TBI is a leading cause of death and disability around the globe and presents a major worldwide social, economic, and health problem. It is the number one cause of coma, it plays the leading role in disability due to trauma, and is the leading cause of brain damage in children and young adults. In Europe it is responsible for more years of disability than any other cause. It also plays a significant role in half of trauma deaths.

Findings on the frequency of each level of severity vary based on the definitions and methods used in studies. A World Health Organization study estimated that between 70 and 90% of head injuries that receive treatment are mild, and a US study found that moderate and severe injuries each account for 10% of TBIs, with the rest mild.

The incidence of TBI varies by age, gender, region and other factors. Findings of incidence and prevalence in epidemiological studies vary based on such factors as which grades of severity are included, whether deaths are included, whether the study is restricted to hospitalized people, and the study's location. The annual incidence of mild TBI is difficult to determine but may be 100–600 people per 100,000.

In the US, the case fatality rate is estimated to be 21% by 30 days after TBI. A study on Iraq War soldiers found that severe TBI carries a mortality of 30–50%. Deaths have declined due to improved treatments and systems for managing trauma in societies wealthy enough to provide modern emergency and neurosurgical services. The fraction of those who die after being hospitalized with TBI fell from almost half in the 1970s to about a quarter at the beginning of the 21st century. This decline in mortality has led to a concomitant increase in the number of people living with disabilities that result from TBI.

Biological, clinical, and demographic factors contribute to the likelihood that an injury will be fatal. In addition, outcome depends heavily on the cause of head injury. In the US, patients with fall-related TBIs have an 89% survival rate, while only 9% of patients with firearm-related TBIs survive. In the US, firearms are the most common cause of fatal TBI, followed by vehicle accidents and then falls. Of deaths from firearms, 75% are considered to be suicides.

The incidence of TBI is increasing globally, due largely to an increase in motor vehicle use in low- and middle-income countries. In developing countries, automobile use has increased faster than safety infrastructure could be introduced. In contrast, vehicle safety laws have decreased rates of TBI in high-income countries, which have seen decreases in traffic-related TBI since the 1970s. Each year in the United States, about two million people suffer a TBI, approximately 675,000 injuries are seen in the emergency department, and about 500,000 patients are hospitalized. The yearly incidence of TBI is estimated at 180–250 per 100,000 people in the US, 281 per 100,000 in France, 361 per 100,000 in South Africa, 322 per 100,000 in Australia, and 430 per 100,000 in England. In the European Union the yearly aggregate incidence of TBI hospitalizations and fatalities is estimated at 235 per 100,000.

Common causes of head injury are motor vehicle traffic collisions, home and occupational accidents, falls, and assaults. Wilson's disease has also been indicative of head injury. According to the United States CDC, 32% of traumatic brain injuries (another, more specific, term for head injuries) are caused by falls, 10% by assaults, 16.5% by being struck or against something, 17% by motor vehicle accidents, 21% by other/unknown ways. In addition, the highest rate of injury is among children ages 0–14 and adults age 65 and older.

A wide range of factors have been identified as being predictive of PCS, including low socioeconomic status, previous mTBI, a serious associated injury, headaches, an ongoing court case, and female gender. Being older than 40 and being female have also been identified as being predictive of a diagnosis of PCS, and women tend to report more severe symptoms. In addition, the development of PCS can be predicted by having a history of alcohol abuse, low cognitive abilities before the injury, a personality disorder, or a medical illness not related to the injury. PCS is also more prevalent in people with a history of psychiatric conditions such as clinical depression or anxiety before the injury.

Mild brain injury-related factors that increase the risk for persisting post-concussion symptoms include an injury associated with acute headache, dizziness, or nausea; an acute Glasgow Coma Score of 13 or 14; and suffering another head injury before recovering from the first. The risk for developing PCS also appears to be increased in people who have traumatic memories of the injury or expect to be disabled by the injury.

In children with uncomplicated minor head injuries the risk of intra cranial bleeding over the next year is rare at 2 cases per 1 million. In some cases transient neurological disturbances may occur, lasting minutes to hours. Malignant post traumatic cerebral swelling can develop unexpectedly in stable patients after an injury, as can post traumatic seizures. Recovery in children with neurologic deficits will vary. Children with neurologic deficits who improve daily are more likely to recover, while those who are vegetative for months are less likely to improve. Most patients without deficits have full recovery. However, persons who sustain head trauma resulting in unconsciousness for an hour or more have twice the risk of developing Alzheimer's disease later in life.

