Auto Accidents impact nearly everyone in the United States each year. If you’re involved in a car accident, statistics show that there’s a significant chance that you or someone you love will be injured in that accident. On average one out of every three motor vehicle accidents results in some type of injury. And, with more than 6 million accidents in the United States, alone, that means there are more than 2 million accidents resulting in more than 3 million injured men, women, and children each year. These injuries range from minor cuts and scrapes to life-changing, and sometimes life-ending, trauma. Some injuries are obvious, but other soft tissue injuries are often undetectable at the time of the accident, showing up as stiffness, numbness, soreness, severe or chronic headaches, and even mild brain injury days or weeks after the event. Because there is such a wide range of medical issues possible with an auto accident, it’s important to seek the best medical treatment snd legal representation related to your particular injury or condition.

Whiplash and whiplash-associated disorders (WAD) represent a range of injuries to the neck caused by or related to a sudden distortion of the neck[1] associated with extension.[2] Whiplash is commonly associated with motor vehicle accidents,[citation needed] usually when the vehicle has been hit in the rear;[3] however, the injury can be sustained in many other ways, including falls from stools, bicycles [4] [citation needed] or horses.[4] [citation needed] It stands out as one of the main injuries covered by the car insurers. [citation needed] In the United Kingdom, 430,000 people made a claim for whiplash in 2007 (75% of the UK's motor insurance claims), accounting for 14% of every driver's premium.[5] Symptoms reported by sufferers include: pain and aching to the neck and back, referred pain to the shoulders, sensory disturbance (such as pins and needles) to the arms & legs and headaches. Symptoms can appear directly after the injury, but often are not felt until days afterwards.[3] Whiplash is usually confined to the spinal cord, and the most common areas of the spinal cord affected by whiplash are the neck, and the mid-back (middle of the spine). [edit] Cause The exact injury mechanism that causes whiplash injuries is unknown.[citation needed] A whiplash injury may be the result of impulsive stretching of the spine, mainly the ligament: anterior longitudinal ligament which is stretched or tears, as the head snaps forward and then back again causing a whiplash injury.[6] [citation needed] Whiplash may be caused by any motion similar to a rear-end collision in a motor vehicle, such as may take place on a roller coaster [7] or other rides at an amusement park, sports injuries such as skiing accidents, other modes of transportation such as airplane travel, or from being hit, kicked or shaken.[8] [citation needed]Shaken baby syndrome can result in a whiplash injury.[6][citation needed] Whiplash symptoms might not always have any pathological (injury) explanation. "Volunteer studies of experimental, low-velocity rear-end collisions have shown a percentage of subjects to report short-lived symptoms", which can not be attributed to any pathogenic effect on the subjects neck.[9] [edit] Diagnosis Diagnosis occurs through a patient history, head and neck examination, X-rays to rule out bone fractures and may involve the use of medical imaging to determine if there are other injuries.[10] [edit] Québec Task Force The Québec Task Force (QTF) has divided whiplash-associated disorders into four grades.[11][citation needed] * Grade 0: no neck pain, stiffness, or any physical signs are noticed * Grade 1: neck complaints of pain, stiffness or tenderness only but no physical signs are noted by the examining physician. * Grade 2: neck complaints and the examining physician finds decreased range of motion and point tenderness in the neck. * Grade 3: neck complaints plus neurological signs such as decreased deep tendon reflexes, weakness and sensory deficits. * Grade 4: neck complaints and fracture or dislocation, or injury to the spinal cord. [edit] Prevention Protection efforts are hampered by lack of knowledge about the causes of whiplash injuries. The focus of preventive measures to date has been on the design of car seats, primarily through the introduction of headrestraints, often called headrests. This approach is potentially problematic given the underlying assumption that purely mechanical factors cause whiplash injuries - an unproven theory. So far the injury reducing effects of head restraints appears to have been low, approximately 5-10%, because car seats have become stiffer in order to increase crash-worthiness of cars in high-speed rear-end collisions which in turn could increase the risk of whiplash injury in low-speed rear impact collisions. Improvements in the geometry of car seats through better design and energy absorption could offer additional benefits. Active devices move the body in a crash in order to shift the loads on the car seat.[3][dead link] Some car manufacturers have begun to implement various whiplash protection devices in their products in order to reduce the risk for and severity of injury, such as * Mercedes-Benz A-Class Active Head Restraint (AHR)[3][12][citation needed], * Saab (Responsible for the first active head restraint), Opel, Ford, Nissan, Subaru, Hyundai, and Peugeot - Active Head restraint (SAHR)[3][13][citation needed], * Volvo and Jaguar - Whiplash Protection System/Whiplash Prevention System (WHIPS)[14][citation needed], and * Toyota - Whiplash Injury Lessening (WIL).[3][citation needed] Whether or not such devices offer a substantial benefit over vehicles without them remains controversial. In a test undertaken by the Swedish National Road Administration and an insurance company (Folksam), one test showed that a whiplash protection device was no guarantee against injury and that the degree of protection varies between vehicles both with and without whiplash protection devices.[15] One study found that an active head restraint system helps reduce the risk of neck injuries by up to 75% in rear-end collisions.[16] [edit] Treatment According to the recommendations made by the Quebec Task Force, treatment for individuals with whiplash associated disorders grade 1-3 should include manipulation, mobilizations and range of motion exercises. Non-narcotic analgesics and non-steroidal anti-inflammatory drugs may also be prescribed in the case of WAD 2 and WAD 3, but their use should be limited to a maximum of 3 weeks. A cervical collar should not be used for longer than 72 hours as it may lead to prolonged inactivity. Return to normal activities of daily living should be encouraged as soon as possible to maximize and expediate full recovery.[17][citation needed] A different approach is taken by the National Institute for Neurological Disorders and Stroke, who suggest that treatment for individuals with whiplash may include pain medications, nonsteroidal anti-inflammatory drugs, antidepressants, muscle relaxants, and a cervical collar (usually worn for 2 to 3 weeks). Range of motion exercises, physical therapy, and cervical traction may also be prescribed. Supplemental heat application may relieve muscle tension. [citation needed] [18] [edit] Prognosis The consequences of whiplash range from mild pain for a few days (which is the case for most people)[19], to severe disability caused by restricted head movement or of the cervical spine, sometimes with persistent pain.[citation needed] Alterations in resting state cerebral blood flow have been demonstrated in patients with chronic pain after whiplash injury [20][citation needed]

Credit for this article is due to Wikipedia, and sources cited within.

