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Friday, June 12, 2020

Concussion

From Wikipedia, the free encyclopedia

Concussion
Other namesMild brain injury, mild traumatic brain injury (mTBI), mild head injury (MHI), minor head trauma
Concussion mechanics.svg
Acceleration (g-forces) can exert rotational forces in the brain, especially the midbrain and diencephalon.
SpecialtyEmergency medicine, neurology
SymptomsHeadache, trouble with thinking, memory or concentration, nausea, blurry vision, sleep disturbances, mood changes
DurationUp to 4 weeks
CausesMotor vehicle collisions, falls, sports injuries, bicycle accidents
Risk factorsDrinking alcohol
Diagnostic methodBased on symptoms
PreventionHelmets when bicycling or motorbiking
TreatmentPhysical and cognitive rest for a day or two with a gradual return to activities
MedicationParacetamol (acetaminophen), NSAIDs
Frequency6 per 1,000 people a year

Concussion, also known as mild traumatic brain injury (mTBI), is typically defined as a head injury that temporarily affects brain functioning. Symptoms may include loss of consciousness (LOC); memory loss; headaches; difficulty with thinking, concentration or balance; nausea; blurred vision; sleep disturbances; and mood changes. Any of these symptoms may begin immediately, or appear days after the injury. It is not unusual for symptoms to last 2 weeks in adults and 4 weeks in children. Fewer than 10% of sports-related concussions among children are associated with loss of consciousness.

Common causes include motor vehicle collisions, falls, sports injuries and bicycle accidents. Risk factors include drinking alcohol and a prior history of concussion. The mechanism of injury involves either a direct blow to the head or forces elsewhere on the body that are transmitted to the head. This is believed to result in neuron dysfunction, as there is increased glucose requirements but not enough blood supply. Diagnosis requires less than 30 minutes of LOC, memory loss of less than 24 hours, and a Glasgow coma scale score of 13 to 15. Otherwise, it is considered a moderate or severe traumatic brain injury.

Prevention of concussions includes the use of a helmet when bicycling or motorbiking. Treatment generally involves physical and cognitive rest for a day or two, with a gradual return to activities. Prolonged periods of rest may slow recovery and result in greater depression and anxiety. Paracetamol (acetaminophen) or NSAIDs may be recommended to help with a headache. Physiotherapy may be useful for persistent balance problems; cognitive behavioral therapy may be useful for mood changes. Evidence to support the use of hyperbaric oxygen therapy and chiropractic therapy is lacking.

Worldwide, concussions are estimated to affect more than 3.5 per 1,000 people a year. Concussions are classified as mild traumatic brain injuries and are the most common type of TBIs. Males and young adults are most commonly affected. Outcomes are generally good. Another concussion before the symptoms of a prior concussion have resolved is associated with worse outcomes. Repeated concussions may also increase the risk in later life of chronic traumatic encephalopathy, Parkinson's disease and depression.

Video explanation of concussions in children

Signs and symptoms

Concussions are associated with a variety of symptoms, which typically occur rapidly after the injury. Early symptoms usually subside within days or weeks. The number and type of symptoms any one individual has varies. The severity of the initial symptoms is the strongest predictor of recovery time.

Physical

Headaches are the most common mTBI symptom. Others include dizziness, vomiting, nausea, lack of motor coordination, difficulty balancing, or other problems with movement or sensation. Visual symptoms include light sensitivity, seeing bright lights, blurred vision, and double vision. Tinnitus, or a ringing in the ears, is also commonly reported. In one in about seventy concussions, concussive convulsions occur, but seizures that take place during or immediately after a concussion are not "post-traumatic seizures", and, unlike post-traumatic seizures, are not predictive of post-traumatic epilepsy, which requires some form of structural brain damage, not just a momentary disruption in normal brain functioning. Concussive convulsions are thought to result from temporary loss or inhibition of motor function and are not associated either with epilepsy or with more serious structural damage. They are not associated with any particular sequelae and have the same high rate of favorable outcomes as concussions without convulsions.

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. Post-traumatic amnesia, in which events following the injury cannot be recalled, is a hallmark of concussions. Confusion, another concussion hallmark, may be present immediately or may develop over several minutes. A person may repeat the same questions, be slow to respond to questions or directions, have a vacant stare, or have slurred or incoherent speech. Other mTBI symptoms include changes in sleeping patterns and difficulty with reasoning, concentrating, and performing everyday activities.

A concussion can result in changes in mood including crankiness, loss of interest in favorite activities or items, tearfulness, and displays of emotion that are inappropriate to the situation. Common symptoms in concussed children include restlessness, lethargy, and irritability.

Mechanism

Rotational force is key in a concussion. Punches in boxing can deliver more rotational force to the head than the typical impact in American football.

Forces

The brain is surrounded by cerebrospinal fluid, which protects it from light trauma. More severe impacts, or the forces associated with rapid acceleration, may not be absorbed by this cushion. 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).

