No medication is approved to halt the progression of the initial injury to secondary injury. The variety of pathological events presents opportunities to find treatments that interfere with the damage processes. Neuroprotection methods to decrease secondary injury, have been the subject of interest follows TBI. However, trials to test agents that could halt these cellular mechanisms have met largely with failure. For example, interest existed in cooling the injured brain; however, a 2014 Cochrane review did not find enough evidence to see if it was useful or not. A 2016 review found that maintaining a normal or low normal temperature appeared useful in adults but not children. High quality evidence to support targeted temperature management below normal however is poor.

In addition, drugs such as NMDA receptor antagonists to halt neurochemical cascades such as excitotoxicity showed promise in animal trials but failed in clinical trials. These failures could be due to factors including faults in the trials' design or in the insufficiency of a single agent to prevent the array of injury processes involved in secondary injury.

Other topics of research have included investigations into mannitol, dexamethasone, progesterone, xenon, barbiturates, magnesium, calcium channel blockers, PPAR-γ agonists, curcuminoids, ethanol, NMDA antagonists, caffeine.

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.

Pharmacotherapy is the utilization of drugs to treat an illness. There are several different drugs that have been used to alleviate symptoms experienced after a head injury including anti-depressants such as amitriptyline and sertraline. Use of these drugs has been associated with a decrease in depression and increased functioning in social and work environments. An antidiuretic called Desmopressin Acetate (DDAVP) has also been shown to improve memory performance in patients

Recent studies have examined the preventative effects of progesterone on brain injuries. Phase III trials are currently being conducted at 17 medical centers across the United States. Preliminary results have shown a 50% reduction in mortality in those treated with progesterone and showed an improved functional outcome.

Overall, the efficacy of pharmacotherapuetic treatments is dependent on the treatment being used and the symptoms being targeted by the treatment.

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

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

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

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

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

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

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

It is important to begin emergency treatment within the so-called "golden hour" following the injury. People with moderate to severe injuries are likely to receive treatment in an intensive care unit followed by a neurosurgical ward. Treatment depends on the recovery stage of the patient. In the acute stage the primary aim of the medical personnel is to stabilize the patient and focus on preventing further injury because little can be done to reverse the initial damage caused by trauma. Rehabilitation is the main treatment for the subacute and chronic stages of recovery. International clinical guidelines have been proposed with the aim of guiding decisions in TBI treatment, as defined by an authoritative examination of current evidence.

Prevention of MTBI involves general measures such as wearing seat belts and using airbags in cars. Older people are encouraged to reduce fall risk by keeping floors free of clutter and wearing thin, flat, shoes with hard soles that do not interfere with balance.

Protective equipment such as headgear has been found to reduce the number of concussions in athletes and improvements in the design of helmets may decrease the number and severity further. New "Head Impact Telemetry System" technology is being placed in helmets to study injury mechanisms and may generate knowledge that will potentially help reduce the risk of concussions among American Football players. Self-reported concussion rates among U-20 and elite rugby union players in Ireland are 45–48%. Half of these injuries go unreported. Changes to the rules or enforcing existing rules in sports, such as those against "head-down tackling", or "spearing", which is associated with a high injury rate, may also prevent concussions.

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.

After exclusion of neck injury, observation should be continued for several hours. If repeated vomiting, worsening headache, dizziness, seizure activity, excessive drowsiness, double vision, slurred speech, unsteady walk, or weakness or numbness in arms or legs, or signs of basilar skull fracture develop, immediate assessment in an emergency department is warranted. After this initial period has passed, there is debate as to whether it is necessary to awaken the person several times during the first night, as has traditionally been done, or whether there is more benefit from uninterrupted sleep.

Physical and cognitive rest should be continued until all symptoms have resolved with most (80–90%) concussions resolving in seven to ten days, although the recovery time may be longer in children and adolescents. Cognitive rest includes reducing activities which require concentration and attention such as school work, video games, and text messaging. It has been suggested that even leisure reading can commonly worsen symptoms in children and adolescents and proposals include time off from school and attending partial days. Since students may appear 'normal', continuing education of relevant school personnel may be needed.

Those with concussion are generally prescribed rest, including adequate nighttime sleep as well as daytime rest. Rest includes both physical and cognitive rest until symptoms clear and a gradual return to normal activities at a pace that does not cause symptoms to worsen is recommended. Education about symptoms, their management, and their normal time course, can lead to an improved outcome.

For persons participating in athletics, the 2008 Zurich Consensus Statement on Concussion in Sport recommends that participants be symptom-free before restarting and then progress through a series of graded steps. These steps include:

- complete physical and cognitive rest

- light aerobic activity (less than 70% of maximum heart rate)

- sport-specific activities such as running drills and skating drills

- non-contact training drills (exercise, coordination, and cognitive load)

- full-contact practice

- full-contact games.

Only when symptom-free for 24 hours, should progression to the next step occur. If symptoms occur, the person should drop back to the previous asymptomatic level for at least another 24 hours. The emphasis is on remaining symptom free and taking it in medium steps, not on the steps themselves.