Post-concussion syndrome, also known as postconcussive syndrome or PCS, and historically called shell shock[1], is a set of symptoms that a person may experience for weeks, months, or occasionally years after a concussion–a mild form of traumatic brain injury (abbreviated TBI). PCS may also occur in moderate and severe cases of traumatic brain injury.[2][3] Symptoms of PCS, which is the most common entity to be diagnosed in people who have suffered TBI,[2] may occur in 38–80% of mild head injuries.[4] A diagnosis may be made when symptoms resulting from concussion last for more than three months after the injury,[5] or it may be made starting within a week[6] or ten days of trauma.[7] In late, persistent, or prolonged PCS (PPCS), symptoms last for over six months,[6][8] or by other standards, three.[9] The condition can cause a variety of symptoms: physical, such as headache; cognitive, such as difficulty concentrating; and emotional and behavioral, such as irritability. As many of the symptoms in PCS are common to, or exacerbated by, other disorders, there is a risk of misdiagnosis. Though there is no treatment for PCS itself, symptoms can be treated; medications and physical and behavioral therapy may be used, and patients can be educated about symptoms and their usual prognosis. The majority of PCS cases disappear after a period of time. It is not known what causes PCS symptoms to occur and persist,[10] or why some people who suffer a mild traumatic brain injury (MTBI) develop PCS while others do not.[11] The nature of the syndrome and the diagnosis itself have been the subject of intense debate since the 19th century. However, certain risk factors have been identified; for example, preexisting medical or psychological conditions, expectations of disability, and older age all increase the chances that someone will suffer PPCS. Physiological and psychological factors present before, during, and after the injury are all thought to be involved in the development of PCS.[12] Symptoms The acronym PCS may also be used to mean post-concussion symptoms.[12] Symptoms can appear immediately, or weeks to months after the initial injury. Their severity lessens progressively over time.[13] The nature of the symptoms tends to change over time: they are most commonly of a physical nature following the injury, but tend to become predominantly psychological later.[14][15] Signs and symptoms such as noise sensitivity, problems with concentration and memory, irritability, depression, anxiety, fatigue, and poor judgment may be called 'late symptoms' because they generally do not occur immediately after the injury, but rather days or weeks after.[12] Nausea and drowsiness commonly occur early after concussion but usually do not last, while headache and dizziness occur immediately after the injury and are long lasting.[12] [edit] Physical The main PCS symptom is headache.[4] While most people have headaches of the same type they experienced before the injury, people with PCS often report more frequent or longer-lasting headaches.[4] Between 30 and 90% of people treated for PCS report having more headaches than they did before the injury, and between 8 and 32% still report them a year after the injury.[4] Dizziness, the second most common symptom, occurs in about half of people with PCS and is still present in up to a quarter of them a year after the injury.[4] Older people are at especially high risk for dizziness.[4] About 10% of people with PCS develop sensitivity to light or noise, about 5% experience a decreased sense of taste or smell, and about 14% have blurred vision.[4] People may also have double vision or ringing in the ears, also called tinnitus.[16] Loss of hearing occurs in 20% of cases.[17] PCS may cause insomnia, fatigue,[18] sleepiness, or other problems with sleep.[13] Other physical symptoms include nausea[19] and vomiting. [edit] Psychological and behavioral Psychological symptoms, which are present in about half of people with PCS, may include irritability, anxiety, depression, and a change in personality.[4] Other emotional and behavioral symptoms include restlessness,[20] aggression,[21] mood swings, anger, decreased libido,[18] impulsiveness, loss of social judgment,[22] and lack of ability to tolerate stress or alcohol.[6] People with PCS may also display a lack of emotion,[23] emotional lability,[19] or mood swings. Another common symptom—apathy, or lack of motivation—may result directly from the syndrome or be secondary to depression.[4] [edit] Higher mental functions Cognitive or mental symptoms can include confusion or impaired cognition,[24] problems with attention,[17] impaired judgment,[12] and amnesia or other problems with memory, especially short-term memory.[4] Problems with memory and attention are the longest-lasting cognitive symptoms;[17] one in four people with PCS still suffer from memory problems a year after the injury.[4] PCS may cause slowed information processing and reactions to stimuli[4] or difficulty with abstract thinking[20] or problem solving.[16] People may also experience a decrease in abilities related to work performance or social interaction.[21] While cognitive symptoms usually resolve within a few months of injury, physical and emotional symptoms can last longer.[25] Most cognitive symptoms clear within half a year of the injury, and the longest-lasting ones, such as memory, attention and language problems, usually resolve within a year.[4] [edit] Controversy No definition of PCS is accepted by all health professionals,[6] and doubt exists about the validity of the diagnosis. One reason for this is that symptoms of PCS also occur in people who have no history of head injury, but who have other medical and psychological complaints.[26] In one study, 80% of healthy, uninjured people reported having three or more symptoms similar to those found after concussion.[15] In another study, 64% of people with TBI met the criteria set out by the ICD-10 for post-concussion syndrome, but so did 40% of people that had injuries not to the head; 11% of those with brain injuries and 7% of those with other injuries met the DSM-IV criteria for post-concussion syndrome (see diagnosis, below).[27] Having depression, post-traumatic stress disorder, or chronic pain virtually guarantees that a person will report symptoms resembling those of PCS.[26] One study found that while people with chronic pain without TBI do report many symptoms similar to those of post-concussion syndrome, they report fewer symptoms related to memory, slowed thinking, and sensitivity to noise and light than people with MTBI do.[12] In a syndrome, a set of symptoms is consistently present, and symptoms are linked such that the presence of one symptom suggests that of others. Because PCS symptoms are so varied and many can be associated with a large number of other conditions, doubt exists about whether the term "syndrome" is appropriate for the constellation of symptoms found after concussion.[28] The fact that the persistence of one symptom is not necessarily linked to that of another has similarly led to doubt about whether "syndrome" is the appropriate term.[29] A longstanding controversy surrounding PCS concerns the nature of its etiology – that is, the cause behind it[22] – and the degree to which psychological factors and organic factors involving brain dysfunction are responsible. The debate has been referred to as 'psychogenesis versus physiogenesis' (psychogenesis referring to a psychological origin for the condition, physiogenesis to a physical one).[22] [edit] Causes The question of the cause or causes of PCS and PPCS has been heavily debated for many years. It is not known to exactly what degree the symptoms are due to organic factors, such as microscopic damage to the brain, and to other factors, such as psychological ones.[23] The subjectivity of the complaints complicates assessment and makes it difficult to determine whether symptoms are being exaggerated or feigned.[4] It is possible that some post-concussion symptoms are due to physical causes while others are psychological.[12] One hypothesis holds that physiological factors are responsible for early symptoms that occur after mild head trauma, whereas symptoms that occur later are due to psychological factors.[22] While the cause of symptoms occurring shortly after head trauma is likely to be physiological, it is less clear whether PPCS has an organic basis,[30][31] and nonorganic factors are likely to be involved in symptoms that last longer than three months.[25] PPCS may be caused by physiological, psychological, or psychosocial factors, chronic pain, or an interaction of some or all of these.[26] The majority of experts believe that PPCS results from a mix of factors, including preexisting psychological factors, and those directly relating to the physical injury.[12] Studies using positron emission tomography have linked PCS to a reduction in glucose use by the brain, and changes in cerebral blood flow have been found to exist for as long as three years after a concussion in studies using single photon emission computed tomography (SPECT).[4] At least one study with functional magnetic resonance imaging (fMRI) has shown differences in brain function during tasks involving memory after MTBI,[32] and fMRI has shown changes in the brains of athletes within a week of a concussion.[26] Not all people with PPCS have abnormalities on imaging, however, and abnormalities found in studies such as fMRI, PET, and SPECT could result from other comorbid conditions such as depression, chronic pain, and post-traumatic stress disorder (PTSD).