (PDF). National Institute for Health and Clinical Excellence. September, 2007. Retrieved 2008-01-26. Check date values in: |date= (help)
  61. ↑ Alexander MP (1995). "Mild traumatic brain injury: Pathophysiology, natural history, and clinical management". Neurology. 45 (7): 1253–1260. PMID 7617178.
  62. ↑ 62.0 62.1 62.2 62.3 62.4 62.5 62.6 62.7 Masferrer R, Masferrer M, Prendergast V, Harrington TR (2000). "Grading scale for cerebral concussions". BNI Quarterly. Barrow Neurological Institute. 16 (1). ISSN 0894-5799.
  63. ↑ Ryan LM, Warden DL (2003). "Post concussion syndrome". International Review of Psychiatry. 15 (4): 310–316. doi:10.1080/09540260310001606692. PMID 15276952.
  64. ↑ 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): 350–356. doi:doi: 10.1176/appi.neuropsych.17.3.350 Check |doi= value (help). PMID 16179657.
  65. ↑ Harmon KG (1999). "Assessment and management of concussion in sports". American Family Physician. 60 (3): 887–892, 894. PMID 10498114.
  66. ↑ 66.0 66.1 Cantu RC (2007). "Chronic traumatic encephalopathy in the National Football League". Neurosurgery. 61 (2): 223–225. doi:10.1227/01.NEU.0000255514.73967.90. PMID 17762733.
  67. ↑ Mendez MF (1995). "The neuropsychiatric aspects of boxing". International Journal of Psychiatry in Medicine. 25 (3): 249–262. PMID 8567192.
  68. ↑ Jordan BD (2000). "Chronic traumatic brain injury associated with boxing". Seminars in Neurology. 20 (2): 179–85. doi:10.1055/s-2000-9826. PMID 10946737.
  69. ↑ McCrory P (2001). "Does second impact syndrome exist?". Clinical Journal of Sport Medicine. 11 (3): 144–149. PMID 11495318.
  70. ↑ 70.0 70.1 Gordon KE, Dooley JM, Wood EP (2006). "Descriptive epidemiology of concussion". Pediatric Neurology. 34 (5): 376–378. doi:10.1016/j.pediatrneurol.2005.09.007. PMID 16647998.
  71. ↑ McKeever CK, Schatz P (2003). "Current issues in the identification, assessment, and management of concussions in sports-related injuries". Applied Neuropsychology. 10 (1): 4–11. PMID 12734070.
  72. ↑ 72.0 72.1 Langlois JA, Rutland-Brown W, Wald MM (2006). "The epidemiology and impact of traumatic brain injury: A brief overview". Journal of Head Trauma Rehabilitation. 21 (5): 375–378. PMID 16983222.
  73. ↑ Cantu RC (1998). "Second-impact syndrome". Clinics in Sports Medicine. 17 (1): 37–44. PMID 9475969.
  74. ↑ Solomon GS, Johnston KM, Lovell MR (2006). The Heads-up on Sport Concussion. Champaign, IL: Human Kinetics Pub. p. 77. ISBN 0736060081. Retrieved 2008-03-06.
  75. ↑ 75.0 75.1 Borg J, Holm L, Peloso PM, Cassidy JD, Carroll LJ, von Holst H; et al. (2004). "Non-surgical intervention and cost for mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury". Journal of Rehabilitation Medicine. 36 (Supplement 43): 76–83. PMID 15083872.
  76. ↑ Kraus JF, Chu LD (2005). "Epidemiology". In Silver JM, McAllister TW, Yudofsky SC. Textbook Of Traumatic Brain Injury. American Psychiatric Pub., Inc. p. 23. ISBN 1585621056.
  77. ↑ 77.0 77.1 77.2 77.3 77.4 77.5 77.6 77.7 77.8 McCrory PR, Berkovic SF (2001). "Concussion: The history of clinical and pathophysiological concepts and misconceptions". Neurology. 57 (12): 2283–89. PMID 11756611.
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