Brain trauma encyclopedia topics

Signs and symptoms

Some symptoms are evident immediately, while others do not surface until several days, weeks, or even years after the injury. In the case of pediatric TBI children are sometimes described as having grown into their deficits years after their injury.

With mild TBI, the patient may remain conscious or may lose consciousness for a few seconds or minutes. The person may also feel dazed or not like him- or herself for several days or weeks after the initial injury. Other symptoms include:

headache
mental confusion
lightheadedness
dizziness
double vision, blurred vision, or tired eyes
ringing in the ears
bad or metallic taste in the mouth
fatigue or lethargy
a change in sleep patterns
behavioral, personality or mood changes
trouble with memory, concentration, or calculation
decreased coordination
symptoms may remain the same or get better; worsening symptoms indicate a more severe injury

With moderate or severe TBI, the patient may show these same symptoms, but may also have:

loss of consciousness
personality change
a severe, persistent, or worsening headache
repeated vomiting or nausea
seizures
inability to awaken
dilation (widening) of one or both pupils
slurred speech
weakness or numbness in the extremities
loss of coordination
increased confusion, restlessness, or agitation
abnormal posturing, ie. decorticate or decerebrate posturing
vomiting and neurological deficit (e.g. weakness in a limb) together are important indicators of prognosis and their presence may warrant early CT scanning and neurosurgical intervention.

Small children with moderate to severe TBI may show some of these signs as well as signs specific to young children, including:

persistent crying
inability to be consoled
refusal to nurse or eat

Head injured people with signs of moderate or severe TBI should receive immediate emergency medical attention. Mild TBI that produces symptoms that do not remit within a short period of time also requires medical attention.

Causes and risk factors

Transportation accidents involving automobiles, motorcycles, bicycles, and pedestrians cause half of all TBIs and the largest portion of TBI in people under age 75. For those aged 75 and older, falls cause the majority of TBIs.

Approximately 20% of TBIs are due to violence, such as firearm assaults and child abuse, and about 3% are due to sports injuries. Half of TBI incidents involve alcohol use.

Traumatic brain injury is a frequent cause of major long-term disability in individuals surviving head injuries sustained in war zones. This is becoming an issue of growing concern in modern warfare, in which rapid deployment of acute interventions are effective in saving the lives of combatants with significant head injuries. Traumatic brain injury has been identified as the "signature injury" among wounded soldiers of the current military engagement in Afghanistan and Iraq.

Outcome for patients with head injury depends heavily on the cause. For example, in the US, patients with TBIs from falls have an 89% survival rate, while only 9% of patients with firearm-related TBIs survive.

Classification and subtypes

Focal vs. diffused

The damage from TBI can be focal or diffuse, confined to one area of the brain or involving more than one area, respectively. Diffused trauma to the brain is frequently associated with concussion (a shaking of the brain in response to sudden motion of the head), diffused axonal injury, or coma. Localized injuries may be associated with neurobehavioral manifestations, hemiparesis or other focal neurologic deficits. Types of focal brain injury include bruising of brain tissue called a contusion and intracranial hemorrhage or hematoma, heavy bleeding in the skull. Hemorrhage, due to rupture of a blood vessel in the head, can be extra-axial, meaning it occurs within the skull but outside of the brain, or intra-axial, occurring within the brain. Extra-axial hemorrhages can be further divided into subdural hematoma, epidural hematoma, and subarachnoid hemorrhage. An epidural hematoma involves bleeding into the area between the skull and the dura. With a subdural hematoma, bleeding is confined to the area between the dura and the arachnoid membrane. A subarachnoid hemorrhage involves bleeding into the space between the surface of the brain and the arachnoid membrane that lies just above the surface of the brain, usually resulting from a tear in a blood vessel on the surface of the brain. Bleeding within the brain itself is called an intracerebral hematoma. Intra-axial bleeds are further divided into intraparenchymal hemorrhage which occurs within the brain tissue itself and intraventricular hemorrhage which occurs into the ventricular system.

Open vs. closed

TBI can result from a closed or penetrating head injury. A closed injury occurs when the skull is not breached, while a penetrating injury occurs when an object pierces the skull and enters brain tissue.

As the first line of defense, the skull is particularly vulnerable to injury. Skull fractures occur when a bone in the skull cracks or breaks. A depressed skull fracture occurs when pieces of the broken skull press into the tissue of the brain. A penetrating skull fracture occurs when something pierces the skull, such as a bullet, leaving a distinct and localized traumatic injury to brain tissue. Skull fractures can cause cerebral contusion.