Head injury may be associated with a neck injury. Bruises on the back or neck, neck pain, or pain radiating to the arms are signs of cervical spine injury and merit spinal immobilization via application of a cervical collar and possibly a long board.If the neurological exam is normal this is reassuring. Reassessment is needed if there is a worsening headache, seizure, one sided weakness, or has persistent vomiting.

To combat overuse of Head CT Scans yielding negative intracranial hemorrhage, which unnecessarily expose patients to radiation and increase time in the hospital and cost of the visit, multiple clinical decision support rules have been developed to help clinicians weigh the option to scan a patient with a head injury. Among these are the Canadian Head CT rule, the PECARN Head Injury/Trauma Algorithm, and the New Orleans/Charity Head Injury/Trauma Rule all help clinicians make these decisions using easily obtained information and noninvasive practices.

Elderly people are the most rapidly growing demographic in developed nations. Although they sustain traumatic injury less commonly than children and young adults, the mortality rate for trauma in the elderly is higher than in younger people. In the United States, this population accounts for 14% of all traumatic injuries, of which a majority are secondary to falls.

It is not known exactly how common PCS is. Estimates of the prevalence at 3 months post-injury are between 24 and 84%, a variation possibly caused by different populations or study methodologies. The estimated incidence of PPCS (persistent postconcussive syndrome) is around 10% of mTBI cases. Since PCS by definition only exists in people who have suffered a head injury, demographics and risk factors are similar to those for head injury; for example, young adults are at higher risk than others for receiving head injury, and, consequently, of developing PCS.

The existence of PCS in children is controversial. It is possible that children's brains have enough plasticity that they are not affected by long-term consequences of concussion (though such consequences are known to result from moderate and severe head trauma). On the other hand, children's brains may be more vulnerable to the injury, since they are still developing and have fewer skills that can compensate for deficits. Clinical research has found higher rates of post-concussion symptoms in children with TBI than in those with injuries to other parts of the body, and that the symptoms are more common in anxious children. Symptoms in children are similar to those in adults, but children exhibit fewer of them. Evidence from clinical studies found that high school-aged athletes had slower recoveries from concussion as measured by neuropsychological tests than college-aged ones and adults. PCS is rare in young children.

Many closed-head injuries can be prevented by proper use of safety equipment during dangerous activities. Common safety features that can reduce the likelihood of experiencing a brain injury include helmets, hard hats, car seats, and safety belts. Another safety precaution that can decrease a person's risk for brain injury is "not" to drink and drive or allow oneself to be driven by a person who has been drinking or who is otherwise impaired.

Helmets can be used to decrease closed-head injuries acquired during athletic activities, and are considered necessary for sports such as American "tackle" football, where frequent head impacts are a normal part of the game. However, recent studies have questioned the effectiveness of even American football helmets, where the assumed protection of helmets promotes far more head impacts, a behavior known as risk compensation. The net result seems to have been an increase, not decrease, in TBI. The similar sports of Australian-rules football and rugby are always played helmetless, and see far fewer traumatic brain injuries. (See Australian rules football injuries.)

Bicycle helmets are perhaps the most promoted variety of helmet, based on the assumption that cycling without a helmet is a dangerous activity, with a large risk of serious brain injury. However, available data clearly shows that to be false. Cycling (with approximately 700 American fatalities per year from all medical causes) is a very minor source of fatal traumatic brain injury, whose American total is approximately 52,000 per year. Similarly, bicycling causes only 3% of America's non-fatal TBI.

Still, bicycle-helmet promotion campaigns are common, and many U.S jurisdictions have enacted mandatory bicycle-helmet laws for children. A few such jurisdictions, a few Canadian provinces, plus Australia and New Zealand mandate bicycle helmets even for adults. A bicycle-helmet educational campaign directed toward children claimed an increase in helmet use from 5.5% to 40.2% leading to a claimed decrease in bicycle-related head injuries by nearly 67%. However, other sources have shown that bicycle-helmet promotion reduces cycling, often with no per-cyclist reduction in TBI.