Forces may cause linear, rotational, or angular movement of the brain or a combination of them. In rotational movement, the head turns around its center of gravity and in angular movement, it turns on an axis, not through its center of gravity. The amount of rotational force is thought to be the major component in concussion and its severity. Studies with athletes have shown that the amount of force and the location of the impact are not necessarily correlated with the severity of the concussion or its symptoms, and have called into question the threshold for concussion previously thought to exist at around 70–75 g.

The parts of the brain most affected by rotational forces are the midbrain and diencephalon. 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. 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. Angular accelerations of 4600, 5900, or 7900 rad/s2 are estimated to have 25, 50, or 80% risk of mTBI respectively.

Pathophysiology

In both animals and humans, mTBI can alter the brain's physiology for hours to years, setting into motion a variety of pathological events. As one example, in animal models, after an initial increase in glucose metabolism, there is a subsequent reduced metabolic state which may persist for up to four weeks after injury. Though these events are thought to interfere with neuronal and brain function, the metabolic processes that follow concussion are reversible in a large majority of affected brain cells; however, a few cells may die after the injury.

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. Excitatory neurotransmitters, chemicals such as glutamate that serve to stimulate nerve cells, are released in excessive amounts. The resulting cellular excitation causes neurons to fire excessively. This creates an imbalance of ions such as potassium and calcium across the cell membranes of neurons (a process like excitotoxicity).

At the same time, cerebral blood flow is relatively reduced for unknown reasons, though the reduction in blood flow is not as severe as it is in ischemia. Thus cells get less glucose than they normally do, which causes an "energy crisis".

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

For a period of minutes to days after a concussion, the brain is especially vulnerable to changes in intracranial pressure, blood flow, and anoxia. According to studies performed on animals (which are not always applicable to humans), large numbers of neurons can die during this period in response to slight, normally innocuous changes in blood flow.

Concussion involves diffuse (as opposed to focal) brain injury, meaning that the dysfunction occurs over a widespread area of the brain rather than in a particular spot. It is thought to be a milder type of diffuse axonal injury, because axons may be injured to a minor extent due to stretching. Animal studies in which rodents were concussed have revealed lifelong neuropathological consequences such as ongoing axonal degeneration and neuroinflammation in subcortical white matter tracts. 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. Findings from a study of the brains of deceased NFL athletes who received concussions suggest that lasting damage is done by such injuries. This damage, the severity of which increases with the cumulative number of concussions sustained, can lead to a variety of other health issues.

The debate over whether concussion is a functional or structural phenomenon is ongoing. Structural damage has been found in the mildly traumatically injured brains of animals, but it is not clear whether these findings would apply to humans. 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. These reversible changes could also explain why dysfunction is frequently temporary. 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."

Using animal studies, the pathology of a concussion seems to start with mechanical shearing and stretching forces disrupting the cell membrane of nerve cells through "mechanoporation". This results in potassium outflow from within the cell into the extracellular space with the subsequent release of excitatory neurotransmitters including glutamate which leads to enhanced potassium extrusion, in turn resulting in sustained depolarization, impaired nerve activity and potential nerve damage. Human studies have failed to identify changes in glutamate concentration immediately post-mTBI, though disruptions have been seen 3 days to 2 weeks post-injury. In an effort to restore ion balance, the sodium-potassium ion pumps increase activity, which results in excessive ATP (adenosine triphosphate) consumption and glucose utilization, quickly depleting glucose stores within the cells. Simultaneously, inefficient oxidative metabolism leads to anaerobic metabolism of glucose and increased lactate accumulation. There is a resultant local acidosis in the brain and increased cell membrane permeability, leading to local swelling. After this increase in glucose metabolism, there is a subsequent lower metabolic state which may persist for up to 4 weeks after injury. A completely separate pathway involves a large amount of calcium accumulating in cells, which may impair oxidative metabolism and begin further biochemical pathways that result in cell death. Again, both of these main pathways have been established from animal studies and the extent to which they apply to humans is still somewhat unclear.

Diagnosis

Seizure
Worsening headache
Red flag
Difficulty waking up
Seeing double
Problem recognizing people or places
Repeated vomiting
Focal neurological problems
Unequal pupil size can be a sign of a brain injury possibly more serious than a concussion.
 

Head trauma recipients are initially assessed to exclude a more severe emergency such as an intracranial hemorrhage. This includes the "ABCs" (airway, breathing, circulation) and stabilization of the cervical spine which is assumed to be injured in any athlete who is found to be unconscious after head or neck injury. Indications that screening for more serious injury is needed include worsening of symptoms such as headaches, persistent vomiting, increasing disorientation or a deteriorating level of consciousness, seizures, and unequal pupil size. Those with such symptoms, or those who are at higher risk of a more serious brain injury, may undergo brain imaging to detect lesions and are frequently observed for 24–48 hours. A brain CT or brain MRI should be avoided unless there are progressive neurological symptoms, focal neurological findings or concern of skull fracture on exam.

Diagnosis of mTBI is based on physical and neurological examination findings, 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). Neuropsychological tests exist to measure cognitive function and the international consensus meeting in Zurich recommended the use of the SCAT2 test. Such tests may be administered hours, days, or weeks after the injury, or at different times to demonstrate any trend. Increasingly, athletes are also being tested pre-season to provide a baseline for comparison in the event of an injury, though this may not reduce risk or affect return to play.