[26] Electroencephalograms, while usually normal in people with PCS, have occasionally been used to detect changes in brain function following mild head injury.[4] Electrophysiological measures of brain function of people with PPCS show abnormal evoked potentials and event-related potentials compared to controls, supporting the hypothesis that PPCS has an organic basis.[12] Proponents of the view that PCS has a physical or organic basis point to findings that people with post-concussive symptoms have deficits on standardized tests of cognitive function as an indication that brain dysfunction is a factor in PCS.[22] Studies have shown that people with PPCS score lower than controls on neuropsychological tests that measure attention, verbal learning, reasoning, and information processing.[12] But although decreased scores on cognitive tests point to brain dysfunction, they cannot diagnose brain damage.[18] Recovery as measured by scores on cognitive tests frequently do not correlate with resolution of symptoms; people may still report subjective symptoms after their cognitive function has returned to normal.[31] Another study found that although children with PPCS had poorer scores on tests of cognitive functioning after the injury, they also had poorer behavioral adjustment before the injury than children with no persistent symptoms; these findings support the idea that PCS may result from a combination of factors such as brain dysfunction resulting from head injury and preexisting psychological or social problems.[22] Different symptoms may be predicted by different factors; for example, one study found that cognitive and physical symptoms were not predicted by the manner in which parents and family members coped with the injury and adjusted to its effects, but psychological and behavioral symptoms were.[22] [edit] Psychological It has been convincingly shown that psychological factors play an important role in the presence of post-concussion symptoms.[33] The development of PCS may be due to a combination of factors such as adjustment to effects of the injury, preexisting vulnerabilities, and brain dysfunction.[34] Setbacks related to the injury, for example problems at work or with physical or social functioning, may act as stressors that interact with preexisting factors such as personality and mental conditions to cause and perpetuate PPCS.[26] In one study, levels of daily stress were found to be correlated to PCS symptoms in both mildly brain injured subjects and controls, but in another, stress was not significantly related to symptoms.[12] Iatrogenic effects (those caused by the medical intervention) may also occur, for example when people focus and dwell on the idea that their brains may be damaged,[26] or when they are led to expect symptoms to occur. Expectation of symptoms may also lead head-injured people to focus on symptoms and therefore perceive them to be more intense, to attribute symptoms that occur for other reasons to the injury, and to underestimate the rate of symptoms before the injury.[31] [edit] Malingering People may malinger (feign or exaggerate symptoms), especially in cases involving litigation or other situations in which they stand to gain from a PCS diagnosis.[4] In countries where lawsuits are less common, PCS symptoms are also less common.[35] Studies have found that people involved in legal proceedings have more severe and longer-lasting post-concussion symptoms than similarly injured people who are not in litigation.[4] One study reviewed over 30,000 court cases and concluded that symptoms were exaggerated or feigned in over a third of those involving mild head trauma.[4] Other studies have failed to show a link between litigation and symptom severity or duration, and that symptoms do not necessarily go away when legal matters come to a close.[13] One explanation for the apparent relative severity of PCS in people involved in litigation is that the stress from these activities could worsen post-concussion symptoms.[36] Another is that people involved in legal proceedings have learned more about PCS, and this relatively greater knowledge of symptoms affects their presentation.[4] People with worse PCS symptoms may also be more likely to become involved in a lawsuit.[31] The International Statistical Classification of Diseases and Related Health Problems (ICD-10) and the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders have set out criteria for PCS and postconcussional disorder (PCD), respectively. The ICD-10 established a set of diagnostic criteria for PCS in 1992.[37] In order to meet these criteria, a patient must have had a head injury with loss of consciousness[22] and develop at least three of the eight symptoms marked with a check mark in the table at right under "ICD-10" within four weeks.[37][38] About 38% of people who suffer a head injury with symptoms of concussion and no radiological evidence of brain lesions meet these criteria.[39] In addition to these symptoms, people that meet the ICD-10 criteria for PCS may fear that they will have permanent brain damage, which may worsen the original symptoms.[3] Preoccupation with the injury may be accompanied by the assumption of a "sick role" and hypochondriasis.[34] The criteria focus on subjective symptoms and mention that neuropsychological evidence of significant impairment are not present.[30] With their focus on psychological factors, the ICD-10 criteria support the idea that the cause of PCS is functional.[22] Like the ICD-10, the ICD-9-CM defines PCS in terms of subjective symptoms and discusses the greater frequency of PCS in people with histories of mental disorders or a financial incentive for a diagnosis.[30] The DSM-IV lists criteria for diagnosis of PCD in people who suffered a head trauma with persistent post-traumatic amnesia, loss of consciousness, or post-traumatic seizures.[22] In addition, for a diagnosis of PCD, patients must have neuropsychological impairment as well as at least three of the symptoms marked with a check mark in the table at right under "DSM-IV".[22] These symptoms must be present for three months after the injury and must have been absent or less severe before the injury.[6] In addition, the patient must experience social problems as a result, and must not meet criteria for another disorder that explains the symptoms better.[6] Neuropsychological tests exist to measure deficits in cognitive functioning that can result from PCS.[4][25] The Stroop Color Test and the 2&7 Processing Speed Test (which both detect deficits in speed of mental processing) can predict the development of cognitive problems from PCS.[4] A test called the Rivermead Postconcussion Symptoms Questionnaire, a set of questions that measure the severity of 16 different post-concussion symptoms, can be self-administered or administered by an interviewer.[3] Other tests that can predict the development of PCS include the Hopkins Verbal Learning A test (HVLA) and the Digit Span Forward examination.[4] The HVLA tests verbal learning and memory by presenting a series of words and assigning points based on the number recalled,[40] and digit span measures attention efficiency by asking the examinee to repeat back digits spoken by the tester in the same order as they are presented.[41] In addition, neuropsychological tests may be performed to detect malingering.[13] [edit] Differential diagnosis PCS, which shares symptoms with a variety of other conditions, is highly likely to be misdiagnosed in people with these conditions.[42] Cognitive and affective symptoms that occur following a traumatic injury may be attributed to MTBI, but in fact be due to another factor such as post-traumatic stress disorder,[33] which is easily misdiagnosed as PCS and vice versa.[42] Affective disorders such as depression have some symptoms that can mimic those of PCS and lead to a wrongful diagnosis of the latter; these include problems with concentration, emotional lability, anxiety, and sleep problems.[4] Depression, which is highly common in persistent PCS, can worsen other PCS symptoms, such as headaches and problems with concentration, memory, and sleep.[43] PCS also shares symptoms with chronic fatigue syndrome, fibromyalgia, and exposure to certain toxins.[18] Traumatic brain injury may cause damage to the hypothalamus or the pituitary gland, and deficiencies of pituitary hormones (hypopituitarism) can cause similar symptoms to post-concussion syndrome; in these cases, symptoms can be treated by replacing any hormone deficiencies. [edit] Treatment Post-concussion syndrome is usually not treated,[23] though specific symptoms can be addressed;[15] for example, people can take pain relievers for headaches and medicine to relieve depression, dizziness,[44] or nausea.[23] Rest is advised, but is only somewhat effective.[45] Physical and behavioral therapy may also be prescribed for problems such as loss of balance and difficulties with attention, respectively.[7] [edit] Medication Though no pharmacological treatments exist especially for PCS, if necessary doctors may prescribe medications used for symptoms that also occur in other conditions; for example, antidepressants are used for the depression that frequently follows MTBI.[29] Side effects of medications may affect people suffering the consequences of MTBI more severely than they do others, and thus it is recommended that medications be avoided if possible;[29] there may be a benefit to avoiding narcotic medications.