Estimates of bicycle-helmet use by American adults vary. One study found that only 25-30% of American adults wear helmets while riding bicycles, despite decades of promotion and despite sport cyclists' adoption of helmets as part of their uniform. It would appear that the typical American adult correctly recognizes ordinary cycling as a very minor risk.

Following the commercial (as opposed to public-health) success of bicycle helmets, there have been successful attempts to promote the sale of ski helmets. Again, results have been less than impressive, with great increases in helmet use yielding no reduction in fatalities, and with most injury reduction confined to lacerations, contusions, and minor concussions, as opposed to more serious head injuries.

There have been rare campaigns for motoring helmets. Unfortunately, just as people greatly overestimate the TBI danger of bicycling, they greatly underestimate the risk of motoring, which remains the largest source of TBI in the developed world, despite the protective effects of seatbelts and airbags.

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 outcome is usually excellent. 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.

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 underreporting 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 underreporting. 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.

Young children have the highest concussion rate among all age groups. However, most people who suffer 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 for suffering concussion than their male counterparts.

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.

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 are 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.

The consequences of whiplash range from mild pain for a few days (which is the case for most people), to severe disability. It seems that around 50% will have some remaining symptoms.

Alterations in resting state cerebral blood flow have been demonstrated in patients with chronic pain after whiplash injury. There is evidence for persistent inflammation in the neck in patients with chronic pain after whiplash injury.

There has long been a proposed link between whiplash injuries and the development of temporomandibular joint dysfunction (TMD). A recent review concluded that although there are contradictions in the literature, overall there is moderate evidence that TMD can occasionally follow whiplash injury, and that the incidence of this occurrence is low to moderate.

Whiplash is the term commonly used to describe hyperflexion and hyperextension, and is one of the most common nonfatal car crash injuries. More than one million whiplash injuries occur each year due to car crashes. This is an estimate because not all cases of whiplash are reported. In a given year, an estimated 3.8 people per 1000 experience whiplash symptoms. "Freeman and co-investigators estimated that 6.2% of the US population have late whiplash syndrome". The majority of cases occur in patients in their late fourth decade. Unless a cervical strain has occurred with additional brain or spinal cord trauma mortality is rare.

Whiplash can occur at speeds of fifteen miles per hour or less; it is the sudden jolt, as one car hits another, that causes ones head to be abruptly thrown back and sideways. The more sudden the motion, the more bones, discs, muscles and tendons in ones neck and upper back will be damaged. Spinal cord injuries are responsible for about 6,000 deaths in the US each year and 5,000 whiplash injuries per year result in quadriplegia.

After 12 months, only 1 in 5 patients remain symptomatic, only 11.5% of individuals were able to return to work a year after the injury, and only 35.4% were able to get back to work at a similar level of performance after 20 years. Estimated indirect costs to industry are $66,626 per year, depending on the level and severity. Lastly, the total cost per year was $40.5 billion in 2008, a 317% increase over 1998.

Virtually all organ systems experience a progressive decline in function as a result of the aging process. One example is a decline in circulatory system function caused in part by thickening of the cardiac muscle. This can lead to congestive heart failure or pulmonary edema.

Atrophy of the brain begins to accelerate at around seventy years of age, which leads to a significant reduction in brain mass. Since the skull does not decrease in size with the brain, there is significant space between the two when this occurs which puts the elderly at a higher risk of a subdural hematoma after sustaining a closed head injury. The reduction of brain size can lead to issues with eyesight, cognition and hearing.

There are several different types of treatment available to those who have suffered a closed-head injury. The treatment type chosen can depend on several factors including the type and severity of injury as well as the effects that injury has on the patient.

The course of treatment differs for each patient and can include several types of treatment, depending on the patient’s specific needs.

Early treatment is vital to recovering lost motor function after an injury, but cognitive abilities can be recovered regardless of time past since injury.

Concussion symptoms can last for an undetermined amount of time depending on the player and the severity of the concussion. A concussion will affect the way a person's brain works.

