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.

Certain facilities are equipped to handle TBI better than others; initial measures include transporting patients to an appropriate treatment center. Both during transport and in hospital the primary concerns are ensuring proper oxygen supply, maintaining adequate blood flow to the brain, and controlling raised intracranial pressure (ICP), since high ICP deprives the brain of badly needed blood flow and can cause deadly brain herniation. Other methods to prevent damage include management of other injuries and prevention of seizures. Some data supports the use of hyperbaric oxygen therapy to improve outcomes.

Neuroimaging is helpful but not flawless in detecting raised ICP. A more accurate way to measure ICP is to place a catheter into a ventricle of the brain, which has the added benefit of allowing cerebrospinal fluid to drain, releasing pressure in the skull. Treatment of raised ICP may be as simple as tilting the patient's bed and straightening the head to promote blood flow through the veins of the neck. Sedatives, analgesics and paralytic agents are often used. Hypertonic saline can improve ICP by reducing the amount of cerebral water (swelling), though it is used with caution to avoid electrolyte imbalances or heart failure. Mannitol, an osmotic diuretic, appears to be equally effective at reducing ICP. Some concerns; however, have been raised regarding some of the studies performed. Diuretics, drugs that increase urine output to reduce excessive fluid in the system, may be used to treat high intracranial pressures, but may cause hypovolemia (insufficient blood volume). Hyperventilation (larger and/or faster breaths) reduces carbon dioxide levels and causes blood vessels to constrict; this decreases blood flow to the brain and reduces ICP, but it potentially causes ischemia and is, therefore, used only in the short term. Administration of corticosteroids is associated with an increased risk of death, and so it is recommended that they not be given routinely.

Endotracheal intubation and mechanical ventilation may be used to ensure proper oxygen supply and provide a secure airway. Hypotension (low blood pressure), which has a devastating outcome in TBI, can be prevented by giving intravenous fluids to maintain a normal blood pressure. Failing to maintain blood pressure can result in inadequate blood flow to the brain. Blood pressure may be kept at an artificially high level under controlled conditions by infusion of norepinephrine or similar drugs; this helps maintain cerebral perfusion. Body temperature is carefully regulated because increased temperature raises the brain's metabolic needs, potentially depriving it of nutrients. Seizures are common. While they can be treated with benzodiazepines, these drugs are used carefully because they can depress breathing and lower blood pressure. TBI patients are more susceptible to side effects and may react adversely or be inordinately sensitive to some pharmacological agents. During treatment monitoring continues for signs of deterioration such as a decreasing level of consciousness.

Traumatic brain injury may cause a range of serious coincidental complications that include cardiac arrhythmias and neurogenic pulmonary edema. These conditions must be adequately treated and stabilised as part of the core care for these patients.

Surgery can be performed on mass lesions or to eliminate objects that have penetrated the brain. Mass lesions such as contusions or hematomas causing a significant mass effect (shift of intracranial structures) are considered emergencies and are removed surgically. For intracranial hematomas, the collected blood may be removed using suction or forceps or it may be floated off with water. Surgeons look for hemorrhaging blood vessels and seek to control bleeding. In penetrating brain injury, damaged tissue is surgically debrided, and craniotomy may be needed. Craniotomy, in which part of the skull is removed, may be needed to remove pieces of fractured skull or objects embedded in the brain. Decompressive craniectomy (DC) is performed routinely in the very short period following TBI during operations to treat hematomas; part of the skull is removed temporarily (primary DC). DC performed hours or days after TBI in order to control high intracranial pressures (secondary DC) has not been shown to improve outcome in some trials and may be associated with severe side-effects.

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.

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.

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.

Patient education has been shown to be one of the most effective ways to decrease secondary symptoms seen with closed-head injuries. Patient education often includes working with a therapist to review symptom management and learn about returning to regular activities. Educational initiatives have also been shown to decrease the occurrence of PTSD in head-injury survivors.

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.

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.

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.

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.

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.

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.

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.

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

Concussions, a type of traumatic brain injury, are a frequent concern for those playing sports, from children and teenagers to professional athletes. Repeated concussions are a known cause of various neurological disorders, most notably chronic traumatic encephalopathy (CTE), which in professional athletes has led to premature retirement, erratic behavior and even suicide. Because concussions cannot be seen on X-rays or CT scans, attempts to prevent concussions have been difficult.

A concussion is defined as a complex pathophysiological process affecting the brain, induced by traumatic forces. Concussion may be caused either by a direct blow to the head, face, neck or elsewhere on the body with an "impulsive" force transmitted to the head. Also, you don't have to pass out when you get a concussion (Aubry et al., 2001).

The dangers of repeated concussions have long been known for boxers and wrestlers; a form of CTE common in these two sports, dementia pugilistica (DP), was first described in 1928. An awareness of the risks of concussions in other sports began to grow in the 1990s, and especially in the mid-2000s, in both the medical and the professional sports communities, as a result of studies of the brains of prematurely deceased American football players, who showed extremely high incidences of CTE (see concussions in American football).