Medications may be prescribed to treat sleep problems and depression. Analgesics such as ibuprofen can be taken for headache, but paracetamol (acetaminophen) is preferred to minimize the risk of intracranial hemorrhage. Concussed individuals are advised not to use alcohol or other drugs that have not been approved by a doctor as they can impede healing. Activation database-guided EEG biofeedback has been shown to return the memory abilities of the concussed individual to levels better than the control group.

About one percent of people who receive treatment for MTBI need surgery for a brain injury. Observation to monitor for worsening condition is an important part of treatment. Health care providers recommend that those suffering from concussion return for further medical care and evaluation 24 to 72 hours after the concussive event if the symptoms worsen. Athletes, especially intercollegiate or professional, are typically followed closely by team athletic trainers during this period but others may not have access to this level of health care and may be sent home with minimal monitoring.

People may be released after assessment from hospital or emergency room to the care of a trusted person with instructions to return if they display worsening symptoms or those that might indicate an emergent condition such as: change in consciousness, convulsions, severe headache, extremity weakness, vomiting, new bleeding or deafness in either or both ears.

Management of post-concussion syndrome typically involves treatments addressing specific symptoms; for example, people can take pain relievers for headaches and medicine to relieve depression or insomnia. Rest is advised, but is only somewhat effective. Physical and behavioral therapy may also be prescribed for problems such as loss of balance and difficulties with attention, respectively.

Though no pharmacological treatments exist for PCS, doctors may prescribe medications used for symptoms that also occur in other conditions; for example, antidepressants are used for the depression that frequently follows mTBI. Side effects of medications may affect people suffering the consequences of mTBI more severely than they do others, and thus it is recommended that medications be avoided if possible; there may be a benefit to avoiding narcotic medications. In addition, some pain medications prescribed for headaches can cause rebound headaches when they are discontinued.

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

The focus of preventive measures to date has been on the design of car seats, primarily through the introduction of head restraints, often called headrests. This approach is potentially problematic given the underlying assumption that purely mechanical factors cause whiplash injuries — an unproven theory. So far the injury reducing effects of head restraints appears to have been low, approximately 5–10%, because car seats have become stiffer in order to increase crashworthiness of cars in high-speed rear-end collisions which in turn could increase the risk of whiplash injury in low-speed rear impact collisions. Improvements in the geometry of car seats through better design and energy absorption could offer additional benefits. Active devices move the body in a crash in order to shift the loads on the car seat.

For the last 40 years, vehicle safety researchers have been designing and gathering information on the ability of head restraints to mitigate injuries resulting from rear-end collisions. As a result, different types of head restraints have been developed by various manufactures to protect their occupants from whiplash.

Below are definitions of different types of head restraints.

Head restraint — refers to a device designed to limit the rearward displacement of an adult occupant’s head in relation to the torso in order to reduce the risk of injury to the cervical vertebrae in the event of a rear impact. The most effective head restraint must allow a backset motion of less than 60 mm to prevent the hyperextension of the neck during impact.

Integrated head restraint or fixed head restraint — refers to a head restraint formed by the upper part of the seat back, or a head restraint that is not height adjustable and cannot be detached from the seat or the vehicle structure except by the use of tools or following the partial or total removal of the seat furnishing".

Adjustable head restraint — refers to a head restraint that is capable of being positioned to fit the morphology of the seated occupant. The device may permit horizontal displacement, known as tilt adjustment, and/or vertical displacement, known as height adjustment.

Active head restraint — refers to a device designed to automatically improve head restraint position and/or geometry during an impact".

Automatically adjusting head restraint — refers to a head restraint that automatically adjusts the position of the head restraint when the seat position is adjusted.

A major issue in whiplash prevention is the lack of proper adjustment of the seat safety system by both drivers and passengers. Studies have shown that a well designed and adjusted head restraint could prevent potentially injurious head-neck kinematics in rear-end collisions by limiting the differential movement of the head and torso. The primary function of a head restraint is to minimize the relative rearward movement of the head and neck during rear impact. During a rear-end collision, the presence of an effective head restraint behind the occupant’s head can limit the differential movement of the head and torso. A properly placed head restraint where one can sufficiently protect his/her head lower the chances of head injury by up to 35% during a rear-end collision.

In contrast to a properly adjusted head restraint, research suggests that there may be an increased risk of neck injuries if the head restraint is incorrectly positioned. More studies by manufacturers and automobile safety organizations are currently undergoing to examine the best ways to reduce head and torso injuries during a rear-end impact with different geometries of the head restraint and seat-back systems.

In most passenger vehicles where manually adjustable head restraints are fitted, proper use requires sufficient knowledge and awareness by occupants. When driving, the height of the head restraint is critical in influencing injury risk. A restraint should be at least as high as the head's center of gravity, or about 9 centimeters (3.5 inches) below the top of the head. The backset, or distance behind the head, should be as small as possible. Backsets of more than 10 centimeters (about 4 inches) have been associated with increased symptoms of neck injury in crashes.

In a sitting position, the minimum height of the restraint should correspond to the top of the driver’s ear or even higher. In addition, there should be minimal distance between the back of head and the point where it first meets the restraint.