If the Glasgow coma scale is less than 15 at two hours or less than 14 at any time, a CT is recommended. In addition, a CT scan is more likely to be performed if observation after discharge is not assured or intoxication is present, there is suspected increased risk for bleeding, age greater than 60, or less than 16. Most concussions, without complication, cannot be detected with MRI or CT scans. However, changes have been reported on MRI and SPECT imaging in those with concussion and normal CT scans, and post-concussion syndrome may be associated with abnormalities visible on SPECT and PET scans. Mild head injury may or may not produce abnormal EEG readings. A blood test known as the Brain Trauma Indicator was approved in the United States in 2018 and may be able to rule out the risk of intracranial bleeding and thus the need for a CT scan for adults.

Concussion may be under-diagnosed because of the lack of the highly noticeable signs and symptoms while athletes may minimize their injuries to remain in the competition. A retrospective survey in 2005 suggested that more than 88% of concussions are unrecognized.

Diagnosis can be complex because concussion shares symptoms with other conditions. For example, post-concussion symptoms such as cognitive problems may be misattributed to brain injury when, in fact, due to post-traumatic stress disorder (PTSD).

Classification

No single definition of concussion, minor head injury, or mild traumatic brain injury is universally accepted. In 2001, the expert Concussion in Sport Group of the first International Symposium on Concussion in Sport defined concussion as "a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces." It was agreed that concussion typically involves temporary impairment of neurological function that heals by itself within time, and that neuroimaging normally shows no gross structural changes to the brain as the result of the condition.

However, although no structural brain damage occurs according to the classic definition, some researchers have included injuries in which structural damage has occurred and the National Institute for Health and Clinical Excellence definition includes physiological or physical disruption in the brain's synapses. Also, by definition, concussion has historically involved a loss of consciousness. However, the definition has evolved over time to include a change in consciousness, such as amnesia, although controversy continues about whether the definition should include only those injuries in which loss of consciousness occurs. This debate resurfaces in some of the best-known concussion grading scales, in which those episodes involving loss of consciousness are graded as being more severe than those without.

Definitions of mild traumatic brain injury (mTBI) were inconsistent until the World Health Organization's International Statistical Classification of Diseases and Related Health Problems (ICD-10) provided a consistent, authoritative definition across specialties in 1992. Since then, various organizations such as the American Congress of Rehabilitation Medicine and the American Psychiatric Association in its Diagnostic and Statistical Manual of Mental Disorders have defined mTBI using some combination of loss of consciousness (LOC), post-traumatic amnesia (PTA), and the Glasgow Coma Scale (GCS).

Concussion falls under the classification of mild TBI, but it is not clear whether concussion is implied in mild brain injury or mild head injury. "mTBI" and "concussion" are often treated as synonyms in medical literature but other injuries such as intracranial hemorrhages (e.g. intra-axial hematoma, epidural hematoma, and subdural hematoma) are not necessarily precluded in mTBI or mild head injury, as they are in concussion. mTBI associated with abnormal neuroimaging may be considered "complicated mTBI". "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. Descriptions of the condition, including the severity and the area of the brain affected, are now used more often than "concussion" in clinical neurology.

Grading systems

At least 41 systems measure the severity, or grade, of a mild head injury, and there is little agreement about which is best. In an effort to simplify, the 2nd International Conference on Concussion in Sport, meeting in Prague in 2004, decided that these systems should be abandoned in favor of a 'simple' or 'complex' classification. However, the 2008 meeting in Zurich abandoned the simple versus complex terminology, although the participants did agree to keep the concept that most (80–90%) concussions resolve in a short period (7–10 days) and although the recovery time frame may be longer in children and adolescents.

In the past, the decision to allow athletes to return to participation was frequently based on the grade of concussion. However, current research and recommendations by professional organizations including the National Athletic Trainers' Association recommend against such use of these grading systems. Currently, injured athletes are prohibited from returning to play before they are symptom-free during both rest and exertion and until results of the neuropsychological tests have returned to pre-injury levels.

Three grading systems have been most widely followed: by Robert Cantu, the Colorado Medical Society, and the American Academy of Neurology. Each employs three grades, as summarized in the following table:

Comparison of historic concussion grading scales – not currently recommended for use by medical professionals
Guidelines  Grade I Grade II Grade III
Cantu Post-traumatic amnesia <30 consciousness="" font="" loss="" minutes="" nbsp="" no="" of=""> Loss of consciousness <5 30="" amnesia="" font="" hours="" lasting="" minutes="" nbsp="" or=""> Loss of consciousness >5 minutes or amnesia >24 hours
Colorado Medical Society Confusion, no loss of consciousness Confusion, post-traumatic amnesia, no loss of consciousness Any loss of consciousness
American Academy of Neurology Confusion, symptoms last <15 consciousness="" font="" loss="" minutes="" nbsp="" no="" of=""> Symptoms last >15 minutes, no loss of consciousness Loss of consciousness (IIIa, coma lasts seconds, IIIb for minutes)

Prevention

Prevention of mTBI involves general measures such as wearing seat belts, using airbags in cars, and protective equipment such as helmets for high-risk sports. Older people are encouraged to reduce fall risk by keeping floors free of clutter and wearing thin, flat, shoes with hard soles that do not interfere with balance.