[35] In addition, headache medications may cause rebound headaches when they are discontinued.[46] [edit] Psychotherapy Psychological treatment, to which about 40% of PCS patients are referred for consultation,[39] has been shown to reduce problems.[3] Ongoing disabilities may be treated with therapy to improve function at work, or in social or other contexts. Therapy aims to aid in the gradual return to work and other preinjury activities, as symptoms permit. A protocol for PCS treatment has been designed based on the principles behind Cognitive behavioral therapy (CBT), a psychotherapy aimed at influencing disturbed emotions by improving thoughts and behaviors.[26] CBT may help prevent persistence of iatrogenic symptoms[29] – those that occur because health care providers create the expectation that they will. A risk exists that the "power of suggestion" may worsen symptoms and cause long-term disabilities;[46] therefore, when counseling is indicated, the therapist must take a psychological origin of symptoms into account and not assume that all symptoms are a direct result of neurological damage from the injury.[47] In situations such as motor vehicle accidents or following a violent attack, the post-concussion syndrome may be accompanied by post-traumatic stress disorder, which is important to recognize and treat in its own right. People with PTSD, depression, and anxiety can be treated with medication and psychotherapy.[29] [edit] Education Education about symptoms and their usual time course is a part of psychological therapy, and is most effective when provided soon after the injury.[29] Since stress exacerbates post-concussion symptoms, and vice versa, an important part of treatment is reassurance that PCS symptoms are normal, and education about how to deal with impairments.[20] One study found that PCS patients who were coached to return to activities gradually, told what symptoms to expect, and trained how to manage them had a reduction in symptoms compared to a control group of uninjured people.[14] Early education has been found to reduce symptoms in children as well.[7] [edit] Prognosis The prognosis for PCS is generally considered excellent, with total resolution of symptoms in the large majority of cases. For most people, post-concussion symptoms go away within a few days to several weeks after the original injury occurs.[23] In others, symptoms may remain for three to six months,[24] but evidence indicates that most cases are completely resolved within that time.[4] Symptoms are largely gone in about half of people with concussion one month after the injury, and about two thirds of people with minor head trauma are symptom-free within three months.[29] It is frequently stated in the literature and considered to be common knowledge that 10–20% of people with PCS have not recovered by a year after the injury, but this may be an overestimate because it is based on studies of people admitted to a hospital, the methodologies of which have been criticized.[26][42][48] In a small minority of people, symptoms may persist for years or be permanent; however, it has not been conclusively shown that permanent neurological symptoms ever result from an uncomplicated concussion.[43] If symptoms are not resolved by one year, they are likely to be permanent, though improvements may occur after even two or three years,[6] or may suddenly occur after a long time without much improvement.[49] Older people and those who have previously suffered another head injury are likely to take longer to recover.[49] The way in which children cope with the injury after it occurs may have more of an impact than factors that existed prior to the injury.[22] Children's mechanisms for dealing with their injuries may have an effect on the duration of symptoms, and parents who do not deal effectively with anxiety about children's post-injury functioning may be less able to help their children recover.[22] If another blow to the head occurs after a concussion but before its symptoms have gone away, there is a very slight risk of developing the extremely rare but deadly second-impact syndrome (SIS). In SIS, the brain rapidly swells, greatly increasing intracranial pressure. People who have repeated mild head injuries over a prolonged period, such as boxers, are at risk for dementia pugilistica, a severe, chronic disorder involving a decline in mental and physical abilities. [edit] Epidemiology It is not known exactly how common PCS is. Estimates of the prevalence at 3 months post-injury are between 24 and 84%, a variation possibly caused by different populations or study methodologies.[12] The estimated incidence of PPCS is around 10% of MTBI cases.[30] Since PCS by definition only exists in people who have suffered a head injury, demographics and risk factors are similar to those for head injury; for example, young adults are at higher risk than others for receiving head injury, and, consequently, of developing PCS.[6] The existence of PCS in children is controversial. It is possible that children's brains have enough plasticity that they are not affected by long-term consequences of concussion (though such consequences are known to result from moderate and severe head trauma).[50] On the other hand, children's brains may be more vulnerable to the injury, since they are still developing and have fewer skills that can compensate for deficits.[51] Clinical research has found higher rates of post-concussion symptoms in children with TBI than in those with injuries to other parts of the body, and that the symptoms are more common in anxious children.[34] Symptoms in children are similar to those in adults, but children exhibit fewer of them.[34] Evidence from clinical studies found that high school-aged athletes had slower recoveries from concussion as measured by neuropsychological tests than college-aged ones and adults.[51] PCS is rare in young children.[35] [edit] Risk factors Factors that predict that a person will suffer PPCS (persistent PCS) include low socioeconomic status, previous MTBI, a serious associated injury, headaches, an ongoing court case, and female gender.[47] Being older than 40 and being female are related to both PCS and PPCS.[12] Women are more likely than men to suffer PCS, and likely to suffer it more severely.[4] In addition, the development of PPCS may be predicted by having a history of alcohol abuse, low cognitive abilities before the injury, a personality disorder or a medical or psychiatric illness.[4] PCS is more prevalent in people who had psychiatric symptoms such as clinical depression or anxiety before the injury.[52] Mild brain injury-related factors that increase the risk for persisting post-concussion symptoms include an injury associated with acute headache, dizziness, or nausea; a Glasgow Coma Score of 13 or 14; post-traumatic amnesia lasting longer than an hour; and suffering another head trauma before recovering from the first.[15] The risk is also increased in people who experience stress, have traumatic memories of the event, or expect to be disabled by the injury.[15] [edit] History The symptoms that occur after a concussion have been known for hundreds of years.[24] The idea that this set of symptoms forms a distinct entity began to attain wide recognition in the latter part of the 19th century.[53] John Erichsen, a surgeon from London, played an important role in developing the study of PCS.[53] The controversy surrounding the cause of PCS was started in 1866 when Erichsen published a paper about persisting symptoms after sustaining mild head trauma.[4] He suggested that the condition was due to injury by "molecular disarrangement" to the spine, and the condition was originally called "railroad spine" because most of the injuries studied had happened to railroad workers.[4] While some of his contemporaries agreed that the syndrome had an organic basis, others attributed the symptoms to psychological factors or to outright feigning.[53] In 1879, the idea that a physical problem was responsible for the symptoms was challenged by Rigler, who suggested that the cause of the persisting symptoms was actually "compensation neurosis": the railroad's practice of compensating workers who had been injured was bringing about the complaints.[4] Later, the idea that hysteria was responsible for the symptoms after a mild head injury was suggested by Charcot.[4][8] Controversy about the syndrome continued through the 20th century.[8] During World War I many soldiers suffered from puzzling symptoms after being close to a detonation but showing no evidence of a head wound. The illness was called shell shock, and a psychological explanation was eventually favoured.[1] The current concept of PCS had replaced ideas of hysteria as the cause of post-concussion symptoms by 1934.[4] British authorities banned the term shell shock during World War II to avoid an epidemic of cases, and the term posttrauma concussion state was coined in 1939 to describe "disturbance of consciousness with no immediate or obvious pathologic change in the brain".[1] The term postconcussion syndrome was in use by 1941.[1] In 1961, H. Miller first used "accident neurosis" to refer to symptoms of PCS and asserted that the condition only ever occurs in situations where people stand to be compensated for the injury, but this contention was widely challenged.[31] The real causes of the condition remain unclear.[4]

Credit for this article is due to Wikipedia, and sources cited within.

