In the past, the term PCS was also used to refer to immediate physical symptoms or post-concussive symptoms following a minor TBI or concussion. The severity of these symptoms typically decreases rapidly. In addition, the nature of the symptoms may change over time: acute symptoms are most commonly of a physical nature, while persisting symptoms tend to be predominantly psychological. Symptoms such as noise sensitivity, problems with concentration and memory, irritability, depression, and anxiety may be called 'late symptoms' because they generally do not occur immediately after the injury, but rather in the days or weeks after the injury. Nausea and drowsiness commonly occur acutely following concussion. Headache and dizziness occur immediately after the injury, but also can be long lasting.

A common condition associated with PCS is headache. While most people have headaches of the same type they experienced before the injury, people diagnosed with PCS often report more frequent or longer-lasting headaches. Between 30% and 90% of people treated for PCS report having more frequent headaches and between 8% and 32% still report them a year after the injury.

Dizziness is another common symptom reported in about half of people diagnosed with PCS and is still present in up to a quarter of them a year after the injury. Older people are at especially high risk for dizziness, which can contribute to subsequent injuries and higher rates of mortality due to falls.

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% report blurred vision. People may also have double vision or ringing in the ears, also called tinnitus. PCS may cause insomnia, fatigue, or other problems with sleep.

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

Severe head injuries can lead to permanent vegetative states or death, therefore being able to recognize symptoms and get medical attention is very important. Symptoms of a severe closed-head injury include:

- coma

- seizures

- loss of consciousness

Cognitive symptoms include confusion, disorientation, and difficulty focusing attention. Loss of consciousness may occur, but is not necessarily correlated with the severity of the concussion if it is brief. Post-traumatic amnesia, in which events following the injury cannot be recalled, is a hallmark of concussion. Confusion, another concussion hallmark, may be present immediately or may develop over several minutes. A person may repeat the same questions, be slow to respond to questions or directions, have a vacant stare, or have slurred or incoherent speech. Other MTBI symptoms include changes in sleeping patterns and difficulty with reasoning, concentrating, and performing everyday activities.

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

Because the brain swelling that produces these symptoms is often a slow process, these symptoms may not surface for days to weeks after the injury.

Common symptoms of a closed-head injury include:

- headache

- dizziness

- nausea

- slurred speech

- vomiting

Symptoms are dependent on the type of TBI (diffuse or focal) and the part of the brain that is affected. Unconsciousness tends to last longer for people with injuries on the left side of the brain than for those with injuries on the right. Symptoms are also dependent on the injury's severity. With mild TBI, the patient may remain conscious or may lose consciousness for a few seconds or minutes. Other symptoms of mild TBI include headache, vomiting, nausea, lack of motor coordination, dizziness, difficulty balancing, lightheadedness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, and changes in sleep patterns. Cognitive and emotional symptoms include behavioral or mood changes, confusion, and trouble with memory, concentration, attention, or thinking. Mild TBI symptoms may also be present in moderate and severe injuries.

A person with a moderate or severe TBI may have a headache that does not go away, repeated vomiting or nausea, convulsions, an inability to awaken, dilation of one or both pupils, slurred speech, aphasia (word-finding difficulties), dysarthria (muscle weakness that causes disordered speech), weakness or numbness in the limbs, loss of coordination, confusion, restlessness, or agitation. Common long-term symptoms of moderate to severe TBI are changes in appropriate social behavior, deficits in social judgment, and cognitive changes, especially problems with sustained attention, processing speed, and executive functioning. Alexithymia, a deficiency in identifying, understanding, processing, and describing emotions occurs in 60.9% of individuals with TBI. Cognitive and social deficits have long-term consequences for the daily lives of people with moderate to severe TBI, but can be improved with appropriate rehabilitation.

When the pressure within the skull (intracranial pressure, abbreviated ICP) rises too high, it can be deadly. Signs of increased ICP include decreasing level of consciousness, paralysis or weakness on one side of the body, and a blown pupil, one that fails to constrict in response to light or is slow to do so. Cushing's triad, a slow heart rate with high blood pressure and respiratory depression is a classic manifestation of significantly raised ICP. Anisocoria, unequal pupil size, is another sign of serious TBI. Abnormal posturing, a characteristic positioning of the limbs caused by severe diffuse injury or high ICP, is an ominous sign.

Small children with moderate to severe TBI may have some of these symptoms but have difficulty communicating them. Other signs seen in young children include persistent crying, inability to be consoled, listlessness, refusal to nurse or eat, and irritability.