Protective equipment such as helmets and other headgear and policy changes such as the banning of body checking in youth hockey leagues have been found to reduce the number and severity of concussions in athletes. Secondary prevention such as a Return to Play Protocol for an athlete may reduce the risk of repeat concussions. New "Head Impact Telemetry System" technology is being placed in helmets to study injury mechanisms and may generate knowledge that will potentially help reduce the risk of concussions among American Football players.

Educational interventions, such as handouts, videos, workshops, and lectures, can improve concussion knowledge of diverse groups, particularly youth athletes and coaches. Strong concussion knowledge may be associated with greater recognition of concussion symptoms, higher rates of concussion reporting behaviors, and reduced body checking-related penalties and injuries, thereby lowering risk of mTBI.

Self-reported concussion rates among U-20 and elite rugby union players in Ireland are 45–48%. Half of these injuries go unreported. Changes to the rules or 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.

Treatment

After exclusion of neck or head injury, observation should be continued for several hours. If repeated vomiting, worsening headache, dizziness, seizure activity, excessive drowsiness, double vision, slurred speech, unsteady walk, or weakness or numbness in arms or legs, or signs of basilar skull fracture develop, immediate assessment in an emergency department is needed. After this initial period has passed, there is debate as to whether it is necessary to awaken the person several times during the first night, as has traditionally been done, or whether there is more benefit from uninterrupted sleep.

Physical and cognitive rest should be continued until all symptoms have resolved with most (80–90%) concussions resolving in seven to ten days, although the recovery time may be longer in children and adolescents. Cognitive rest includes reducing activities which require concentration and attention such as school work, video games, and text messaging. It has been suggested that even leisure reading can commonly worsen symptoms in children and adolescents and proposals include time off from school and attending partial days. Since students may appear 'normal', continuing education of relevant school personnel may be needed.

Those with concussion are generally prescribed rest, including adequate nighttime sleep as well as daytime rest. Rest includes both physical and cognitive rest until symptoms clear and a gradual return to normal activities at a pace that does not cause symptoms to worsen is recommended. Education about symptoms, their management, and their normal time course, can lead to an improved outcome.

For persons participating in athletics, the 2008 Zurich Consensus Statement on Concussion in Sport recommends that participants be symptom-free before restarting and then progress through a series of graded steps. These steps include:
  • complete physical and cognitive rest
  • light aerobic activity (less than 70% of maximum heart rate)
  • sport-specific activities such as running drills and skating drills
  • non-contact training drills (exercise, coordination, and cognitive load)
  • full-contact practice
  • full-contact games.
Only when symptom-free for 24 hours, should progression to the next step occur. If symptoms occur, the person should drop back to the previous asymptomatic level for at least another 24 hours. The emphasis is on remaining symptom-free and taking it in medium steps, not on the steps themselves.

Medications may be prescribed to treat sleep problems and depression. Analgesics such as ibuprofen can be taken for headaches, but paracetamol (acetaminophen) is preferred to minimize the risk of intracranial hemorrhage. Concussed individuals are advised not to use alcohol or other drugs that have not been approved by a doctor as they can impede healing. Activation database-guided EEG biofeedback has been shown to return the memory abilities of the concussed individual to levels better than the control group.

About one percent of people who receive treatment for mTBI need surgery for a brain injury. Observation to monitor for worsening condition is an important part of treatment. 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, are typically followed closely by team athletic trainers during this period but others may not have access to this level of health care and may be sent home with minimal monitoring.

People may be released after assessment from hospital or emergency room to the care of a trusted person with instructions to return if they display worsening symptoms or those that might indicate an emergent condition such as change in consciousness, convulsions, severe headache, extremity weakness, vomiting, new bleeding or deafness in either or both ears.

Prognosis

People who have had a concussion seem more susceptible to another one, particularly if the new injury occurs before symptoms from the previous concussion have completely gone away. It is also a negative process if smaller impacts cause the same symptom severity. Repeated concussions may increase a person's risk in later life for dementia, Parkinson's disease, and depression.

mTBI has a mortality rate of almost zero. The symptoms of most concussions resolve within weeks, but problems may persist. These are seldom permanent, and the outcome is usually excellent. About 75% of children recover within three months.

The overall prognosis for recovery may be influenced by a variety of factors that include age at the 
time of injury, intellectual abilities, family environment, social support system, occupational status, coping strategies, and financial circumstances. People over age 55 may take longer to heal from mTBI or may heal incompletely. Similarly, factors such as a previous head injury or a coexisting medical condition have been found to predict longer-lasting post-concussion symptoms. 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. Longer periods of amnesia or loss of consciousness immediately after the injury may indicate longer recovery times from residual symptoms. For unknown reasons, having had one concussion significantly increases a person's risk of having another. Having previously sustained a sports concussion has been found to be a strong factor increasing the likelihood of a concussion in the future. Other strong factors include participation in a contact sport and body mass size. The prognosis may differ between concussed adults and children; little research has been done on concussion in the pediatric population, but concern exists that severe concussions could interfere with brain development in children.

