Diagnosis is suspected based on lesion circumstances and clinical evidence, most prominently a neurological examination, for example checking whether the pupils constrict normally in response to light and assigning a Glasgow Coma Score. Neuroimaging helps in determining the diagnosis and prognosis and in deciding what treatments to give.

The preferred radiologic test in the emergency setting is computed tomography (CT): it is quick, accurate, and widely available. Follow-up CT scans may be performed later to determine whether the injury has progressed.

Magnetic resonance imaging (MRI) can show more detail than CT, and can add information about expected outcome in the long term. It is more useful than CT for detecting injury characteristics such as diffuse axonal injury in the longer term. However, MRI is not used in the emergency setting for reasons including its relative inefficacy in detecting bleeds and fractures, its lengthy acquisition of images, the inaccessibility of the patient in the machine, and its incompatibility with metal items used in emergency care. A variant of MRI since 2012 is High definition fiber tracking (HDFT).

Other techniques may be used to confirm a particular diagnosis. X-rays are still used for head trauma, but evidence suggests they are not useful; head injuries are either so mild that they do not need imaging or severe enough to merit the more accurate CT. Angiography may be used to detect blood vessel pathology when risk factors such as penetrating head trauma are involved. Functional imaging can measure cerebral blood flow or metabolism, inferring neuronal activity in specific regions and potentially helping to predict outcome. Electroencephalography and transcranial doppler may also be used. The most sensitive physical measure to date is the quantitative EEG, which has documented an 80% to 100% ability in discriminating between normal and traumatic brain-injured subjects.

Neuropsychological assessment can be performed to evaluate the long-term cognitive sequelae and to aid in the planning of the rehabilitation. Instruments range from short measures of general mental functioning to complete batteries formed of different domain-specific tests.

The need for imaging in patients who have suffered a minor head injury is debated. A non-contrast CT of the head should be performed immediately in all those who have suffered a moderate or severe head injury, an MRI is also an option. Computed tomography (CT) has become the diagnostic modality of choice for head trauma due to its accuracy, reliability, safety, and wide availability. The changes in microcirculation, impaired auto-regulation, cerebral edema, and axonal injury start as soon as head injury occurs and manifest as clinical, biochemical, and radiological changes.

Since a major cause of TBI are vehicle accidents, their prevention or the amelioration of their consequences can both reduce the incidence and gravity of TBI. In accidents, damage can be reduced by use of seat belts, child safety seats and motorcycle helmets, and presence of roll bars and airbags. Education programs exist to lower the number of crashes. In addition, changes to public policy and safety laws can be made; these include speed limits, seat belt and helmet laws, and road engineering practices.

Changes to common practices in sports have also been discussed. An increase in use of helmets could reduce the incidence of TBI. Due to the possibility that repeatedly "heading" a ball practicing soccer could cause cumulative brain injury, the idea of introducing protective headgear for players has been proposed. Improved equipment design can enhance safety; softer baseballs reduce head injury risk. Rules against dangerous types of contact, such as "spear tackling" in American football, when one player tackles another head first, may also reduce head injury rates.

Falls can be avoided by installing grab bars in bathrooms and handrails on stairways; removing tripping hazards such as throw rugs; or installing window guards and safety gates at the top and bottom of stairs around young children. Playgrounds with shock-absorbing surfaces such as mulch or sand also prevent head injuries. Child abuse prevention is another tactic; programs exist to prevent shaken baby syndrome by educating about the dangers of shaking children. Gun safety, including keeping guns unloaded and locked, is another preventative measure. Studies on the effect of laws that aim to control access to guns in the United States have been insufficient to determine their effectiveness preventing number of deaths or injuries.