Concussion, from the Latin concutere ("to shake violently")[1] or the Latin concussus ("action of striking together"),[2] is the most common 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,[3][4] although the latter is often treated as a narrower category.[5] 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 temporary loss of brain function, concussion can cause a variety of physical, cognitive, and emotional symptoms. Treatment of concussion involves monitoring and rest. Symptoms usually go away entirely within three weeks, though they may persist, or complications may occur.[6] 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 1,000 people.[7] Common causes include sports injuries, bicycle accidents, car accidents, and falls; the latter two are the most frequent causes among adults.[8] Concussion may be caused by a blow to the head, or by acceleration forces without a direct impact. The forces involved disrupt cellular processes in the brain for days or weeks. On the battlefield, MTBI is a potential consequence of nearby explosions.[9] 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.[10] Cellular damage has reportedly been found in concussed brains, but it may have been due to artifacts from the studies.[11] A debate about whether structural damage exists in concussion has raged for centuries and is ongoing. No single definition of concussion mild head injury,[12] or mild traumatic brain injury is universally accepted, though a variety of definitions have been offered.[13] In 2001, the first International Symposium on Concussion in Sport was organized by the International Olympic Committee Medical Commission and other sports federations.[14] 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."[15] They agreed that concussion typically involves temporary impairment of neurological function that quickly resolves by itself, and that neuroimaging normally shows no gross structural changes to the brain as the result of the condition.[6] According to the classic definition, no structural brain damage occurs in concussion;[16] 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.[6] 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.[17] Definitions of mild traumatic brain injury (M.T.B.I) 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.[4] 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.[18] In 1994, the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders defined MTBI using PTA and LOC.[4] Other definitions of MTBI incorporate focal neurological deficit and altered mental status, in addition to PTA and GCS.[13] Concussion falls under the classification of mild TBI.[19] It is not clear whether concussion is implied in mild brain injury or mild head injury.[20] "MTBI" and "concussion" are often treated as synonyms in medical literature.[18] However, other injuries such as intracranial hemorrhages (e.g. intra-axial hematoma, epidural hematoma, and subdural hematoma) are not necessarily precluded in MTBI[6] or mild head injury,[21][22] but they are in concussion.[23] MTBI associated with abnormal neuroimaging may be considered "complicated MTBI".[24] "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.[6] Descriptions of the condition, including the severity and the area of the brain affected, are now used more often than "concussion" in clinical neurology.[25] 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.[26] 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.[27] 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.[28] [edit] Grading systems Main article: Concussion grading systems At least 41 systems exist to measure the severity, or grade, of a mild head injury,[6] and there is little agreement among professionals about which is the best.[29] Several of the systems use loss of consciousness and amnesia as the primary determinants of the severity of the concussion.[29] 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 neuropsychological tests are normal again This is to avoid 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.[28] Each divides concussion into three grades, as summarized in the following table:[29] Signs and symptoms Concussion can be associated with a variety of symptoms, which typically occur rapidly after the injury.[14] Early symptoms usually subside within days or weeks.[11] The number and type of symptoms a person suffers varies widely.[13] [edit] Physical Headache is the most common MTBI symptom.[18] Other symptoms include dizziness, vomiting, nausea, lack of motor coordination, difficulty balancing,[18] or other problems with movement or sensation. Visual symptoms include light sensitivity,[30] seeing bright lights,[29] blurred vision,[11] and double vision.[31] Tinnitus, or a ringing in the ears, is also commonly reported.[11] In one in about seventy concussions, concussive convulsions occur, but these are not actual post-traumatic seizures and are not predictive of post-traumatic epilepsy, which results from structural brain damage.[32] Concussive convulsions are thought to result from temporary loss of 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.[33] [edit] 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.[15] 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.[18] Confusion, another concussion hallmark, may be present immediately or may develop over several minutes.[18] A patient may, for example, repeatedly ask the same questions,[34] be slow to respond to questions or directions, have a vacant stare, or have slurred[18] or incoherent speech.[35] Other MTBI symptoms include changes in sleeping patterns[11] and difficulty with reasoning,[31] concentrating, and performing everyday activities.[18] Affective results of concussion include crankiness, loss of interest in favorite activities or items,[36] tearfulness,[5] and displays of emotion that are inappropriate to the situation.[35] Common symptoms in concussed children include restlessness, lethargy, and irritability.[37] Mechanism. 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 may not be absorbed by this cushion.[10] 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).[5] Forces may cause linear, rotational, or angular movement of the brain, or a combination of these types of motion.[5] 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.[5] The amount of rotational force is thought to be the major type of force to cause concussion[39] and the largest component in its severity.[6] 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.[40][41] The parts of the brain most affected by rotational forces are the midbrain and diencephalon.[1][8] 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.[8] 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.[42]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.[43] 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.[24] 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.[24] Excitatory neurotransmitters, chemicals such as glutamate that serve to stimulate nerve cells, are released in excessive amounts as the result of the injury.[44] The resulting cellular excitation causes neurons to fire excessively.[45] This creates an imbalance of ions such as potassium and calcium across the cell membranes of neurons (a process like excitotoxicity).[24] 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.[24] 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.[24] The brain may stay in this state of hypermetabolism for days or weeks.[37] At the same time, cerebral blood flow is relatively reduced for unknown reasons,[30] though the reduction in blood flow is not as severe as it is in ischemia.[24] Thus cells get less glucose than they normally do, which causes an "energy crisis".[30] 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.[24] For a period of minutes to days after a concussion, the brain is especially vulnerable to changes in intracranial pressure, blood flow, and anoxia.[30] 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.[30] 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.[46] Concussion is thought to be a milder type of diffuse axonal injury because axons may be injured to a minor extent due to stretching.[5] Animal studies in which primates were concussed have revealed damage to brain tissues such as small petechial hemorrhages and axonal injury.[47] 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.[11] Findings from a study of the brains of dead NFL athletes who received concussions suggest there is lasting damage to the brain after experiencing one; this damage can lead to a variety of other health issues.[48] The debate over whether concussion is a functional or structural phenomenon is ongoing.[49] 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.