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).

Improvement of neurological function usually occurs for two or more years after the trauma. For many years it was believed that recovery was fastest during the first six months, but there is no evidence to support this. It may be related to services commonly being withdrawn after this period, rather than any physiological limitation to further progress. Children recover better in the immediate time frame and improve for longer periods.

Complications are distinct medical problems that may arise as a result of the TBI. The results of traumatic brain injury vary widely in type and duration; they include physical, cognitive, emotional, and behavioral complications. TBI can cause prolonged or permanent effects on consciousness, such as coma, brain death, persistent vegetative state (in which patients are unable to achieve a state of alertness to interact with their surroundings), and minimally conscious state (in which patients show minimal signs of being aware of self or environment). Lying still for long periods can cause complications including pressure sores, pneumonia or other infections, progressive multiple organ failure, and deep venous thrombosis, which can cause pulmonary embolism. Infections that can follow skull fractures and penetrating injuries include meningitis and abscesses. Complications involving the blood vessels include vasospasm, in which vessels constrict and restrict blood flow, the formation of aneurysms, in which the side of a vessel weakens and balloons out, and stroke.

Movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), myoclonus (shock-like contractions of muscles), and loss of movement range and control (in particular with a loss of movement repertoire). 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. 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). People may lose or experience altered vision, hearing, or smell.

Hormonal disturbances may occur secondary to hypopituitarism, occurring immediately or years after injury in 10 to 15% of TBI patients. Development of diabetes insipidus or an electrolyte abnormality acutely after injury indicate need for endocrinologic work up. Signs and symptoms of hypopituitarism may develop and be screened for in adults with moderate TBI and in mild TBI with imaging abnormalities. Children with moderate to severe head injury may also develop hypopituitarism. Screening should take place 3 to 6 months, and 12 months after injury, but problems may occur more remotely.

Cognitive deficits that can follow TBI include impaired attention; disrupted insight, judgement, and thought; reduced processing speed; distractibility; and deficits in executive functions such as abstract reasoning, planning, problem-solving, and multitasking. Memory loss, the most common cognitive impairment among head-injured people, occurs in 20–79% of people with closed head trauma, depending on severity. People who have suffered TBI may also have difficulty with understanding or producing spoken or written language, or with more subtle aspects of communication such as body language. Post-concussion syndrome, a set of lasting symptoms experienced after mild TBI, can include physical, cognitive, emotional and behavioral problems such as headaches, dizziness, difficulty concentrating, and depression. Multiple TBIs may have a cumulative effect. A young person who receives a second concussion before symptoms from another one have healed may be at risk for developing a very rare but deadly condition called second-impact syndrome, in which the brain swells catastrophically after even a mild blow, with debilitating or deadly results. About one in five career boxers is affected by chronic traumatic brain injury (CTBI), which causes cognitive, behavioral, and physical impairments. Dementia pugilistica, the severe form of CTBI, affects primarily career boxers years after a boxing career. It commonly manifests as dementia, memory problems, and parkinsonism (tremors and lack of coordination).

TBI may cause emotional, social, or behavioral problems and changes in personality. These may include emotional instability, depression, anxiety, hypomania, mania, apathy, irritability, problems with social judgment, and impaired conversational skills. TBI appears to predispose survivors to psychiatric disorders including obsessive compulsive disorder, substance abuse, dysthymia, clinical depression, bipolar disorder, and anxiety disorders. In patients who have depression after TBI, suicidal ideation is not uncommon; the suicide rate among these persons is increased 2- to 3-fold. Social and behavioral symptoms that can follow TBI include disinhibition, inability to control anger, impulsiveness, lack of initiative, inappropriate sexual activity, asociality and social withdrawal, and changes in personality.

TBI also has a substantial impact on the functioning of family systems Caregiving family members and TBI survivors often significantly alter their familial roles and responsibilities following injury, creating significant change and strain on a family system. Typical challenges identified by families recovering from TBI include: frustration and impatience with one another, loss of former lives and relationships, difficulty setting reasonable goals, inability to effectively solve problems as a family, increased level of stress and household tension, changes in emotional dynamics, and overwhelming desire to return to pre-injury status. In addition, families may exhibit less effective functioning in areas including coping, problem solving and communication. Psychoeducation and counseling models have been demonstrated to be effective in minimizing family disruption

Presentation varies according to the injury. Some patients with head trauma stabilize and other patients deteriorate. A patient may present with or without neurological deficit. Patients with concussion may have a history of seconds to minutes unconsciousness, then normal arousal. Disturbance of vision and equilibrium may also occur. Common symptoms of head injury include coma, confusion, drowsiness, personality change, seizures, nausea and vomiting, headache and a lucid interval, during which a patient appears conscious only to deteriorate later.