Due to low public awareness of the consequence of incorrect positioning of head restraints, some passenger vehicle manufactures have designed and implemented a range of devices into their models to protect their occupants.

Some current systems are:

- Mercedes-Benz A-Class Active Head Restraint (AHR),

- Saab (Responsible for the first active head restraint), Opel, Ford, Nissan, Subaru, Hyundai, and Peugeot — Active Head restraint (SAHR),

- Volvo and Jaguar — Whiplash Protection System/Whiplash Prevention System (WHIPS), and

- Toyota — Whiplash Injury Lessening (WIL).

The Insurance Institute for Highway Safety (IIHS) and other testing centers around the world have been involved in testing the effectiveness of head restraint and seat systems in laboratory conditions to assess their ability to prevent or mitigate whiplash injuries. They have found that over 60% of new motor vehicles on the market have "good" rated head restraints. Various organisations exist which list such vehicles

According to the recommendations made by the Quebec Task Force, treatment for individuals with whiplash associated disorders grade 1–3 may include non-narcotic analgesics. Non-steroidal anti-inflammatory drugs may also be prescribed in the case of WAD 2 and WAD 3, but their use should be limited to a maximum of three weeks. Botulinum toxin A is used to treat involuntary muscle contraction and spasms. Botulinum toxin type-A is only temporary and repeated injections need to take place in order to feel the effects.

According to a year long follow-up study in 2008 on 186 patients, the WAD-classification and Quebec Task Force regimen were not linked to better clinical outcomes.

A progressive decline in central nervous system function leads to a loss of proprioception, balance and overall motor coordination, as well as a reduction in eye–hand coordination, reaction time and an unsteady gait. These degenerative changes are often accompanied by osteoarthritis (degenerative joint disease), which leads to a reduction in the range of motion of the head, neck and extremities. Furthermore, elderly people frequently take multiple medications for control of various diseases and conditions. The side effects of some of these medications may either predispose to injury, or may cause a minor trauma to result in a much more severe condition. For example, a person taking warfarin (Coumadin) and/or clopidogrel (Plavix) may experience a life-threatening intracranial hemorrhage after sustaining a relatively minor closed head injury, as a result of the defect in the hemostatic mechanism caused by such medications. The combined effects of these changes greatly predisposes elderly people to traumatic injury. Both the incidence of falls and the severity of associated complications increase with advancing age.

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.

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, 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.

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.

It is estimated that as many as 1.6-3.8 million concussions occur in the US per year in competitive sports and recreational activities; this is a rough estimate, since as many as 50% of concussions go unreported. Concussions occur in all sports with the highest incidence in American football, hockey, rugby, soccer, and basketball. In addition to concussions caused by a single severe impact, multiple minor impacts may also cause brain injury.

Stingers can be prevented by wearing protective gear, such as butterfly restrictors, designed to protect the head and neck from being forced into unnatural positions. This equipment is more feasible in positions where unrestricted head and neck movement is not required, such as American football lineman, than in positions like quarterback, where such movement is integral. Regardless of equipment, it is important to report even minor symptoms to an athletic trainer or team physician, and to allow appropriate recovery time.

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.

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.

A cerebral laceration is a type of traumatic brain injury that occurs when the tissue of the brain is mechanically cut or torn. The injury is similar to a cerebral contusion; however, according to their respective definitions, the pia-arachnoid membranes are torn over the site of injury in laceration and are not torn in contusion. Lacerations require greater physical force to cause than contusions, but the two types of injury are grouped together in the ICD-9 and ICD-10 classification systems.

Despite the success of goggles and lenses against ballistic and secondary trauma, BLPS, SPECS, and SWDG forms of eye armor do not protect against primary-blast injuries. The space between the lenses and the eyes promotes sonic wave diffraction, and current efforts to eradicate ocular trauma due to the primary blast wave have been unsuccessful due to this lens-eye air interface.

Prevention of ocular trauma is most effective when soldiers wear polycarbonate eye armor correctly in the battlefield. For Operation Iraqi Freedom and Operation Enduring Freedom, the United States Military have made Ballistic Laser Protective Spectacles (BLPS), Special Protective Eyewear Cylindrical System (SPECS), and Sun/Wind/Dust Goggles (SWDG) available to combatants and associated personnel. These forms of eye protection are available in non-prescription and prescription lenses, and their use has been made mandatory at all times when soldiers are in areas of potential conflict. Despite their proven record of protection against secondary blast trauma, soldier compliance remains low: 85% of soldiers afflicted ocular trauma in the first year of OEF were not wearing their protective lenses at the time of detonation. While 41% of soldiers could not recall whether or not they were wearing eye protection at the time of detonation, 17% of casualties were wearing eye protection while 26% of casualties were not. Among this group, the poorest visual prognoses were documented in individuals who did not wear eye protection. The lack of compliance has been attributed to complaints about comfort, stylishness, and “misting” of the lenses when in the field. BLPS and SPECS offer the same line of protection against secondary trauma as the SWD goggles, and these lenses may overcome the complaints many soldiers have with their military-issue goggles.