As of 2012, the four major professional sports leagues in the United States and Canada have concussion policies. Sports-related concussions are generally analyzed by athletic training or medical staff on the sidelines using an evaluation tool for cognitive function known as the Sport Concussion Assessment Tool (SCAT), a symptom severity checklist, and a balance test.

Concussion symptoms can last for an undetermined amount of time depending on the player and the severity of the concussion. A concussion will affect the way a person's brain works.

There is the potential of post-concussion syndrome, post-concussion syndrome is defined as a set of symptoms that may continue after a concussion is sustained. Post-concussion symptoms can be classified into physical, cognitive, emotional, and sleep symptoms. Physical symptoms include a headache, nausea, and vomiting. Athletes may experience cognitive symptoms that include speaking slowly, difficulty remembering and concentrating. Emotional and sleep symptoms include irritability, sadness, drowsiness, and trouble falling asleep.

Along with the classification of post-concussion symptoms, the symptoms can also be described as immediate and delayed. The immediate symptoms are experienced immediately after a concussion such as: memory loss, disorientation, and poor balance. Delayed symptoms are experienced in the later stages and include sleeping disorders and behavioral changes. Both immediate and delayed symptoms can continue for long periods of time and have a negative impact on recovery. According to research, 20-25% of individuals who have sustained a concussion experienced chronic, delayed symptoms.

Playing through concussion makes people more vulnerable to getting hit again, and that is why most sports have test that trainers will perform to prevent getting hit a second time. A second blow can cause a rare condition known as second-impact syndrome, which can result in severe injury or death. Second-impact syndrome is when an athlete suffers a second head injury before the brain has adequate time to heal in between concussions.

Repeated concussions have been linked to a variety of neurological disorders among athletes, including CTE, Alzheimer's Disease, Parkinsonism and Amyotrophic lateral sclerosis (ALS).

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).

Neurapraxia is often treated and cured by non-operative means. The primary goals of treatment are to maintain the proper nutrition of the paralyzed muscles, prevent contraction by the antagonists of the paralyzed muscles, and to consistently keep the joints mobile. A splint is often used in cases of neurapraxia because it is able to maintain a relaxed position of the paralyzed muscle. The splint prevents the paralyzed muscle from being overstretched either by the force of gravity or by other non-paralyzed antagonists. During the recovery period of neurapraxia, it is essential that the joints constantly undergo passive movement in order to preserve proper mobility. If joints are kept mobile, the limb has the best possible chance of benefit from the return of nervous function. Non-steroidal anti-inflammatory medications can also help to reduce swelling at the injury site. In addition to these non-operative remedies, it is suggested that muscles affected by neurapraxia be kept warm at all times. Circulation in the limb is stimulated with the use of heat.

Once voluntary movement has returned to the muscle, recovery and treatment continues by the participation in active exercises. Physical Therapy and Occupational Therapy are common sources of treatment during these early stages of restoration of active movement. Almost all cases of neurapraxia can be completely treated by non-operative means.

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

Medical treatment with anti-vertigo medications may be considered in acute, severe exacerbation of BPPV, but in most cases are not indicated. These primarily include drugs of the anti-histamine and anti-cholinergic class, such as meclizine and hyoscine butylbromide (scopolamine) respectively. The medical management of vestibular syndromes has become increasingly popular over the last decade, and numerous novel drug therapies (including existing drugs with new indications) have emerged for the treatment of vertigo/dizziness syndromes. These drugs vary considerably in their mechanisms of action, with many of them being receptor- or ion channel-specific. Among them are betahistine or dexamethasone/gentamicin for the treatment of Ménière's disease, carbamazepine/oxcarbazepine for the treatment of paroxysmal dysarthria and ataxia in multiple sclerosis, metoprolol/topiramate or valproic acid/tricyclic antidepressant for the treatment of vestibular migraine, and 4-aminopyridine for the treatment of episodic ataxia type 2 and both downbeat and upbeat nystagmus. These drug therapies offer symptomatic treatment, and do not affect the disease process or resolution rate. Medications may be used to suppress symptoms during the positioning maneuvers if the patient's symptoms are severe and intolerable. More dose-specific studies are required, however, in order to determine the most effective drug(s) for both acute symptom relief and long-term remission of the condition.

According to medical professionals with the Cleveland Clinic, once an athlete suffers from an episode of cervical spinal cord, team physician or athletic trainer first stabilize the head and neck followed by a thorough neurologic inspection. If the injury is deemed severe, injured parties should be taken to a hospital for evaluation. Athletes that suffer from severe episodes of neurapraxia are urged to consult orthopaedic or spinal medical specialists. In mild cases of neurapraxia, the athlete is able to remove themselves from the field of play. However, the athlete is still advised to seek medical consultation.