There is the potential of post-concussion syndrome, post-concussion syndrome is defined as a set of symptoms that may continue after a concussion is sustained. Post-concussion symptoms can be classified into physical, cognitive, emotional, and sleep symptoms. Physical symptoms include a headache, nausea, and vomiting. Athletes may experience cognitive symptoms that include speaking slowly, difficulty remembering and concentrating. Emotional and sleep symptoms include irritability, sadness, drowsiness, and trouble falling asleep.

Along with the classification of post-concussion symptoms, the symptoms can also be described as immediate and delayed. The immediate symptoms are experienced immediately after a concussion such as: memory loss, disorientation, and poor balance. Delayed symptoms are experienced in the later stages and include sleeping disorders and behavioral changes. Both immediate and delayed symptoms can continue for long periods of time and have a negative impact on recovery. According to research, 20-25% of individuals who have sustained a concussion experienced chronic, delayed symptoms.

Playing through concussion makes people more vulnerable to getting hit again, and that is why most sports have test that trainers will perform to prevent getting hit a second time. A second blow can cause a rare condition known as second-impact syndrome, which can result in severe injury or death. Second-impact syndrome is when an athlete suffers a second head injury before the brain has adequate time to heal in between concussions.

Repeated concussions have been linked to a variety of neurological disorders among athletes, including CTE, Alzheimer's Disease, Parkinsonism and Amyotrophic lateral sclerosis (ALS).

Concussions, a type of traumatic brain injury, are a frequent concern for those playing sports, from children and teenagers to professional athletes. Repeated concussions are a known cause of various neurological disorders, most notably chronic traumatic encephalopathy (CTE), which in professional athletes has led to premature retirement, erratic behavior and even suicide. Because concussions cannot be seen on X-rays or CT scans, attempts to prevent concussions have been difficult.

A concussion is defined as a complex pathophysiological process affecting the brain, induced by traumatic forces. Concussion may be caused either by a direct blow to the head, face, neck or elsewhere on the body with an "impulsive" force transmitted to the head. Also, you don't have to pass out when you get a concussion (Aubry et al., 2001).

The dangers of repeated concussions have long been known for boxers and wrestlers; a form of CTE common in these two sports, dementia pugilistica (DP), was first described in 1928. An awareness of the risks of concussions in other sports began to grow in the 1990s, and especially in the mid-2000s, in both the medical and the professional sports communities, as a result of studies of the brains of prematurely deceased American football players, who showed extremely high incidences of CTE (see concussions in American football).

As of 2012, the four major professional sports leagues in the United States and Canada have concussion policies. Sports-related concussions are generally analyzed by athletic training or medical staff on the sidelines using an evaluation tool for cognitive function known as the Sport Concussion Assessment Tool (SCAT), a symptom severity checklist, and a balance test.

Concussions in England's professional rugby union are the most common injury gained. Concussion can occur where an individual experiences a minor injury to the head. Commonly occurring in high contact sporting activities; American football, boxing, and rugby. It can also occur in recreational activities like horse riding, jumping, cycling, and skiing. The reason being that it doesn't have to be something to strike you in the proximity of your brain, but can also be caused by rapid change of movement, giving the skull not enough time to move with your body, causing your brain to press against your skull. With rugby being such a contact and fast moving sport, it is no wonder why there is concussion and other head injuries occurring. With the development of equipment and training methods, these will help benefit the players on the field know what could happen and how they can help with preventing it.

Pain, especially headache, is a common complication following a TBI. Being unconscious and lying still for long periods can cause blood clots to form (deep venous thrombosis), which can cause pulmonary embolism. Other serious complications for patients who are unconscious, in a coma, or in a vegetative state include pressure sores, pneumonia or other infections, and progressive multiple organ failure.

The risk of post-traumatic seizures increases with severity of trauma (image at right) and is particularly elevated with certain types of brain trauma such as cerebral contusions or hematomas. As many as 50% of people with penetrating head injuries will develop seizures. People with early seizures, those occurring within a week of injury, have an increased risk of post-traumatic epilepsy (recurrent seizures occurring more than a week after the initial trauma) though seizures can appear a decade or more after the initial injury and the common seizure type may also change over time. Generally, medical professionals use anticonvulsant medications to treat seizures in TBI patients within the first week of injury only and after that only if the seizures persist.