Severity

Levels of TBI severity
	GCS	PTA	LOC
Mild	13 to 15	<1 hour	<30 minutes
Moderate	9 to 12	30 minutes to 24 hours	1 to 24 hours
Severe	3 to 8	>1 day	>24 hours

Head injuries can be subdivided into mild, moderate, and severe TBI to help predict outcome. One common classification system determines severity based on the Glasgow Coma Scale (GCS) and duration of post-traumatic amnesia (PTA) and loss of consciousness (LOC) according to the table at right. Other classification systems use GCS alone or PTA or LOC alone or together. Prognosis worsens with the severity of injury, but mild TBI is more poorly defined and prognosis is not as clear with it.

Mild TBI is also commonly called concussion. Though prognosis for concussion is usually very good, a portion of people may suffer lasting problems associated with the injury, such as post-concussion syndrome. A young person who receives a second concussion before symptoms from another one have healed is at risk for developing a very rare but deadly condition called second-impact syndrome, in which the brain swells catastrophically after even a mild blow.

Pathophysiology

Unlike most forms of traumatic death, a large percentage of the people killed by brain trauma do not die right away but rather days to weeks after the event. Rather than improving after being hospitalized, some 40% of TBI patients deteriorate. Primary brain injury (the damage that occurs at the moment of trauma when tissues and blood vessels are stretched, compressed, and torn) is not adequate to explain this degeneration. Rather, the deterioration is caused by secondary injury, a complex set of biochemical cascades that occur in the minutes to days following the trauma and contribute a large amount to disability and mortality from TBI.

Secondary injury events are poorly understood but are thought to include brain swelling, alterations in cerebral blood flow, a decrease in the tissues' pH, free radical overload, and excitotoxicity. These secondary processes damage neurons that were not directly harmed by the primary injury.

Effects

The results of traumatic brain injury vary widely in type and duration. A head injured patient may experience physical effects of the trauma such as headaches, movement disorders (e.g. Parkinsonism), seizures, difficulty walking, sexual dysfunction, lethargy, or coma. Cognitive symptoms include changes in judgment or ability to reason or plan, memory problems, and loss of mathematical ability. Emotional problems include mood swings, poor impulse control, agitation, low frustration threshold, self-centeredness, clinical depression, and psychotic symptoms such as hallucinations and delusions.

Effects on consciousness

Generally, there are six abnormal states of consciousness that can result from a TBI: stupor, coma, persistent vegetative state, minimally conscious state, locked-in syndrome, and brain death.

Stupor is a state in which the patient is unresponsive but can be aroused briefly by a strong stimulus, such as sharp pain. Coma is a state in which the patient is totally unconscious, unresponsive, unaware, and unarousable.

Patients in a persistent vegetative state are unconscious and unaware of their surroundings, but they continue to have a sleep-wake cycle and can have periods of alertness. A vegetative state can result from diffuse injury to the cerebral hemispheres of the brain without damage to the lower brain and brainstem.

Patients in a minimally conscious state have a reduced level of arousal and may appear, on the surface, to be in a persistent vegetative state but are capable of demonstrating the ability to actively process information. In the minimally conscious state a patient exhibits deliberate, or cognitively mediated, behavior often enough, or consistently enough, for clinicians to be able to distinguish it from the entirely unconscious, reflexive responses that are seen in the persistent vegetative state. Differentiating a patient in a persistent vegetative state from one in a minimally conscious state can be challenging but remains a critically important clinical task.

Locked-in syndrome is a condition in which a patient is aware and awake, but cannot move or communicate due to complete paralysis of the body. Voluntary control of eye movements or blinking may be spared permitting the detection of conscious awareness and enabling the establishment of functional communication.

Brain death is the lack of measurable brain function due to diffuse damage to the cerebral hemispheres and the brainstem, with loss of any integrated activity among distinct areas of the brain. Brain death is irreversible. Removal of assistive devices will result in immediate cardiac arrest and cessation of breathing.

Studies have brought into question the nature of coma and consciousness in TBI. For example, a 23 year old woman in a vegetative state after a severe brain injury due to a car accident was able to communicate with a team of British researchers at Cambridge University in England via functional magnetic resonance imaging. While cautious about accepting the study's results, Nicholas Schiff, a neurologist at the Weill Cornell Medical College in New York, agrees that the research was groundbreaking. "It's the first time we've ever seen something like this. It really is kind of shocking," he said.

Complications

Health complications may occur in the period immediately following a TBI. These complications are not types of TBI, but are distinct medical problems that arise as a result of the injury. The risk of complications increases with the severity of the trauma. Complications of TBI include immediate seizures, hydrocephalus or post-traumatic ventricular enlargement, cerebrospinal fluid leaks, infections, vascular injuries, and cranial nerve injuries. Pain, especially headache, is a common complication following a TBI. Serious complications for patients who are unconscious, in a coma, or in a vegetative state include pressure sores of the skin, pneumonia or other infections, and progressive multiple organ failure.