[6] These reversible changes could also explain why dysfunction is frequently temporary.[49] 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."[14] [edit] DiagnosisDiagnosis 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).[50] Neuropsychological tests exist to measure cognitive function.[11] 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.[51] Athletes may be tested before a sports season begins to provide a baseline comparison in the event of an injury.[52] 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,[53] increasing disorientation or a deteriorating level of consciousness,[54] seizures, and unequal pupil size.[55] People with such symptoms, or who are at higher risk for a more serious brain injury, are CT scaned to detect brain lesions and are frequently observed for 24 - 48 hours. If the Glasgow Coma Scale is less than 15 at two hours or less than 14 at any time a CT recommended.[8] 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,[8] or younger than 16. Most concussions cannot be detected with MRI or CT scans.[39] 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.[24] Mild head injury may or may not produce abnormal EEG readings.[56] 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 to remain in the competition.[26] A retrospective survey in 2005 found that more than 88% of concussions go unrecognized;[57]. 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).[58] [edit] Prevention Further information: Association football headgear, Bicycle helmet, Football helmet, Hockey helmet, Motorcycle helmet, and Ski helmet Prevention of MTBI involves taking general measures to prevent traumatic brain injury, such as wearing seat belts and using airbags in cars.[18] 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.[36] Use of protective equipment such as headgear has been found to reduce the number of concussions in athletes.[38] Improvements in the design of protective athletic gear such as helmets may decrease the number and severity of such injuries.[59] New "Head Impact Telemetry System" technology is being placed in helmets to study injury mechanisms and potentially help reduce the risk of concussions among American Football players. 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.[38] [edit] Treatment Usually concussion symptoms go away without treatment,[60] and no specific treatment exists.[61] About one percent of people who receive treatment for MTBI need surgery for a brain injury.[50] Traditionally, concussion sufferers are prescribed rest,[61] including plenty of sleep at night plus rest during the day.[55] Health care providers recommend a gradual return to normal activities at a pace that does not cause symptoms to worsen.[55] Education about symptoms, how to manage them, and their normal time course can lead to an improved outcome.[13] Medications may be prescribed to treat symptoms such as sleep problems and depression.[13] Analgesics such as ibuprofen can be taken for the headaches that frequently occur after concussion,[6] but paracetamol (acetaminophen) is preferred to minimize the risk for complications such as intracranial hemorrhage.[62] Concussed individuals are advised not to drink alcohol or take drugs that have not been approved by a doctor, as they could impede healing.[55] Observation to monitor for worsening condition is an important part of treatment.[63] 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[8] or those that 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.[64] 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.[8] [edit] Prognosis MTBI has a mortality rate of almost zero.[50] The symptoms of most concussions resolve within weeks, but problems may persist.[6] Problems are seldom permanent, and outcome is usually excellent.[24] People over age 55 may take longer to heal from MTBI or may heal incompletely.[65] Similarly, factors such as a previous head injury or a coexisting medical condition have been found to predict longer-lasting post-concussion symptoms.[47] 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.[24] Longer periods of amnesia or loss of consciousness immediately after the injury may indicate longer recovery times from residual symptoms.[66] For unknown reasons, having had one concussion significantly increases a person's risk of having another.[51] 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.[67] 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.[51] A 2009 study published in Brain 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.[68] [edit] 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.[69] Symptoms may include headaches, dizziness, fatigue, anxiety, memory and attention problems, sleep problems, and irritability.[70] There is no scientifically established treatment, and rest, a recommended recovery technique, has limited effectiveness.[61] Symptoms usually go away on their own within months.[23] 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.[58] [edit] 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.[71] Symptoms may be more severe and changes in neurophysiology can occur with the third and subsequent concussions.[51] 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.[38] 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.[72] Three or more concussions is also associated with a fivefold greater chance of developing Alzheimer's disease earlier and a three-fold greater chance of developing memory deficits.[72] [edit] 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.[73] It shares features with Alzheimer's disease.[74] [edit] 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.[30] 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.[51] As the brain swells, intracranial pressure rapidly rises.[53] The brain can herniate, and the brain stem can fail within five minutes.[30] Except in boxing, all cases have occurred in athletes under age 20.[44] Due to the very small number of documented cases, the diagnosis is controversial, and doubt exists about its validity.[75] Epidemiology. 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.[7] However, due to underreporting and to the widely varying definitions of concussion and MTBI, it is difficult to estimate how common the condition is.[4] 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.[24] 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.[7] Young children have the highest concussion rate among all age groups.[8] However, most people who suffer concussion are young adults.[69] A Canadian study found that the yearly incidence of MTBI is lower in older age groups (graph at right).[76] Studies suggest males suffer MTBI at about twice the rate of their female counterparts.[7] However, female athletes may be at a higher risk for suffering concussion than their male counterparts.[77] Up to five percent of sports injuries are concussions.[44] 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.[78] Since loss of consciousness is thought to occur in less than 10% of concussions,[79] the CDC estimate is likely lower than the real number.[78] 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.[80] Due to the lack of a consistent definition, the economic costs of MTBI are not known, but they are estimated to be very high.[81] These high costs are due in part to the large percentage of hospital admissions for head injury that are due to mild head trauma,[20] but indirect costs such as lost work time and early retirement account for the bulk of the costs.[81] These direct and indirect costs cause the expense of mild brain trauma to rival that of moderate and severe head injuries.[82]