Recent clinical and laboratory research by neurosurgeon Julian Bailes, M.D., and his colleagues from West Virginia University, has resulted in papers showing that dietary supplementation with omega-3 DHA offers protection against the biochemical brain damage that occurs after a traumatic injury. Rats given DHA prior to induced brain injuries suffered smaller increases in two key markers for brain damage (APP and caspase-3), as compared with rats given no DHA. “The potential for DHA to provide prophylactic benefit to the brain against traumatic injury appears promising and requires further investigation. The essential concept of daily dietary supplementation with DHA, so that those at significant risk may be preloaded to provide protection against the acute effects of TBI, has tremendous public health implications.”

Furthermore, acetylcysteine has been confirmed, in a recent double-blind placebo-controlled trial conducted by the US military, to reduce the effects of blast induced mild traumatic brain and neurological injury in soldiers. Multiple animal studies have also demonstrated its efficacy in reducing the damage associated with moderate traumatic brain or spinal injury, and also ischemia-induced brain injury. In particular, it has been demonstrated through multiple studies to significantly reduce neuronal losses and to improve cognitive and neurological outcomes associated with these traumatic events. Acetylcysteine has been safely used to treat paracetamol overdose for over forty years and is extensively used in emergency medicine.

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

Diagnosis of MTBI is based on physical and neurological examination findings, duration of unconsciousness (usually less than 30 minutes) and post-traumatic amnesia (PTA; usually less than 24 hours), and the Glasgow Coma Scale (MTBI sufferers have scores of 13 to 15). Neuropsychological tests exist to measure cognitive function and the international consensus meeting in Zurich recommended the use of the SCAT2 test.

If the Glasgow Coma Scale is less than 15 at two hours, or less than 14 at any time, a CT is recommended. In addition, a CT scan is more likely to be performed if observation after discharge is not assured or intoxication is present, there is suspected increased risk for bleeding, age greater than 60, or less than 16. Most concussions, without complication, cannot be detected with MRI or CT scans. However, changes have been reported on MRI and SPECT imaging in those with concussion and normal CT scans, and post-concussion syndrome may be associated with abnormalities visible on SPECT and PET scans. Mild head injury may or may not produce abnormal EEG readings.

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

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

Most head injuries are of a benign nature and require no treatment beyond analgesics and close monitoring for potential complications such as intracranial bleeding. If the brain has been severely damaged by trauma, neurosurgical evaluation may be useful. Treatments may involve controlling elevated intracranial pressure. This can include sedation, paralytics, cerebrospinal fluid diversion. Second line alternatives include decompressive craniectomy (Jagannathan et al. found a net 65% favorable outcomes rate in pediatric patients), barbiturate coma, hypertonic saline and hypothermia. Although all of these methods have potential benefits, there has been no randomized study that has shown unequivocal benefit.

Clinicians will often consult clinical decision support rules such as the Canadian CT Head Rule or the New Orleans/Charity Head injury/Trauma Rule to decide if the patient needs further imaging studies or observation only. Rules like these are usually studied in depth by multiple research groups with large patient cohorts to ensure accuracy given the risk of adverse events in this area.

The ASCOT probability of survival encapsulates several of the variables measured in the Glasgow Coma Scale but also includes systolic blood pressure, respiration rates upon admission, and anatomic injuries. The ASCOT was found to be the most sensitive tool for determining severity of head injuries in children and is effective in predicting the outcome of injury.

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

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

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

A mechanism-based TBI classification system divides traumatic brain injuries (TBI) into closed and penetrating head trauma; based on the way in which the person was injured.

The International Statistical Classification of Diseases and Related Health Problems (ICD-10) and the American Psychiatric Association's "Diagnostic and Statistical Manual of Mental Disorders" have set out criteria for post-concussion syndrome (PCS) and post-concussional disorder (PCD), respectively.

The ICD-10 established a set of diagnostic criteria for PCS in 1992. In order to meet these criteria, a patient has had a head injury "usually sufficiently severe to result in loss of consciousness" and then develop at least three of the eight symptoms marked with a check mark in the table at right under "ICD-10" within four weeks.

