Diagnosis can be difficult as symptoms may be nonspecific. A CT scan of the head is typically recommended if a concern is present. While retinal bleeding is common, it can also occur in other conditions.

Interventions by neonatal nurses including giving parents information about abusive head trauma, normal infant crying and reasons for crying, teaching how to calm an infant, and how to cope if the infant was inconsolable may reduce rates of AHT.

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) .

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.

PCS, which shares symptoms with a variety of other conditions, is highly likely to be misdiagnosed in people with these conditions. Cognitive and affective symptoms that occur following a traumatic injury may be attributed to mTBI, but in fact be due to another factor such as post-traumatic stress disorder, which is easily misdiagnosed as PCS and vice versa. Affective disorders such as depression have some symptoms that can mimic those of PCS and lead to a wrongful diagnosis of the latter; these include problems with concentration, emotional lability, anxiety, and sleep problems. Depression, which is highly common in persistent PCS, can worsen other PCS symptoms, such as headaches and problems with concentration, memory, and sleep. PCS also shares symptoms with chronic fatigue syndrome, fibromyalgia, and exposure to certain toxins. Traumatic brain injury may cause damage to the hypothalamus or the pituitary gland, and deficiencies of pituitary hormones (hypopituitarism) can cause similar symptoms to post-concussion syndrome; in these cases, symptoms can be treated by replacing any hormones that are deficient.

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).

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:

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.

DAI currently lacks a specific treatment beyond what is done for any type of head injury, including stabilizing the patient and trying to limit increases in intracranial pressure (ICP).

DAI is difficult to detect since it does not show up well on CT scans or with other macroscopic imaging techniques, though it shows up microscopically. However, there are characteristics typical of DAI that may or may not show up on a CT scan. Diffuse injury has more microscopic injury than macroscopic injury and is difficult to detect with CT and MRI, but its presence can be inferred when small bleeds are visible in the corpus callosum or the cerebral cortex. MRI is more useful than CT for detecting characteristics of diffuse axonal injury in the subacute and chronic time frames. Newer studies such as Diffusion Tensor Imaging are able to demonstrate the degree of white matter fiber tract injury even when the standard MRI is negative. Since axonal damage in DAI is largely a result of secondary biochemical cascades, it has a delayed onset, so a person with DAI who initially appears well may deteriorate later. Thus injury is frequently more severe than is realized, and medical professionals should suspect DAI in any patients whose CT scans appear normal but who have symptoms like unconsciousness.

MRI is more sensitive than CT scans, but MRI may also miss DAI, because it identifies the injury using signs of edema, which may not be present.

DAI is classified into grades based on severity of the injury. In Grade I, widespread axonal damage is present but no focal abnormalities are seen. In Grade II, damage found in Grade I is present in addition to focal abnormalities, especially in the corpus callosum. Grade III damage encompasses both Grades I and II plus rostral brain stem injury and often tears in the tissue.

While any number of injuries may occur during the birthing process. A number of specific conditions are well described. Brachial plexus palsy occurs in 0.4 to 5.1 infants per 1000 live birth. Head trauma and brain damage during delivery can lead to a number of conditions include: caput succedaneum, cephalohematoma, subgaleal hemorrhage, subdural hemorrhage, subarachnoid hemorrhage, epidural hemorrhage, and intraventricular hemorrhage.

The most common fracture during delivery is that of the clavicle (0.5%).

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.

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".

Sequelae can occur in both the mother and the infant after a traumatic birth.

Birth trauma is uncommon in the Western world in relation to rates in the third world. In the West injury occurs in 1.1% of C-sections.

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.

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.

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.

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.

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.

Diagnosis occurs through a patient history, head and neck examination, X-rays to rule out bone fractures and may involve the use of medical imaging to determine if there are other injuries.

Management consists of vigilant observation over days to detect progression. The subgaleal space is capable of holding up to 50% of a newborn baby's blood and can therefore result in acute shock and death. Fluid bolus may be required if blood loss is significant and patient becomes tachycardic. Transfusion and phototherapy may be necessary. Investigation for coagulopathy may be indicated.

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.

It may cause seizures but cephalohematoma and caput will not cause seizure

Stingers are best diagnosed by a medical professional. This person will assess the athlete's pain, range of head and neck motion, arm numbness, and muscle strength. Often, the affected athlete is allowed to return to play within a short time, but persistent symptoms will result in removal. Athletes are also advised to receive

regular evaluations until symptoms have ceased. If they have not after two weeks, or increase, additional tests such as magnetic resonance imaging (MRI) can be performed to detect a more serious injury, such as a herniated disc.

The order of treatments applied depends on whether the athlete's main complaint is pain or weakness. Both can be treated with an analgesic, anti-inflammatory medication, ice and heat, restriction of movement, and if necessary, cervical collar or traction. Surgery is only necessary in the most severe cases.

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

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

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