Neurostorms may occur after a severe TBI. The lower the Glasgow Coma Score (GCS), the higher the chance of Neurostorming. Neurostorms occur when the patient's Autonomic Nervous System (ANS), Central Nervous System (CNS), Sympathetic Nervous System (SNS), and ParaSympathetic Nervous System (PSNS) become severely compromised https://www.brainline.org/story/neurostorm-century-part-1-3-medical-terminology . This in turn can create the following potential life-threatening symptoms: increased IntraCranial Pressure (ICP), tachycardia, tremors, seizures, fevers, increased blood pressure, increased Cerebral Spinal Fluid (CSF), and diaphoresis https://www.brainline.org/story/neurostorm-century-part-1-3-medical-terminology. A variety of medication may be used to help decrease or control Neurostorm episodes https://www.brainline.org/story/neurostorm-century-part-3-3-new-way-life.

Parkinson's disease and other motor problems as a result of TBI are rare but can occur. Parkinson's disease, a chronic and progressive disorder, may develop years after TBI as a result of damage to the basal ganglia. Other movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), and myoclonus (shock-like contractions of muscles).

Skull fractures can tear the meninges, the membranes that cover the brain, leading to leaks of cerebrospinal fluid (CSF). A tear between the dura and the arachnoid membranes, called a CSF fistula, can cause CSF to leak out of the subarachnoid space into the subdural space; this is called a subdural hygroma. CSF can also leak from the nose and the ear. These tears can also allow bacteria into the cavity, potentially causing infections such as meningitis. Pneumocephalus occurs when air enters the intracranial cavity and becomes trapped in the subarachnoid space. Infections within the intracranial cavity are a dangerous complication of TBI. They may occur outside of the dura mater, below the dura, below the arachnoid (meningitis), or within the brain itself (abscess). Most of these injuries develop within a few weeks of the initial trauma and result from skull fractures or penetrating injuries. Standard treatment involves antibiotics and sometimes surgery to remove the infected tissue.

Injuries to the base of the skull can damage nerves that emerge directly from the brain (cranial nerves). Cranial nerve damage may result in:

- Paralysis of facial muscles

- Damage to the nerves responsible for eye movements, which can cause double vision

- Damage to the nerves that provide sense of smell

- Loss of vision

- Loss of facial sensation

- Swallowing problems

Hydrocephalus, post-traumatic ventricular enlargement, occurs when CSF accumulates in the brain, resulting in dilation of the cerebral ventricles and an increase in ICP. This condition can develop during the acute stage of TBI or may not appear until later. Generally it occurs within the first year of the injury and is characterized by worsening neurological outcome, impaired consciousness, behavioral changes, ataxia (lack of coordination or balance), incontinence, or signs of elevated ICP.

Any damage to the head or brain usually results in some damage to the vascular system, which provides blood to the cells of the brain. The body can repair small blood vessels, but damage to larger ones can result in serious complications. Damage to one of the major arteries leading to the brain can cause a stroke, either through bleeding from the artery or through the formation of a blood clot at the site of injury, blocking blood flow to the brain. Blood clots also can develop in other parts of the head. Other types of vascular complications include vasospasm, in which blood vessels constrict and restrict blood flow, and the formation of aneurysms, in which the side of a blood vessel weakens and balloons out.

Fluid and hormonal imbalances can also complicate treatment. Hormonal problems can result from dysfunction of the pituitary, the thyroid, and other glands throughout the body. Two common hormonal complications of TBI are syndrome of inappropriate secretion of antidiuretic hormone and hypothyroidism.

Another common problem is spasticity. In this situation, certain muscles of the body are tight or hypertonic because they cannot fully relax.

The nature of the head trauma also influences the risk of PTE. People who suffer depressed skull fractures, penetrating head trauma, early PTS, and intracerebral and subdural haematomas due to the TBI are especially likely to suffer PTE, which occurs in more than 30% of people with any one of these findings. About 50% of patients with penetrating head trauma develop PTE, and missile injuries and loss of brain volume are associated with an especially high likelihood of developing the condition. Injuries that occur in military settings carry higher-than-usual risk for PTE, probably because they more commonly involve penetrating brain injury and brain damage over a more widespread area. Intracranial hematomas, in which blood accumulates inside the skull, are one of the most important risk factors for PTE. Subdural hematoma confers a higher risk of PTE than does epidural hematoma, possibly because it causes more damage to brain tissue. Repeated intracranial surgery confers a high risk for late PTE, possibly because people who need more surgery are more likely to have factors associated with worse brain trauma such as large hematomas or cerebral swelling. In addition, the chances of developing PTE differ by the location of the brain lesion: brain contusion that occurs on in one or the other of the frontal lobes has been found to carry a 20% PTE risk, while a contusion in one of the parietal lobes carries a 19% risk and one in a temporal lobe carries a 16% chance. When contusions occur in both hemispheres, the risk is 26% for the frontal lobes, 66% for the parietal, and 31% for the temporal.