Hydrocephalus or post-traumatic ventricular enlargement occurs when cerebrospinal fluid (CSF) accumulates in the brain resulting in dilation of the cerebral ventricles (cavities in the brain filled with CSF) 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. The condition may develop as a result of meningitis, subarachnoid hemorrhage, intracranial hematoma, or other injuries. Treatment includes shunting and draining of CSF as well as any other appropriate treatment for the root cause of the condition.

Skull fractures can tear the meninges, the membranes that cover the brain, leading to CSF leaks. 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 that let CSF out of the brain cavity 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. Meningitis may be especially dangerous, with the potential to spread to the rest of the brain and nervous system.

Skull fractures, especially at the base of the skull, can also cause cranial nerve injuries that result in compressive cranial neuropathies. All but three of the twelve cranial nerves project out from the brain stem to the head and face. Damage to the seventh cranial nerve, the most commonly injured one in TBI, can result in paralysis of facial muscles.

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 damage to small blood vessels, but damage to larger vessels 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 (hemorrhagic stroke) or through the formation of a clot at the site of injury, called a thrombus or thrombosis, blocking blood flow to the brain (ischemic stroke). Blood clots also can develop in other parts of the head. Symptoms such as headache, vomiting, seizures, paralysis on one side of the body, and semiconsciousness developing within several days of a head injury may be caused by a blood clot that forms in the tissue of one of the sinuses, or cavities, adjacent to the brain. Other types of vascular injuries include vasospasm and the formation of aneurysms.

Fluid and hormonal imbalances can complicate the treatment of hypermetabolism and high intracranial pressure (ICP). 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 (SIADH) and hypothyroidism.

Trauma victims often develop hypermetabolism or an increased metabolic rate, which leads to an increase in the amount of heat the body produces. The body redirects into heat the energy needed to keep organ systems functioning, causing muscle wasting and the starvation of other tissues. The nutritional management of patients with TBI, including the provision of adequate calories and protein through an available route of administration to balance consumption, is thus critically important in order to avoid complications related to hypermetabolism and resulting malnutrition. Provision of food through a feeding tube may be temporarily necessary to meet the nutritional needs of the patient with a severe TBI, until they are awake and able to eat and swallow safely without risking pulmonary aspiration and the development of aspiration pneumonia. Sometimes the use of parenteral feeding is necessary if the patient has associated injuries or complications that prevent direct access to the digestive system.

Disabilities resulting from TBI

Disabilities resulting from a TBI depend upon the severity of the injury, the location of the injury, and the age and general health of the patient. Some common disabilities include problems with cognition (attention, calculation, memory, judgment, insight, and reasoning), sensory processing (sight, hearing, touch, taste, and smell), communication (language expression and understanding), social function (empathy, capacity for compassion, interpersonal social awareness and facility) and mental health (depression, anxiety, personality changes, aggression, acting out, and social inappropriateness).

Postconcussion syndrome

The term post-concussion syndrome (PCS) is defined in the DSM-IV, requiring both neuropsychological testing demonstrating attention and concentration difficulties, as well as 3 of the following symptoms being present for at least 3 months since the time of a specific incident:

1. Fatigue 2. Sleep Disorder 3. Headache 4. Dizziness/Vertigo 5. Irritability/Aggression 6. Anxiety 7. Depression/Lability 8. Personality Changes 9. Apathy

There is significant controversy in the medical literature regarding PCS, as these symptoms are not specific to brain trauma, and are commonly present in people with psychological issues, chronic pain, or other medical conditions. The syndrome is more prevalent in patients who have had a prior history of psychiatric symptoms, such as depression or anxiety, before the injury. Treatment can be variable, but typically includes counseling and education, and potentially use of medications and/or specific therapy, including cognitive therapy and psychological counseling.

Cognitive problems

Most patients with severe TBI who recover consciousness suffer from cognitive disabilities, including the loss of many higher level mental skills. Memory loss, the most common cognitive impairment among head-injured patients, occurs in 20–79% of people with closed head trauma, depending on severity. Memory loss is characterized by some loss of specific memories or the partial inability to form or store new ones. Some of these patients may experience post-traumatic amnesia (PTA), either anterograde or retrograde. Anterograde PTA is impaired memory of events that happened after the TBI, while retrograde PTA is impaired memory of events that happened before the TBI.

Patients with mild to moderate head injuries who experience cognitive deficits may become easily confused or distracted and have problems with concentration and attention. They may also have problems with higher level, executive functions, such as planning, organizing, abstract reasoning, problem solving, and making judgments, which may make it difficult to resume pre-injury activities. Recovery from cognitive deficits is greatest within the first six months after the injury and more gradual after that.

