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.

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.

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.

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.

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.

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

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

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.

The chances that a person will suffer PTS are influenced by factors involving the injury and the person. The largest risks for PTS are having an altered level of consciousness for a protracted time after the injury, severe injuries with focal lesions, and fractures. The single largest risk for PTS is penetrating head trauma, which carries a 35 to 50% risk of seizures within 15 years. If a fragment of metal remains within the skull after injury, the risk of both early and late PTS may be increased. Head trauma survivors who abused alcohol before the injury are also at higher risk for developing seizures.

Occurrence of seizures varies widely even among people with similar injuries. It is not known whether genetics play a role in PTS risk. Studies have had conflicting results with regard to the question of whether people with PTS are more likely to have family members with seizures, which would suggest a genetic role in PTS. Most studies have found that epilepsy in family members does not significantly increase the risk of PTS. People with the ApoE-ε4 allele may also be at higher risk for late PTS.

Risks for late PTS include hydrocephalus, reduced blood flow to the temporal lobes of the brain, brain contusions, subdural hematomas, a torn dura mater, and focal neurological deficits. PTA that lasts for longer than 24 hours after the injury is a risk factor for both early and late PTS. Up to 86% of people who have one late post-traumatic seizure have another within two years.

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.

It is not known whether PTS increase the likelihood of developing PTE. Early PTS, while not necessarily epileptic in nature, are associated with a higher risk of PTE. However, PTS do not indicate that development of epilepsy is certain to occur, and it is difficult to isolate PTS from severity of injury as a factor in PTE development. About 3% of patients with no early seizures develop late PTE; this number is 25% in those who do have early PTS, and the distinction is greater if other risk factors for developing PTE are excluded. Seizures that occur immediately after an insult are commonly believed not to confer an increased risk of recurring seizures, but evidence from at least one study has suggested that both immediate and early seizures may be risk factors for late seizures. Early seizures may be less of a predictor for PTE in children; while as many as a third of adults with early seizures develop PTE, the portion of children with early PTS who have late seizures is less than one fifth in children and may be as low as one tenth. The incidence of late seizures is about half that in adults with comparable injuries.

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.

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 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.

Head injuries in sports of any level (junior, amateur, professional) are the most dangerous and sickening kind of injuries that can occur in sport, and are becoming more common in Australian sport. Concussions are the most common side effect of a head injury and are defined as "temporary unconsciousness or confusion and other symptoms caused by a blow to the head." A concussion also falls under the category of Traumatic Brain Injury (TBI). Especially in contact sports like Australian rules football and Rugby issues with concussions are prevalent, and methods to deal with, prevent and treat concussions are continuously being updated and researched to deal with the issue. Concussions pose a serious threat to the patients’ mental and physical health, as well as their playing career, and can result in lasting brain damage especially if left untreated. The signs that a player may have a concussion are: loss of consciousness or non-responsiveness, balance problems (unsteadiness on feet, poor co-ordination), a dazed, blank or vacant look and/or confusion and unawareness of their surroundings. Of course the signs are relevant only after the player experiences a blow to the head.

Concussions and other types of repetitive play-related head blows in American football have been shown to be the cause of chronic traumatic encephalopathy (CTE), which has led to player suicides and other debilitating symptoms after retirement, including memory loss, depression, anxiety, headaches, and also sleep disturbances.

The list of ex-NFL players that have either been diagnosed "post-mortem" with CTE or have reported symptoms of CTE continues to grow.

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.

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 occurrence of concussion in children during sport is significantly more likely compared to other levels of athletes. Roughly 20% of children playing sport are diagnosed with concussion. Despite the lower level of impact compared to the professional or amateur levels, children's neck muscles are quite weak and most lack the awareness and skill level to cushion or prepare themselves for a blow leading to a high concussion rate. The guidelines and protocols for a child suffering a concussion are basically the same as if an adult received one.

For a child diagnosed with a concussion, the real issue is returning to school rather than the sporting field, as a concussion can affect a child's learning ability. A medical clearance is required before a return to school is possible and parents are recommended to properly manage their child through the first 72 hours after experiencing a concussion.

Concussions are proven to cause loss of brain function. This can lead to physical and emotional symptoms such as attention disorders, depression, headaches, nausea, and amnesia. These symptoms can last for days or week and even after the symptoms have gone, the brain still won't be completely normal. Players with multiple concussions can have drastically worsened symptoms and exponentially increased recovery time.

Researchers at UCLA have, for the first time, used a brain-imaging tool to identify a certain protein found in five retired NFL players. The presence and accumulation of tau proteins found in the five living players, are associated with Alzheimer's disease. Previously, this type of exam could only be performed with an autopsy. Scientists at UCLA created a chemical marker that binds to the abnormal proteins and they are able to view this with Positron Emission Tomography (PET) scan. Researcher at UCLA, Gary Small explains, "Providing a non-invasive method for early detection is a critical first step in developing interventions to prevent symptom onset and progression in CTE".

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease found in people who have had multiple head injuries. Symptoms may include behavioral problems, mood problems, and problems with thinking. This typically does not begin until years after the injuries. It often gets worse over time and can result in dementia. It is unclear if the risk of suicide is altered.

Most documented cases have occurred in athletes involved in contact sports such as football, wrestling, ice hockey, and soccer. Other risk factors include being in the military, prior domestic violence, and repeated banging of the head. The exact amount of trauma required for the condition to occur is unknown. Definitive diagnosis can only occur at autopsy. It is a form of tauopathy.

As of 2017 there is no specific treatment. Rates of disease have been found to be about 30% among those with a history of multiple head injuries. Population rates, however, are unclear. Research into brain damage as a result of repeated head injuries began in the 1920s, at which time the condition was known as "punch drunk". Changing the rules in some sports has been discussed as a means of prevention.

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.

Those at the overall highest risk for lateral medullary syndrome are men at an average age of 55.06. Having a history of hypertension, diabetes and smoking all increase the risk of large artery atherosclerosis. Large artery atherosclerosis is thought to be the greatest risk factor for lateral medullary syndrome due to the deposits of cholesterol, fatty substances, cellular waste products, calcium and fibrin. Otherwise known as plaque build up in the arteries.