About 38% of people who suffer a head injury with symptoms of concussion and no radiological evidence of brain lesions meet these criteria. In addition to these symptoms, people that meet the ICD-10 criteria for PCS may fear that they will have permanent brain damage, which may worsen the original symptoms. Preoccupation with the injury may be accompanied by the assumption of a "sick role" and hypochondriasis. The criteria focus on subjective symptoms and mention that neuropsychological evidence of significant impairment is not present. With their focus on psychological factors, the ICD-10 criteria support the idea that the cause of PCS is functional. Like the ICD-10, the ICD-9-CM defines PCS in terms of subjective symptoms and discusses the greater frequency of PCS in people with histories of mental disorders or a financial incentive for a diagnosis.

The DSM-IV lists criteria for diagnosis of PCD in people who have suffered a head trauma with persistent post-traumatic amnesia, loss of consciousness, or post-traumatic seizures. In addition, for a diagnosis of PCD, patients must have neuropsychological impairment as well as at least three of the symptoms marked with a check mark in the table at right under "DSM-IV". These symptoms must be present for three months after the injury and must have been absent or less severe before the injury. In addition, the patient must experience social problems as a result, and must not meet criteria for another disorder that explains the symptoms better.

Neuropsychological tests exist to measure deficits in cognitive functioning that can result from PCS. The Stroop Color Test and the 2&7 Processing Speed Test (which both detect deficits in speed of mental processing) can predict the development of cognitive problems from PCS. A test called the Rivermead Postconcussion Symptoms Questionnaire, a set of questions that measure the severity of 16 different post-concussion symptoms, can be self-administered or administered by an interviewer. Other tests that can predict the development of PCS include the Hopkins Verbal Learning A test (HVLA) and the Digit Span Forward examination. The HVLA tests verbal learning and memory by presenting a series of words and assigning points based on the number recalled, and digit span measures attention efficiency by asking the examinee to repeat back digits spoken by the tester in the same order as they are presented. In addition, neuropsychological tests may be performed to detect malingering (exaggerating or making up symptoms) .

Medical personnel aim to determine whether a seizure is caused by a change in the patient's biochemistry, such as hyponatremia. Neurological examinations and tests to measure levels of serum electrolytes are performed.

Not all seizures that occur after trauma are PTS; they may be due to a seizure disorder that already existed, which may even have caused the trauma. In addition, post-traumatic seizures are not to be confused with concussive convulsions, which may immediately follow a concussion but which are not actually seizures and are not a predictive factor for epilepsy.

Neuroimaging is used to guide treatment. Often, MRI is performed in any patient with PTS, but the less sensitive but more easily accessed CT scan may also be used.

Seizures that result from TBI are often difficult to treat. Antiepileptic drugs that may be given intravenously shortly after injury include phenytoin, sodium valproate, carbamazepine, and phenobarbital. Antiepileptic drugs do not prevent all seizures in all people, but phenytoin and sodium valproate usually stop seizures that are in progress.

Currently, CTE can only be definitively diagnosed by direct tissue examination after death, including full and immunohistochemical brain analyses.

The lack of "in vivo" techniques to show distinct biomarkers for CTE is the reason CTE cannot currently be diagnosed while a person is alive. The only known diagnosis for CTE occurs by studying the brain tissue after death. Concussions are non-structural injuries and do not result in brain bleeding, which is why most concussions cannot be seen on routine neuroimaging tests such as CT or MRI. Acute concussion symptoms (those that occur shortly after an injury) should not be confused with CTE. Differentiating between prolonged post-concussion syndrome (PCS, where symptoms begin shortly after a concussion and last for weeks, months, and sometimes even years) and CTE symptoms can be difficult. Research studies are currently examining whether neuroimaging can detect subtle changes in axonal integrity and structural lesions that can occur in CTE. Recently, more progress in in-vivo diagnostic techniques for CTE has been made, using DTI, fMRI, MRI, and MRS imaging; however, more research needs to be done before any such techniques can be validated.