A 2009 study found that individuals with a history of concussions might demonstrate a decline in both physical and mental performance for longer than 30 years. Compared to their peers with no history of brain trauma, sufferers of concussion exhibited effects including loss of episodic memory and reduced muscle speed.

Post-concussion syndrome

In post-concussion syndrome, symptoms do not resolve for weeks, months, or years after a concussion, and may occasionally be permanent. About 10% to 20% of people have post-concussion syndrome for more than a month. Symptoms may include headaches, dizziness, fatigue, anxiety, memory and attention problems, sleep problems, and irritability. There is no established treatment, and rest, a recommended recovery technique, has limited effectiveness. Symptoms usually go away on their own within months but may last for years. 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.

Cumulative effects

Cumulative effects of concussions are poorly understood, especially the effects on children. 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. Symptoms may be more severe and changes in neurophysiology can occur with the third and subsequent concussions. 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.

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 American football players with a history of three or more concussions than for those with no concussion history. Three or more concussions is also associated with a fivefold greater chance of developing Alzheimer's disease earlier and a threefold greater chance of developing memory deficits.

CTE

Chronic traumatic encephalopathy, or "CTE", 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 was previously referred to as "dementia pugilistica", or "punch drunk" syndrome, as it was first noted in boxers. The disease can lead to cognitive and physical handicaps such as parkinsonism, speech and memory problems, slowed mental processing, tremor, depression, and inappropriate behavior. It shares features with Alzheimer's disease.

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 second blow days or weeks after an initial concussion before its symptoms have gone away. 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. As the brain swells, intracranial pressure rapidly rises. The brain can herniate, and the brain stem can fail within five minutes. Except in boxing, all cases have occurred in athletes under age 20. Due to the very small number of documented cases, the diagnosis is controversial, and doubt exists about its validity. A 2010 Pediatrics review article stated that there is debate whether the brain swelling is due to two separate hits or to just one hit, but in either case, catastrophic football head injuries are three times more likely in high school athletes than in college athletes.

Epidemiology

Annual incidence of MTBI by age group in Canada
 
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. However, due to under reporting and to the widely varying definitions of concussion and mTBI, it is difficult to estimate how common the condition is. Estimates of the incidence of concussion may be artificially low, for example, due to under reporting. At least 25% of mTBI sufferers fail to get assessed by a medical professional. 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.

Age

Young children have the highest concussion rate among all age groups. However, most people who suffer a concussion are young adults. A Canadian study found that the yearly incidence of mTBI is lower in older age groups (graph at right). Studies suggest males suffer mTBI at about twice the rate of their female counterparts. However, female athletes may be at a higher risk of suffering a concussion than their male counterparts.

Sports

Up to five percent of sports injuries are concussions. 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. Since loss of consciousness is thought to occur in less than 10% of concussions, the CDC estimate is likely lower than the real number. 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 US, Australia, and Canada.

History

The Hippocratic Corpus mentioned concussion.
 
The Hippocratic Corpus, a 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". This idea of disruption of mental function by "shaking of the brain" remained the widely accepted understanding of concussion until the 19th century. In the 10th century, the Persian physician Muhammad ibn Zakarīya Rāzi was the first to write about concussion as distinct from other types of head injury. 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.

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. 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. In the 16th-century, the term "concussion" came into use, and symptoms such as confusion, lethargy, and memory problems were described. The 16th century physician Ambroise Paré used the term commotio cerebri, as well as "shaking of the brain", "commotion", and "concussion".
Guillaume Dupuytren distinguished between concussion and unconsciousness associated with brain contusion.
 
Until the 17th century, a concussion was usually described by its clinical features, but after the invention of the microscope, more physicians began exploring underlying physical and structural mechanisms. 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. 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. 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. In 1941, animal experiments showed that no macroscopic damage occurs in concussion.

Society and culture

Costs

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

Terminology

The terms mild brain injury, mild traumatic brain injury (mTBI), mild head injury (MHI), and concussion may be used interchangeably; although the term "concussion" is still used in sports literature as interchangeable with "MHI" or "mTBI", the general clinical medical literature uses "mTBI" instead, since a 2003 CDC report outlined it as an important strategy. In this article, "concussion" and "mTBI" are used interchangeably. 

The term "concussion" is from Latin concutere, "to shake violently" or concussus, "action of striking together".

Research

Minocycline, lithium, and N-acetylcysteine show tentative success in animal models.

Measurement of predictive visual tracking is being studied as a screening technique to identify mild traumatic brain injury. A head-mounted display unit with eye-tracking capability shows a moving object in a predictive pattern for the person to follow with their eyes. People without brain injury will be able to track the moving object with smooth pursuit eye movements and correct trajectory while it is hypothesized that those with mild traumatic brain injury cannot.