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Knee Pain / Knee Injuries Knee pain can be related to overuse where small stresses are repeated a large number of times without allowing adequate recovery, for example running too much too soon, or excessive jumping. Or injuries can be acute where the injury is caused by an impact or twisting such as an anterior cruciate ligament injury. An overuse injury can also be considered to be acute if it is painful or inflammed. Knee Joint Injuries Anterior cruciate ligament injury, Medial ligament sprain, Lateral ligament sprain, Posterior cruciate ligament injury....more Anterior (Front) Injuries Jumpers knee (patella tendinitis), Osgood Schlatters disease, Patellofemoral pain syndrome, Chondromalacia Patellae, Housemaids knee..more Medial (Inside) Injuries Medial Cartilage Meniscus Injury, Medial Ligament Sprain, Osteoarthritis of the knee, Synovial Plica / Patella Plica...more Lateral (Outside) Pain Iliotibial band friction syndrome (runners knee), Patellofemoral instability, Lateral cartilage injury...more Posterior (Back) Pain Posterior cruciate ligament injury, Bakers Cyst, Hamstring tendon strain...more Acute Pain Acute patella injury, Patella dislocation, Patella tendon rupture....more. line line Anterior (front) Knee Pain Patellofemoral Pain Syndrome One of the most common knee injuries with pain originating from the patella or kneecap. A common overuse injury and running injury. Chondromalacia Patellae Damage to the cartilage lining the back of the patella. Fat Pad Impingement The fat pad is soft tissue between the patella and the femoral condyle (end of the thigh bone). It gets pinched, often as the result of a hyperextension (bending back) of the knee. Housemaid's Knee / Prepatella Bursitis Inflammation or swelling of the bursa or sac of fluid on the front of the patella. Infrapatellar Bursitis (Clergyman's Knee) Pain at the front of the patella from and inflamed bursa Jumpers knee (patella tendon inflammation / rupture) Inflammation of the patella tendon or from a partial rupture of the tendon. Osgood Schlatters disease An overuse injury mainly affecting young people undergoing a growth spurt. Symptoms include pain below the knee on the tibial tuberosity which becomes worse with use. Patellofemoral Instability Patellofemoral instability usually presents with the patient having a sensation of their kneecap (patella) 'slipping away' or feeling loose on movement. Patella tendonitis / Jumper's Knee Inflammation of the patella tendon or from a partial rupture of the tendon. Pre Patella Bursitis / Housemaids Knee Inflammation or swelling of the bursa or sac of fluid on the front of the patella. Quadriceps tendinopathy / inflammation at insertion at the Patella An overuse injury where the quadriceps tendon becomes inflamed and painful at the point it inserts into the patella. Quadriceps Haematoma Caused by a direct blow can cause bleeding withing the muscle or a haematoma. Synovial Plica / Patella Plica The synovial plica is a synovial fold found along the inside border of the patella. Patella Dislocation Where the patella (knee cap) moves out of the grove in which it normally runs Lateral (outer) Knee Pain Runners Knee (Iliotibial band syndrome) An overuse injury caused by the ilitibial band rubbing on the outside of the joint Lateral Meniscus Tear / cartilage tear Torn cartilage or meniscus towards the outside of the knee. Caused by internally rotating the knee with the foot, over bending the knee backwards or forwards, or from over use. Lateral Cartilage Meniscus Abnormality Knee injury involving pain similar to that in Iliotibial Band Friction syndrome. The lateral meniscus becomes inflammed or has degenerated. Osteoarthritis of the knee. Osteoarthritis (also called degenerative joint disease) is the degradation and degeneration of this articular cartilage. As the disease progresses, the cartilage itself becomes thinner and in some cases may wear away altogether. Patellofemoral Pain Syndrome One of the most common knee injuries with pain originating from the patella or kneecap. A common overuse injury and running injury. Medial (inner) Knee Pain Medial Cartilage Meniscus Injury Damage to the medial cartilage or meniscus causing pain to the inside of the knee. Can be caused by twisting the knee, over flexing (bending) or over use. Medial Ligament Sprain Sprain or tear to the medial colateral ligament. Often caused by impact to the outside of the knee. This injury is common in contact sports such as football and rugby. Osteoarthritis of the knee. Osteoarthritis (also called degenerative joint disease) is the degradation and degeneration of the articular cartilage. As the disease progresses, the cartilage itself becomes thinner and in some cases may wear away altogether. Synovial Plica / Patella Plica The synovial plica is a synovial fold found along the inside border of the patella. Posterior (back) Knee Pain Bakers cyst (Popliteal cyst) A prominent swelling at the back of the knee, often caused by some disorder within the joint. Biceps Femoris Tendinopathy Inflammation of the hamstring tendons at the back of the joint. Biceps Femoris Avulsion Avulsion of the biceps femoris tendon, is the complete pulling away of the tendon from the bone. Deep Vein Thrombosis / DVT Deep Vein Thrombosis is a blood clot in a vein. It is more common in the calf muscle area, particularly following surgery. Inflammation of hamstring tendons / tendinitis Inflammation of the hamstring tendons as they insert into the knee. Posterior cruciate ligament sprain Injury to the posterior cruciate ligament, often caused by hyperextension or bending the knee back the wrong way. Rupture of hamstring tendons / tendon strain Rupture or partial rupture of one of the hamstring tendons at the back of the joint. Popliteus injury Overuse of the Popliteus muscle at the back of the knee joint. Knee joint injuries (sprains and other conditions) Anterior cruciate ligament sprain Sprain or rupture of the anterior cruciate ligament, often caused by twisting or an impact to the side. Articular Cartilage Injury Or Osteochondritis dessicans - damage or flakes off the hard cartilage that lines the ends of bones. Lateral Ligament Sprain Sprain or tear to the lateral ligament on the outside of the joint, often caused by impact to the inside which over-stretches the ligament. Lateral Meniscus Tear / cartilage tear Torn cartilage or meniscus towards the outside of the joint. Caused by internally rotating the knee, over bending the knee backwards or forwards, or from over use. Medial Ligament Sprain Sprain or tear to the medial collateral ligament. Often caused by impact to the outside of the joint. Common in contact sports such as football and rugby. Medial Cartilage Meniscus Injury Medial cartilage or meniscus tear causing pain to the inside of the joint. Can be caused by twisting, over-flexing (bending) or over use. Posterior cruciate ligament sprain Injury to the posterior cruciate ligament, often caused by hyperextension or bending back the wrong way. Patella Disclocation Dislocation of the patella. Tibiofibular Joint Dislocation Dislocation of the proximal tibiofibular joint occurs most commonly when the athlete sustains an impact or falls with their knee in a fully flexed position, with their foot pointing inwards (inversion) and downwards. Acute Injuries (sudden onset knee pain) Acute Patellar Injury Contusion to the patella or fracture of the patella Anterior cruciate ligament sprain Sprain or rupture of the anterior cruciate ligament, often caused by twisting or an impact to the side of the knee. Articular Cartilage Injury Or Osteochondritis dessicans - damage or flakes off the hard cartilage that lines the ends of bones. Biceps femoris avulsion Avulsion of the biceps femoris tendon, is the complete pulling away of the tendon from the bone. Coronary Ligament Sprain The coronary ligament is part of the fibrous joint capsule. It attaches to the edge of the cartilage meniscis and to the adjacent part of the tibia or shin bone. Fat Pad Impingement The fat pad is soft tissue between the patella and the femoral condyle (end of the thigh bone). It gets pinched, often as the result of a hyperextension (over straightening). Hamstring tendon rupture / strain Rupture of the hamstring tendons as they insert into the back of the knee. Lateral Ligament Sprain Sprain or tear to the lateral ligament on the outside, often caused by impact to the inside of the knee which over-stretches the ligament. Lateral Meniscus Tear / cartilage tear Injury involving torn cartilage or meniscus towards the outside of the joint. Caused by internally rotating the knee, over bending the knee backwards or forwards, or from over use. Medial Ligament Sprain Sprain or tear to the medial collateral ligament. Often caused by impact to the outside of the knee. A common injury in contact sports such as football and rugby. Medial Cartilage Meniscus Injury Injury to the medial cartilage or meniscus causing pain to the inside of the joint. Can be caused by twisting, over-flexing (bending) or over use. Posterior cruciate ligament sprain Injury to the posterior cruciate ligament, often caused by hyperextension or over-straightening. Patella Disclocation Dislocation of the patella or kneecap. Patella Tendon Rupture Rupture or tear of the patella tendon. Pre Patella Bursitis / Housemaids Knee Inflammation or swelling of the bursa or sac of fluid on the front of the patella. Quadriceps Tendon Rupture Ruptures of the quadriceps tendon mainly occur in middle aged individuals during sporting activities. Tibial Plateau Fracture Fracture to the upper surface of the tibia or shin boneusually from high velocity accidents Tibiofibular Joint Dislocation Dislocation of the proximal tibiofibular joint occurs most commonly when the athlete sustains an impact or falls with their knee in a fully flexed position, with their foot pointing inwards (inversion) and downwards.