PET tracers that bind specifically to tau protein are desired to aid diagnosis of CTE in living individuals. One candidate is the tracer [F]FDDNP, which is retained in the brain in individuals with a number of dementing disorders such as Alzheimer's disease, Down syndrome, progressive supranuclear palsy, familial frontotemporal dementia, and Creutzfeldt–Jakob disease. In a small study of 5 retired NFL players with cognitive and mood symptoms, the PET scans revealed accumulation of the tracer in their brains. However, [F]FDDNP binds to beta-amyloid and other proteins as well. Moreover, the sites in the brain where the tracer was retained were not consistent with the known neuropathology of CTE. A more promising candidate is the tracer [F]-T807, which binds only to tau. It is being tested in several clinical trials.

A putative biomarker for CTE is the presence in serum of autoantibodies against the brain. The autoantibodies were detected in football players who experienced a large number of head hits but no concussions, suggesting that even sub-concussive episodes may be damaging to the brain. The autoantibodies may enter the brain by means of a disrupted blood-brain barrier, and attack neuronal cells which are normally protected from an immune onslaught. Given the large numbers of neurons present in the brain (86 billion), and considering the poor penetration of antibodies across a normal blood-brain barrier, there is an extended period of time between the initial events (head hits) and the development of any signs or symptoms. Nevertheless, autoimmune changes in blood of players may consist the earliest measurable event predicting CTE.

Robert A. Stern, one of the scientists at the Boston University CTE Center, said in 2015 that "he expected a test to be developed within a decade that will be able to diagnose C.T.E. in living people".

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.

To be diagnosed with PTE, a person must have a history of head trauma and no history of seizures prior to the injury. Witnessing a seizure is the most effective way to diagnose PTE. Electroencephalography (EEG) is a tool used to diagnose a seizure disorder, but a large portion of people with PTE may not have the abnormal "epileptiform" EEG findings indicative of epilepsy. In one study, about a fifth of people who had normal EEGs three months after an injury later developed PTE. However, while EEG is not useful for predicting who will develop PTE, it can be useful to localize the epileptic focus, to determine severity, and to predict whether a person will suffer more seizures if they stop taking antiepileptic medications.

Magnetic resonance imaging (MRI) is performed in people with PTE, and CT scanning can be used to detect brain lesions if MRI is unavailable. However, it is frequently not possible to detect the epileptic focus using neuroimaging.

For a diagnosis of PTE, seizures must not be attributable to another obvious cause. Seizures that occur after head injury are not necessarily due to epilepsy or even to the head trauma. Like anyone else, TBI survivors may suffer seizures due to factors including imbalances of fluid or electrolytes, epilepsy from other causes, hypoxia (insufficient oxygen), and ischemia (insufficient blood flow to the brain). Withdrawal from alcohol is another potential cause of seizures. Thus these factors must be ruled out as causes of seizures in people with head injury before a diagnosis of PTE can be made.

Shortly after TBI, people are given anticonvulsant medication, because seizures that occur early after trauma can increase brain damage through hypoxia, excessive release of excitatory neurotransmitters, increased metabolic demands, and increased pressure within the intracranial space. Medications used to prevent seizures include valproate, phenytoin, and phenobarbital. It is recommended that treatment with anti-seizure medication be initiated as soon as possible after TBI. Prevention of early seizures differs from that of late seizures, because the aim of the former is to prevent damage caused by the seizures, whereas the aim of the latter is to prevent epileptogenesis. Strong evidence from clinical trials suggests that antiepileptic drugs given within a day of injury prevent seizures within the first week of injury, but not after. For example, a 2003 review of medical literature found phenytoin to be preventative of early, but probably not late PTS. In children, anticonvulsants may be ineffective for both early and late seizures. For unknown reasons, prophylactic use of antiepileptic drugs over a long period is associated with an increased risk for seizures. For these reasons, antiepileptic drugs are widely recommended for a short time after head trauma to prevent immediate and early, but not late, seizures. No treatment is widely accepted to prevent the development of epilepsy. However, medications may be given to repress more seizures if late seizures do occur.