Agnosia

From Wikipedia, the free encyclopedia

Agnosia
Image of a question mark in a speech bubble.
Agnosia causes the victims to lose the ability to recognize or comprehend the meaning of objects even with intact senses.
SpecialtyPsychiatry, Neurology, Neuropsychology
Picture of the ventral and dorsal streams. The ventral stream is depicted in purple and the dorsal stream is depicted in green.
 
Agnosia is the inability to process sensory information. Often there is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream. Agnosia only affects a single modality, such as vision or hearing. More recently, a top-down interruption is considered to cause the disturbance of handling perceptual information.

Types

Name Description
Akinetopsia Also known as cerebral akinetopsia, this is associated with the inability to perceive visual motion. One cause of cerebral akinetopsia is lesions outside the striate cortex.
Allotopagnosia Patients cannot point at external targets located outside their own body, whether other persons' body parts or objects, but they perfectly point at their own body parts.
Anosognosia This is the inability to gain feedback about one's own condition and can be confused with lack of insight but is caused by problems in the feedback mechanisms in the brain. It is caused by neurological damage and can occur in connection with a range of neurological impairments but is most commonly referred to in cases of paralysis following stroke. Those with Anosognosia with multiple impairments may even be aware of some of their impairments but completely unable to perceive others.
Apperceptive visual agnosia Patients are unable to distinguish visual shapes and so have trouble recognizing, copying, or discriminating between different visual stimuli. Unlike patients suffering from associative agnosia, those with apperceptive agnosia are unable to copy images.[7]
Associative visual agnosia Patients can describe visual scenes and classes of objects but still fail to recognize them. They may, for example, know that a fork is something you eat with but may mistake it for a spoon. Patients suffering from associative agnosia are still able to reproduce an image through copying.
Astereognosis Also known as somatosensory agnosia, it is connected to tactile sense—that is, touch. Patient finds it difficult to recognize objects by touch based on its texture, size and weight. However, they may be able to describe it verbally or recognize same kind of objects from pictures or draw pictures of them. Thought to be connected to lesions or damage in somatosensory cortex.
Auditory agnosia Auditory agnosia has been recognized since 1877. With auditory agnosia, there is difficulty distinguishing environmental and non-verbal auditory cues including difficulty distinguishing speech from non-speech sounds even though hearing is usually normal. There are two types of auditory agnosia: semantic associative and discriminative agnosia. Semantic associative agnosia is associated with lesions to the left hemisphere, whereas discriminative agnosia is associated with lesions to the right hemisphere.
Auditory verbal agnosia Also known as pure word deafness (PWD). This presents as a form of meaning 'deafness' in which hearing is intact but there is significant difficulty recognising spoken words as semantically meaningful.
Autotopagnosia Is associated with the inability to orient parts of the body, and is often caused by a lesion in the parietal part of the posterior thalmic radiations.
Cerebral achromatopsia A difficulty in perceiving colors in which the world may appear drab or in shades of gray. Cerebral achromatopsia is caused by neurological damage. There are two regions of the brain which specialize for color recognition, areas V4 and V8. If there is a unilateral lesion to area V4, a loss of color perception in only half of the visual field may result known as hemiachromatopsia. Similar, but distinct, is color agnosia, which involves having difficulty recognizing colors, while still being able to perceive them as measured by a color matching or categorizing task.
Cortical deafness Refers to people who do not perceive any auditory information but whose hearing is intact.
Environmental agnosia It is the inability to locate a specific room or building that one is familiar with, as well as the inability to provide directions for how to arrive at a particular location. These individuals experience difficulty with learning routes. This form of agnosia is often associated with lesions to the bilateral or right hemisphere posterior regions. It is also associated with prosopagnosia and Parkinson's disease.
Finger agnosia Is the inability to distinguish the fingers on the hand. It is present in lesions of the dominant parietal lobe, and is a component of Gerstmann syndrome.
Form agnosia Patients perceive only parts of details, not the whole object.
Heterotopagnosia Patients cannot point at another person's body parts, but can point at their own body parts.
Integrative agnosia Usually a patient has a form of associative agnosia or apperceptive agnosia. However, in the case of integrative agnosia a patient falls in between a form of associative and apperceptive agnosia. This is where one has the ability to recognize elements of something but yet be unable to integrate these elements together into comprehensible perceptual wholes.
Pain agnosia Also referred to as congenital analgesia, this is the difficulty perceiving and processing pain; thought to underpin some forms of self injury.
Phonagnosia Is the inability to recognize familiar voices, even though the hearer can understand the words used.
Prosopagnosia Also known as faceblindness and facial agnosia: Patients cannot consciously recognize familiar faces, sometimes even including their own. This is often misperceived as an inability to remember names.
Pure alexia Inability to recognize text. Patients with pure alexia often have damage to their corpus callosum, as well as damage to the left visual association areas. Pure alexia involves not being able to read printed material, but these individuals still have the ability to write. Individuals with pure alexia usually read words letter by letter. However, individuals with pure alexia show a frequency effect. They are able to read high frequency words better and faster than they can read low frequency words.
Semantic agnosia Those with this form of agnosia are effectively 'object blind' until they use non-visual sensory systems to recognise the object. For example, feeling, tapping, smelling, rocking or flicking the object, may trigger realisation of its semantics (meaning).
Social-emotional agnosia Sometimes referred to as expressive agnosia, this is a form of agnosia in which the person is unable to perceive facial expression, body language and intonation, rendering them unable to non-verbally perceive people's emotions and limiting that aspect of social interaction.
Simultagnosia The inability to process visual input as a whole. The person instead processes faces, bodies, objects, rooms, places, pictures in a bit-by-bit fashion. When looking at a picture they can describe the parts of the picture but struggle to comprehend the picture as a whole. Simultagnosia occurs in Bálint syndrome but may also occur in brain injury. This condition can also be described by only seeing one object at a time. An example is having two cups in your visual field and only being able to see one at a time.
Tactile agnosia Impaired ability to recognize or identify objects by touch alone.
Time agnosia Is the loss of comprehension of the succession and duration of events.
Topographical disorientation Also known as topographical agnosia or topographagnosia, this is a form of visual agnosia in which a person cannot rely on visual cues to guide them directionally due to the inability to recognize objects. Nevertheless, they may still have an excellent capacity to describe the visual layout of the same place. Patients with topographical agnosia have the ability to read maps, but become lost in familiar environments.
Visuospatial dysgnosia This is a loss of the sense of "whereness" in the relation of oneself to one's environment and in the relation of objects to each other. It may include constructional apraxia, topographical disorientation, optic ataxia, ocular motor apraxia, dressing apraxia, and right-left confusion.
Visual agnosia Is associated with lesions of the left occipital lobe and temporal lobes. Many types of visual agnosia involve the inability to recognize objects.