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Hip pain is common problem, and it can be confusing because there are many causes. It is important to make an accurate diagnosis of the cause of your symptoms so that appropriate treatment can be directed at the underlying problem. If you have hip pain, some common causes include: * Arthritis Arthritis is among the most frequent causes of hip pain, and there are many treatments available. If conservative treatments fail, hip replacement surgery is an option. * Trochanteric Bursitis Trochanteric bursitis is an extremely common problem that causes inflammation of the bursa over the outside of the hip joint. * Tendonitis Tendonitis can occur in any of the tendons that surround the hip joint. The most frequently encountered tendonitis around the hip is iliotibial band (IT band) tendonitis. * Osteonecrosis Osteonecrosis is a condition that occurs when blood flow to an area of bone is restricted. If an inadequate amount of blood flow reaches the bone, the cells will die and the bone may collapse. One of the most common places for osteonecrosis to occur is in the hip joint. * Lumbar Pain - Referred Symptoms Many back and spine problems can cause symptoms around the buttocks and hip. The most common problems that refer pain to the hip region are herniated discs and sciatica. * Snapping Hip Syndrome Snapping hip syndrome is a word used to describe three distinct hip problems. The first is when the IT band snaps over the outside of the thigh. The second occurs when the deep hip flexor snaps over the front of the hip joint. Finally, tears of the cartilage, or labrum, around the hip socket can cause a snapping sensation. * Muscle Strains Strains of the muscles around the hip and pelvis can cause pain and spasm. The most common strains are groin pulls and hamstring strains. * Hip Fracture Hip fractures are most common in elderly patients with osteoporosis. Treatment of broken hips requires surgery to either replace the broken portion or repair it with a metal plate and screws. * Stress Fracture Stress fractures of the hip are most common in athletes who participate in high-impact sports, such as long distance runners. Treatment usually is successful by avoiding the impact activities. Childhood Hip Problems: * Developmental Dysplasia When the hips are dislocated or out of position in infancy, the joint may not develop properly. While this is not usually painful as a child, it will lead to early arthritis and problems with walking. * Legg-Calve-Perthes Disease Also called Perthes disease, this is a problem similar to osteonecrosis (see above) but in childhood. If severe, it can lead to permanent damage to this hip joint and early arthritis. When do you need to call your doctor about your hip pain? If you are unsure of the cause of your symptoms, or if you do not know the specific treatment recommendations for your condition, you should seek medical attention. Treatment of hip pain must be directed at the specific cause of your problem. Some signs that you should be seen by a doctor include: o Inability to walk comfortably on the affected side o Injury that causes deformity around the joint o Hip pain that occurs at night or while resting o Hip pain that persists beyond a few days o Inability to bend the hip o Swelling of the hip or the thigh area o Signs of an infection, including fever, redness, warmth o Any other unusual symptoms What are the best treatments for hip pain? Treatment depends entirely on the cause of the problem. Therefore, it is of utmost importance that you understand the cause of your symptoms before embarking on a treatment program. If you are unsure of your diagnosis, or the severity of your condition, you should seek medical advice before beginning any treatment plan. Some common treatments for hip pain are listed here. Not all of these treatments are appropriate for every condition, but they may be helpful in your situation. * Rest: The first treatment for most conditions that cause hip pain is to rest the joint, and allow the acute inflammation to subside. Often this is the only step needed to relieve hip pain. If the symptoms are severe, crutches or a cane may be helpful as well. * Ice and Heat Application: Ice packs and heat pads are among the most commonly used treatments for inflammation. So which one is the right one to use, ice or heat? And how long should the ice or heat treatments last? Read on for more information about ice and heat treatment. * Stretching: Stretching the muscles and tendons that surround the joint can help with some causes of hip pain. A good routine should be established, and following some specific suggestions will help you on your way. * Physical Therapy: Physical therapy is an important aspect of treatment of almost all orthopedic conditions. Physical therapists use different modalities to increase strength, regain mobility, and help return patients to their pre-injury level of activity. * Anti-Inflammatory Medication: Nonsteroidal anti-inflammatory medications, commonly referred to as NSAIDs, are some of the most frequently prescribed medications, especially for patients with hip pain caused by problems such as arthritis, bursitis, and tendonitis.

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The rotator cuff is a group of muscles which work together to provide the Glenohumeral (shoulder) joint with dynamic stability, helping to control the joint during rotation (hence the name). The rotator cuff muscles include: Supraspinatus and Infraspinatus are the most commonly injured rotator cuff muscles. Due to the function of these muscles, sports which involve a lot of shoulder rotation – for example, bowling in cricket, pitching in baseball, swimming, kayaking – often put the rotator cuff muscles under a lot of stress. Problems with the rotator cuff muscles can be classed into two categories – Tears of the tendons/muscles, and inflammation of structures in the joint. Acute Tear This tends to happen as a result of a sudden, powerful movement. This might include falling over onto an outstretched hand at speed, making a sudden thrust with the paddle in kayaking, or following a powerful pitch/throw. The symptoms will usually include: * Sudden, tearing feeling in the shoulder, followed by severe pain through the arm * Limited movement of the shoulder due to pain or muscle spasm * Severe pain for a few days (due to bleeding and muscle spasm) which usually resolves quickly * Specific tenderness (“x marks the spot”) over the point of rupture/tear * If there is a severe tear, you will not be able to abduct your arm (raise it out to the side) without assistance Chronic Tear A chronic tear develops over a period of time. They usually occur at or near the tendon, as a result of the tendon rubbing against the overlying bone. This is usually associated with an impingement syndrome. * Usually found on the dominant side * More often an affliction of the 40+ age group * Pain is worse at night, and can affect sleeping * Gradual worsening of pain, eventually some weakness * Eventually unable to abduct arm (lift out to the side) without assistance or do any activities with the arm above the head * Some limitations of other movements depending on the tendon affected

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