Once taken off the field of play due to possible concussion, being unconscious, or showing the symptoms post game, getting medical advice as soon as possible is recommended. At the hospital or medical practice, the player will be under observation, if they are experiencing a headache, mild pain killers will be given. The medical professional will request that no food or drink is to be consumed until advised. They will then assess whether the player needs an x-ray, to check for any possible cervical vertebrae damage, or a computerised axial tomography (CT Scan) to check for any brain or cranium damage. With a mild head injury being sent home to take care and doing activities slower than usual, and maintaining painkillers. If symptoms of concussion don't disappear in the average of seven to ten days, then seek medical advice again as injury could be worse. In post-concussion syndrome, symptoms do not resolve for weeks, months, or years after a concussion, and may occasionally be permanent. About 10% to 20% of people have post concussion syndrome for more than a month.

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.

Prevention of PTE involves preventing brain trauma in general; protective measures include bicycle helmets and child safety seats. No specific treatment exists to prevent the development of epilepsy after TBI occurs. In the past, antiepileptic drugs were used with the intent of preventing the development of PTE. However, while antiepileptic drugs can prevent early PTS, clinical studies have failed to show that prophylactic use of antiepileptic drugs prevents the development of PTE. Why antiepileptic drugs in clinical trials have failed to stop PTE from developing is not clear, but several explanations have been offered. The drugs may simply not be capable of preventing epilepsy, or the drug trials may have been set up in a way that did not allow a benefit of the drugs to be found (e.g. drugs may have been given too late or in inadequate doses). Animal studies have similarly failed to show much protective effect of the most commonly used seizure medications in PTE trials, such as phenytoin and carbamazepine. Antiepileptic drugs are recommended to prevent late seizures only for people in whom PTE has already been diagnosed, not as a preventative measure. On the basis of the aforementioned studies, no treatment is widely accepted to prevent the development of epilepsy. However, it has been proposed that a narrow window of about one hour after TBI may exist during which administration of antiepileptics could prevent epileptogenesis (the development of epilepsy).

Corticosteroids have also been investigated for the prevention of PTE, but clinical trials revealed that the drugs did not reduce late PTS and were actually linked to an increase in the number of early PTS.

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.

As with other types of intracranial hematomas, the blood may be removed surgically to remove the mass and reduce the pressure it puts on the brain. The hematoma is evacuated through a burr hole or craniotomy. If transfer to a facility with neurosurgery is prolonged trephination may be performed in the emergency department.

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.

On images produced by CT scans and MRIs, epidural hematomas usually appear convex in shape because their expansion stops at the skull's sutures, where the dura mater is tightly attached to the skull. Thus they expand inward toward the brain rather than along the inside of the skull, as occurs in subdural hematoma. The lens-like shape of the hematoma causes the appearance of these bleeds to be "lentiform".

Epidural hematomas may occur in combination with subdural hematomas, or either may occur alone. CT scans reveal subdural or epidural hematomas in 20% of unconscious patients. In the hallmark of epidural hematoma, patients may regain consciousness and appear completely normal during what is called a lucid interval, only to descend suddenly and rapidly into unconsciousness later. The lucid interval, which depends on the extent of the injury, is a key to diagnosing epidural hemorrhage. If the patient is not treated with prompt surgical intervention, death is likely to follow.

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.

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.

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.

Every disease has different signs and symptoms. Some of them are persistent headache; pain in the face, back, arms, or legs; an inability to concentrate; loss of feeling; memory loss; loss of muscle strength; tremors; seizures; increased reflexes, spasticity, tics; paralysis; and slurred speech. One should seek medical attention if affected by these.