Visual agnosia

Visual agnosia is a broad category that refers to a deficiency in the ability to recognize visual objects. Visual agnosia can be further subdivided into two different subtypes: apperceptive visual agnosia and associative visual agnosia.

Individuals with apperceptive visual agnosia display the ability to see contours and outlines when shown an object, but they experience difficulty if asked to categorize objects. Apperceptive visual agnosia is associated with damage to one hemisphere, specifically damage to the posterior sections of the right hemisphere.

In contrast, individuals with associative visual agnosia experience difficulty when asked to name objects. Associative agnosia is associated with damage to both the right and left hemispheres at the occipitotemporal border. A specific form of associative visual agnosia is known as prosopagnosia. Prosopagnosia is the inability to recognize faces. For example, these individuals have difficulty recognizing friends, family and coworkers. However, individuals with prosopagnosia can recognize all other types of visual stimuli.

Speech agnosia

Speech agnosia, or auditory verbal agnosia, refers to "an inability to comprehend spoken words despite intact hearing, speech production and reading ability". Patients report that they do indeed hear sounds being produced, but that the sounds are fundamentally unrecognizable/untranslatable.
  1. EXAMINER: What did you eat for breakfast?
  2. PATIENT: Breakfast, breakfast, it sounds familiar but it doesn't speak to me. (Obler & Gjerlow 1999:45)
Despite an inability to process what the speaker is saying, some patients have been reported to recognize certain characteristic information about the speaker's voice (such as being a man or woman).

Causes

Agnosia can result from strokes, dementia, or other neurological disorders. It may also be trauma-induced by a head injury, brain infection, or hereditary. Additionally, some forms of agnosia may be the result of developmental disorders. Damage causing agnosia usually occurs in either the occipital or parietal lobes of the brain. Although one modality may be affected, cognitive abilities in other areas are preserved.

Patients who experience dramatic recovery from blindness experience significant to total agnosia.

The effect of damage to the superior temporal sulcus is consistent with several types of neurolinguistic deficiencies, and some contend that agnosia is one of them. The superior temporal sulcus is vital for speech comprehension because the region is highly involved with the lexical interface. According to the 1985 TRACE II Model, the lexical interface associates sound waves (phonemes) with morphological features to produce meaningful words. This association process is accomplished by lateral inhibition/excitement of certain words within an individual's lexicon (vocabulary). For instance, if an experimenter were to say DOG aloud, the utterance would activate and inhibit various words within the subjects lexical interface:
  • DOG activates 3, and inhibits 0 letters in DOG. – +3
  • DOG activates 2, and inhibits 1 letters in FOG. – +2
  • DOG activates 1, and inhibits 2 letters in DAN. – +1
The consistency of this model to agnosia is shown by evidence that bilateral lesions to the superior temporal sulcus produces 'pure word deafness' (Kussmaul, 1877), or as it's understood today—speech agnosia. Patients with pure word deafness demonstrate the inability to recognize and process speech sounds with normal auditory processing for non-speech sounds below the level of the cortex.