To minimise the risks of concussion the mild traumatic brain injury, using the method of the 6 R's. Firstly Recognising and Removing a suspected player of concussion, to stop the injury from getting worse. Secondly Refer, whether the player is either recognised or suspected with concussion they must see a medical doctor as soon as possible. 90.8% of players knew they should not continue playing when concussed. 75% of players would continue an important game even if concussed. Of those concussed, 39.1% have tried to influence medical assessment with 78.2% stating it is possible or quite easy to do so. If the player is diagnosed with concussion, they then must Rest, until all signs of concussion are gone. The player must then Recover by just returning to general activities in life, then progressing back to playing. Returning to play, must follow the Graduated Return to Play (GRTP) protocol, by having clearance from a medical professional, and no symptoms of concussion. Despite good knowledge of concussion complications, management players engage in unsafe behaviour with little difference between gender and competition grades. Information regarding symptoms and management should be available to all players, coaches, and parents. On-going education is needed to assist coaches in identifying concussion signs and symptoms. Provision of medical care should be mandatory at every level of competition.

The more severe the brain trauma is, the more likely a person is to suffer late PTE. Evidence suggests that mild head injuries do not confer an increased risk of developing PTE, while more severe types do. In simple mild TBI, the risk for PTE is about 1.5 times that of the uninjured population. By some estimates, as many as half of sufferers of severe brain trauma experience PTE; other estimates place the risk at 5% for all TBI patients and 15–20% for severe TBI. One study found that the 30-year risk of developing PTE was 2.1% for mild TBI, 4.2% for moderate, and 16.7% for severe injuries, as shown in the chart at right.

A cerebral laceration with large amounts of blood apparent on a CT scan is an indicator of poor prognosis. The progression and course of complications (health effects that result from but are distinct from the injury itself) do not appear to be affected by a cerebral laceration's location or a mass effect it causes.

Cerebral lacerations usually accompany other brain injuries and are often found with skull fractures on both sides of the head. Frequently occurring in the same areas as contusions, lacerations are particularly common in the inferior frontal lobes and the poles of the temporal lobes. When associated with diffuse axonal injury, the corpus callosum and the brain stem are common locations for laceration. Lacerations are very common in penetrating and perforating head trauma and frequently accompany skull fractures; however, they may also occur in the absence of skull fracture. Lacerations, which may result when brain tissue is stretched, are associated with intraparenchymal bleeding (bleeding into the brain tissue).

Traumatic brain injury (TBI, physical trauma to the brain) can cause a variety of complications, health effects that are not TBI themselves but that result from it. The risk of complications increases with the severity of the trauma; however even mild traumatic brain injury can result in disabilities that interfere with social interactions, employment, and everyday living. TBI can cause a variety of problems including physical, cognitive, emotional, and behavioral complications.

Symptoms that may occur after a concussion – a minor form of traumatic brain injury – are referred to as post-concussion syndrome.

DAI is the result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated, as may occur in car accidents, falls, and assaults. Vehicle accidents are the most frequent cause of DAI; it can also occur as the result of child abuse such as in shaken baby syndrome.

Immediate disconnection of axons could be observed in severe brain injury, but the major damage of DAI is delayed secondary axon disconnections slowly developed over an extended time course. Tracts of axons, which appear white due to myelination, are referred to as white matter. Lesions in both grey and white matters are found in postmortem brains in CT and MRI exams.

Besides mechanical breaking of the axonal cytoskeleton, DAI pathology also includes secondary physiological changes such as interrupted axonal transport, progressive swellings and degeneration. Recent studies have linked these changes to twisting and misalignment of broken axon microtubules, as well as tau and APP deposition.