Symptoms of skull fracture can include:

- leaking cerebrospinal fluid (a clear fluid drainage from nose, mouth or ear) may be and is strongly indicative of basilar skull fracture and the tearing of sheaths surrounding the brain, which can lead to secondary brain infection.

- visible deformity or depression in the head or face; for example a sunken eye can indicate a maxillar fracture

- an eye that cannot move or is deviated to one side can indicate that a broken facial bone is pinching a nerve that innervates eye muscles

- wounds or bruises on the scalp or face.

- Basilar skull fractures, those that occur at the base of the skull, are associated with Battle's sign, a subcutaneous bleed over the mastoid, hemotympanum, and cerebrospinal fluid rhinorrhea and otorrhea.

Because brain injuries can be life-threatening, even people with apparently slight injuries, with no noticeable signs or complaints, require close observation; They have a chance for severe symptoms later on. The caretakers of those patients with mild trauma who are released from the hospital are frequently advised to rouse the patient several times during the next 12 to 24 hours to assess for worsening symptoms.

The Glasgow Coma Scale (GCS) is a tool for measuring degree of unconsciousness and is thus a useful tool for determining severity of injury. The Pediatric Glasgow Coma Scale is used in young children. The widely used PECARN Pediatric Head Injury/Trauma Algorithm helps physicians weigh risk-benefit of imaging in a clinical setting given multiple factors about the patient—including mechanism/location of injury, age of patient, and GCS score.

Diffuse axonal injury, or DAI, usually occurs as the result of an acceleration or deceleration motion, not necessarily an impact. Axons are stretched and damaged when parts of the brain of differing density slide over one another. Prognoses vary widely depending on the extent of damage.

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.

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.

A concussion, which is known as a subset traumatic brain injury (TBI), is when a force comes in contact with the head, neck or face, or fast movement of the head, causing a functional injury to the brain. Depending on where the location of impact, depends on the severity of the injury. It is short-lived impairment of neurological function, the brains ability to process information, which can be resolved in seven to ten days. Not all concussion involves the loss of consciousness, with it occurring in less than 10% of concussions. Second-impact syndrome is when a player has obtained a second concussion when you either return to field the same day, or return to play before a complete recovery from a previous concussion. This is a result from brain swelling, from vascular congestion and increased intracranial pressure, this can be fatal to a player as it is a very difficult medical injury to control. The brain is surrounded by cerebrospinal fluid, which protects it from light trauma. More severe impacts, or the forces associated with rapid acceleration, may not be absorbed by this cushion. Concussion may be caused by impact forces, in which the head strikes or is struck by something, or impulsive forces, in which the head moves without itself being subject to blunt trauma (for example, when the chest hits something and the head snaps forward). Chronic traumatic encephalopathy, or "CTE", is an example of the cumulative damage that can occur as the result of multiple concussions or less severe blows to the head. The condition was previously referred to as "dementia pugilistica", or "punch drunk" syndrome, as it was first noted in boxers. The disease can lead to cognitive and physical handicaps such as parkinsonism, speech and memory problems, slowed mental processing, tremor, depression, and inappropriate behavior. It shares features with Alzheimer's disease. Lamont sai od th PSCA after his incident::

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.

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.

Symptoms of CTE, which occur in four stages, generally appear 8 to 10 years after an athlete experiences repetitive mild traumatic brain injury.

First-stage symptoms include attention deficit hyperactivity disorder as well as confusion, disorientation, dizziness, and headaches. Second-stage symptoms include memory loss, social instability, impulsive behavior, and poor judgment. Third and fourth stages include progressive dementia, movement disorders, hypomimia, speech impediments, sensory processing disorder, tremors, vertigo, deafness, depression and suicidality.

Additional symptoms include dysarthria, dysphagia, cognitive disorder such as amnesia, and ocular abnormalities, such as ptosis.

The condition manifests as dementia, or declining mental ability, problems with memory, dizzy spells or lack of balance to the point of not being able to walk under one's own power for a short time and/or Parkinsonism, or tremors and lack of coordination. It can also cause speech problems and an unsteady gait. Patients with DP may be prone to inappropriate or explosive behavior and may display pathological jealousy or paranoia.