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

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

Pain, especially headache, is a common complication following a TBI. Being unconscious and lying still for long periods can cause blood clots to form (deep venous thrombosis), which can cause pulmonary embolism. Other serious complications for patients who are unconscious, in a coma, or in a vegetative state include pressure sores, pneumonia or other infections, and progressive multiple organ failure.

The risk of post-traumatic seizures increases with severity of trauma (image at right) and is particularly elevated with certain types of brain trauma such as cerebral contusions or hematomas. As many as 50% of people with penetrating head injuries will develop seizures. People with early seizures, those occurring within a week of injury, have an increased risk of post-traumatic epilepsy (recurrent seizures occurring more than a week after the initial trauma) though seizures can appear a decade or more after the initial injury and the common seizure type may also change over time. Generally, medical professionals use anticonvulsant medications to treat seizures in TBI patients within the first week of injury only and after that only if the seizures persist.

Neurostorms may occur after a severe TBI. The lower the Glasgow Coma Score (GCS), the higher the chance of Neurostorming. Neurostorms occur when the patient's Autonomic Nervous System (ANS), Central Nervous System (CNS), Sympathetic Nervous System (SNS), and ParaSympathetic Nervous System (PSNS) become severely compromised https://www.brainline.org/story/neurostorm-century-part-1-3-medical-terminology . This in turn can create the following potential life-threatening symptoms: increased IntraCranial Pressure (ICP), tachycardia, tremors, seizures, fevers, increased blood pressure, increased Cerebral Spinal Fluid (CSF), and diaphoresis https://www.brainline.org/story/neurostorm-century-part-1-3-medical-terminology. A variety of medication may be used to help decrease or control Neurostorm episodes https://www.brainline.org/story/neurostorm-century-part-3-3-new-way-life.

Parkinson's disease and other motor problems as a result of TBI are rare but can occur. Parkinson's disease, a chronic and progressive disorder, may develop years after TBI as a result of damage to the basal ganglia. Other movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), and myoclonus (shock-like contractions of muscles).

Skull fractures can tear the meninges, the membranes that cover the brain, leading to leaks of cerebrospinal fluid (CSF). A tear between the dura and the arachnoid membranes, called a CSF fistula, can cause CSF to leak out of the subarachnoid space into the subdural space; this is called a subdural hygroma. CSF can also leak from the nose and the ear. These tears can also allow bacteria into the cavity, potentially causing infections such as meningitis. Pneumocephalus occurs when air enters the intracranial cavity and becomes trapped in the subarachnoid space. Infections within the intracranial cavity are a dangerous complication of TBI. They may occur outside of the dura mater, below the dura, below the arachnoid (meningitis), or within the brain itself (abscess). Most of these injuries develop within a few weeks of the initial trauma and result from skull fractures or penetrating injuries. Standard treatment involves antibiotics and sometimes surgery to remove the infected tissue.

Injuries to the base of the skull can damage nerves that emerge directly from the brain (cranial nerves). Cranial nerve damage may result in:

- Paralysis of facial muscles

- Damage to the nerves responsible for eye movements, which can cause double vision

- Damage to the nerves that provide sense of smell

- Loss of vision

- Loss of facial sensation

- Swallowing problems

Hydrocephalus, post-traumatic ventricular enlargement, occurs when CSF accumulates in the brain, resulting in dilation of the cerebral ventricles and an increase in ICP. This condition can develop during the acute stage of TBI or may not appear until later. Generally it occurs within the first year of the injury and is characterized by worsening neurological outcome, impaired consciousness, behavioral changes, ataxia (lack of coordination or balance), incontinence, or signs of elevated ICP.

Any damage to the head or brain usually results in some damage to the vascular system, which provides blood to the cells of the brain. The body can repair small blood vessels, but damage to larger ones can result in serious complications. Damage to one of the major arteries leading to the brain can cause a stroke, either through bleeding from the artery or through the formation of a blood clot at the site of injury, blocking blood flow to the brain. Blood clots also can develop in other parts of the head. Other types of vascular complications include vasospasm, in which blood vessels constrict and restrict blood flow, and the formation of aneurysms, in which the side of a blood vessel weakens and balloons out.

Fluid and hormonal imbalances can also complicate treatment. Hormonal problems can result from dysfunction of the pituitary, the thyroid, and other glands throughout the body. Two common hormonal complications of TBI are syndrome of inappropriate secretion of antidiuretic hormone and hypothyroidism.

Another common problem is spasticity. In this situation, certain muscles of the body are tight or hypertonic because they cannot fully relax.

Surgical treatments, such as a semi-circular canal occlusion, do exist for BPPV, but carry the same risk as any neurosurgical procedure. Surgery is reserved as a last resort option for severe and persistent cases which fail vestibular rehabilitation (including particle repositioning and habituation therapy).