Diagnosis

In order to assess an individual for agnosia, it must be verified that the individual is not suffering from a loss of sensation, and that both their language abilities and intelligence are intact. In order for an individual to be diagnosed with agnosia, they must only be experiencing a sensory deficit in a single modality. To make a diagnosis, the distinction between apperceptive and associative agnosia must be made. This distinction can be made by having the individual complete copying and matching tasks. If the individual is suffering from a form of apperceptive agnosia they will not be able to match two stimuli that are identical in appearance. In contrast, if an individual is suffering from a form of associative agnosia, they will not be able to match different examples of a stimulus. For example, an individual who has been diagnosed with associative agnosia in the visual modality would not be able to match pictures of a laptop that is open with a laptop that is closed.

Pure alexia

Individuals with pure alexia usually have difficulty reading words as well as difficulty with identifying letters. In order to assess whether an individual has pure alexia, tests of copying and recognition must be performed. An individual with pure alexia should be able to copy a set of words, and should be able to recognize letters.

Prosopagnosia

Individuals are usually shown pictures of human faces that may be familiar to them such as famous actors, singers, politicians or family members. The pictures shown to the patient are selected to be age and culture appropriate. The task involves the examiner asking the individual to name each face. If the individual cannot name whose face appears in the picture, the examiner may ask a question that would help to recognize the face in the picture.

Treatment

For all practical purposes, there is no direct cure. Patients may improve if information is presented in other modalities than the damaged one. Different types of therapies can help to reverse the effects of agnosia. In some cases, occupational therapy or speech therapy can improve agnosia, depending on its cause.

Initially many individuals with a form of agnosia are unaware of the extent to which they have either a perceptual or recognition deficit. This may be caused by anosognosia which is the lack of awareness of a deficit. This lack of awareness usually leads to a form of denial and resistance to any form of help or treatment. There are various methods that can be used which can help the individual recognize the impairment in perception or recognition that they may have. A patient can be presented with a stimulus to the impaired modality only to help increase their awareness of their deficit. Alternatively, a task can be broken down into its component parts so that the individual can see each part of the problem caused by the deficit. Once the individual acknowledges their perceptual or recognition deficit, a form of treatment may be recommended. There are various forms of treatment such as compensatory strategies with alternate modalities, verbal strategies, alternate cues and organizational strategies.

Verbal strategies

Using verbal descriptions may be helpful for individuals with certain types of agnosia. Individuals such as prosopagnosics may find it useful to listen to a description of their friend or family member and recognize them based on this description more easily than through visual cues.

Alternate cues

Alternate cues may be particularly useful to an individual with environmental agnosia or prosopagnosia. Alternate cues for an individual with environmental agnosia may include color cues or tactile markers to symbolize a new room or to remember an area by. Prosopagnosics may use alternate cues such as a scar on an individual's face or crooked teeth in order to recognize the individual. Hair color and length can be helpful cues as well.

Organizational strategies

Organizational strategies may be extremely helpful for an individual with visual agnosia. For example, organizing clothes according to different hangers provides tactile cues for the individual, making it easier to identify certain forms of clothing as opposed to relying solely on visual cues.

Alternative medicine

These strategies elicit the use of an unaffected modality. For example, visual agnosics can use tactile information in replacement of visual information. Alternatively, an individual with prosopagnosia can use auditory information in order to replace visual information. For example, an individual with prosopagnosia can wait for someone to speak, and will usually recognize the individual from their speech.

Current research

There are clinical trials being done to further research for treatments. At the National Institute of Neurological Disorders and Stroke (NINDS) they support research for rare diseases like agnosia. Some organizations that are recruiting for trials are using clincaltrials.gov and give status updates on the trials.

History

The term 'agnosia' comes from the Ancient Greek ἀγνωσία (agnosia), "ignorance", "absence of knowledge". It was introduced by Sigmund Freud in 1891: "For disturbances in the recognition of objects, which Finkelnburg classes as asymbolia, I should like to propose the term 'agnosia'." Prior to Freud's introduction of the term, some of the first ideas about agnosia came from Carl Wernicke, who created theories about receptive aphasia in 1874. He noted that individuals with receptive aphasia did not possess the ability to understand speech or repeat words. He believed that receptive aphasia was due to lesions of the posterior third of the left superior temporal gyrus. Due to these lesions, Wernicke believed that individuals with receptive aphasia had a limited deafness for certain sounds and frequencies in speech.

After Wernicke, came Kussmaul in 1877 who attempted to explain why auditory verbal agnosia, also known as word deafness, occurs. Contrary to Wernicke's explanations, Kussmaul believed auditory verbal agnosia was the result of major destruction to the first left temporal gyrus. Kussmaul also posited about the origins of alexia (acquired dyslexia) also known as word blindness. He believed that word blindness was the result of lesions to the left angular and supramarginal gyri.

Heinrich Lissauer shared his ideas about agnosia after Wernicke and Kussmaul. In 1890, he theorized that there were two ways in which object recognition impairment could occur. One way in which impairment could occur was if there was damage to early perceptual processing or if there was damage to the actual object representation. If the actual object representation was damaged, this would not allow the object to be stored in visual memory, and therefore the individual would not be able to recognize the object. During the time of Wernicke, Kussmaul and Lissauer there was little known about the cerebral cortex. Today, with new neuroimaging techniques, we have been able to expand our knowledge on agnosia greatly.

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