TBI patients may have sensory problems, especially problems with vision; they may not be able to register what they are seeing or may be slow to recognize objects. Also, TBI patients often have difficulty with hand–eye coordination, causing them to seem clumsy or unsteady. Other sensory deficits include problems with hearing, smell, taste, or touch. Tinnitus, a ringing or roaring in the ears, may occur. A person with damage to the part of the brain that processes taste or smell may perceive a persistent bitter taste or noxious smell. Damage to the part of the brain that controls the sense of touch may cause a TBI patient to develop persistent skin tingling, itching, or pain. These conditions are rare and difficult to treat.

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.

In the mid 1970s, PTS was first classified by Bryan Jennett into early and late seizures, those occurring within the first week of injury and those occurring after a week, respectively. Though the seven-day cutoff for early seizures is used widely, it is arbitrary; seizures occurring after the first week but within the first month of injury may share characteristics with early seizures. Some studies use a 30‑day cutoff for early seizures instead. Later it became accepted to further divide seizures into immediate PTS, seizures occurring within 24 hours of injury; early PTS, with seizures between a day and a week after trauma; and late PTS, seizures more than one week after trauma. Some consider late PTS to be synonymous with post-traumatic epilepsy.

Early PTS occur at least once in about 4 or 5% of people hospitalized with TBI, and late PTS occur at some point in 5% of them. Of the seizures that occur within the first week of trauma, about half occur within the first 24 hours. In children, early seizures are more likely to occur within an hour and a day of injury than in adults. Of the seizures that occur within the first four weeks of head trauma, about 10% occur after the first week. Late seizures occur at the highest rate in the first few weeks after injury. About 40% of late seizures start within six months of injury, and 50% start within a year.

Especially in children and people with severe TBI, the life-threatening condition of persistent seizure called status epilepticus is a risk in early seizures; 10 to 20% of PTS develop into the condition. In one study, 22% of children under 5 years old developed status seizures, while 11% of the whole TBI population studied did. Status seizures early after a TBI may heighten the chances that a person will suffer unprovoked seizures later.

Diffuse axonal injury (DAI) is a brain injury in which damage in the form of extensive lesions in white matter tracts occurs over a widespread area. DAI is one of the most common and devastating types of traumatic brain injury, and is a major cause of unconsciousness and persistent vegetative state after severe head trauma. It occurs in about half of all cases of severe head trauma and may be the primary damage that occurs in concussion. The outcome is frequently coma, with over 90% of patients with severe DAI never regaining consciousness. Those who do wake up often remain significantly impaired.

DAI can occur in every degree of severity from very mild or moderate to very severe. Concussion may be a milder type of diffuse axonal injury.

Post-traumatic seizures (PTS) are seizures that result from traumatic brain injury (TBI), brain damage caused by physical trauma. PTS may be a risk factor for post-traumatic epilepsy (PTE), but a person who has a seizure or seizures due to traumatic brain injury does not necessarily have PTE, which is a form of epilepsy, a chronic condition in which seizures occur repeatedly. However, "PTS" and "PTE" may be used interchangeably in medical literature.

Seizures are usually an indication of a more severe TBI. Seizures that occur shortly after a person suffers a brain injury may further damage the already vulnerable brain. They may reduce the amount of oxygen available to the brain, cause excitatory neurotransmitters to be released in excess, increase the brain's metabolic need, and raise the pressure within the intracranial space, further contributing to damage. Thus, people who suffer severe head trauma are given anticonvulsant medications as a precaution against seizures.

Around 5–7% of people hospitalized with TBI have at least one seizure. PTS are more likely to occur in more severe injuries, and certain types of injuries increase the risk further. The risk that a person will suffer PTS becomes progressively lower as time passes after the injury. However, TBI survivors may still be at risk over 15 years after the injury. Children and older adults are at a higher risk for PTS.

In the short term, concussions do not pose a serious problem and a player suffering may experience: headache, dizziness, loss of memory, blurred vision, confusion, disorientation and /or sensitiveness to bright light and loud noises. However, the real danger occurs after repeated concussions suffered by the same player, if the player returns to play immediately after contracting a concussion or too soon after suffering one. If the player returns to play immediately or too soon after, there is an increased risk of another concussion (which is much more serious) as well as to the rest of the body due to a slower reaction time. The player can also suffer from a number of psychological issues like depression, as well as permanent brain damage and severe brain swelling. A player, regardless of age or level of competition, should not return to play or training following a concussion, without a medical clearance from a registered medical doctor.

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.