Patients with moderate to severe TBI have more problems with cognitive deficits than patients with mild TBI, but a history of several mild TBIs may have an additive or multiplicative effect.

Language and communication problems are common disabilities in TBI patients. Some may experience aphasia, defined as difficulty with understanding and producing spoken and written language; others may have difficulty with the more subtle aspects of communication, such as body language and emotional, non-verbal signals. TBI patients may have problems with spoken language if the part of the brain that controls speech muscles is damaged. In this disorder, called dysarthria, the patient can think of the appropriate language, but cannot easily speak the words because they are unable to use the muscles needed to form the words and produce the sounds. Speech is often slow, slurred, and garbled. Some may have problems with intonation or inflection, called prosodic dysfunction.

Alzheimer's disease (AD) is a progressive, neurodegenerative disease characterized by dementia, memory loss, and deteriorating cognitive abilities. Research suggests an association between head injury in early adulthood and the development of AD later in life; the more severe the head injury, the greater the risk of developing AD. Some evidence indicates that a head injury may interact with other factors to trigger the disease and may hasten the onset of the disease in individuals already at risk. For example, people who have a particular form of the protein apolipoprotein E (apoE4) and suffer a head injury fall into this increased risk category. (ApoE4 is a naturally occurring protein that helps transport cholesterol through the bloodstream.)

Dementia pugilistica, also called chronic traumatic encephalopathy, primarily affects career boxers. The most common symptoms of the condition are dementia and parkinsonism caused by repetitive blows to the head over a long period of time. Symptoms begin anywhere between 6 and 40 years after the start of a boxing career, with an average onset of about 16 years.

Post-traumatic dementia is another potential long-term effect of TBI. The symptoms of post-traumatic dementia are very similar to those of dementia pugilistica, except that post-traumatic dementia is also characterized by long-term memory problems and is caused by a single, severe TBI that results in a coma.

Sensory deficits

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

Emotional and behavioral problems

TBI may cause emotional or behavioral problems that fit under the broad category of psychiatric health, including personality changes. Psychiatric problems that may persist for one half year to two years after the injury may include irritability, suicidal ideation, insomnia, and loss of the ability to experience pleasure from previously enjoyable experiences. Other problems include apathy, anxiety, anger, paranoia, confusion, frustration, agitation, and mood swings. About one quarter of people with TBI suffer from clinical depression, and about 9% suffer mania.

Different behavioral problems are characteristic of the location of injury; for instance, frontal lobe injuries often result in disinhibition and inappropriate or childish behavior, and temporal lobe injuries often cause irritability and aggression.

Problem behaviors may include violence, impulsivity, acting out, noncompliance, social inappropriateness, emotional outbursts, impaired self-control, impaired self-awareness, inability to take responsibility or accept criticism, egocentrism, inappropriate sexual activity, and alcohol or drug abuse or addiction. Some patients' personality problems may be so severe that they are diagnosed with organic personality disorder, a psychiatric condition characterized by many of these problems. Sometimes TBI patients suffer from developmental stagnation, meaning that they fail to mature emotionally, socially, or psychologically after the trauma. This is a serious problem for children and young adults who suffer from a TBI, because attitudes and behaviors that are appropriate for a child or teenager become inappropriate in adulthood. TBI patients who show psychiatric or behavioral problems may be helped with medication and psychotherapy, although the effectiveness of psychotherapy may be limited by the residual neurocognitive impairment. Technological improvements and emergency care have diminished the incidence of devastating TBI while increasing the numbers of patients with mild or moderate TBI. Such patients are more adversely affected by their emotional problems (such as post traumatic stress disorder) and neurocognitive difficulties than by their residual physical disabilities. One study found that the prevalence of all psychiatric illnesses was 49% in moderate to severe TBI and 34% in mild TBI within a year of injury, compared with 18% of controls. People with TBI continue to be at greater risk for psychiatric problems than others years after an injury.

Physical problems

As many as 50% of patients with penetrating head injuries will develop post-traumatic seizures. The risk of seizures is elevated with other types of brain trauma such as cerebral contusions or hematomas, and it increases with severity of trauma (image at right). 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). 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.

Parkinson's disease and other motor problems as a result of TBI are rare but can occur. Parkinson's disease may develop years after TBI as a result of damage to the basal ganglia. Symptoms of Parkinson's disease include tremor or trembling, rigidity or stiffness, slow movement (bradykinesia), inability to move (akinesia), shuffling walk, and stooped posture. Despite many scientific advances in recent years, Parkinson's disease remains a chronic and progressive disorder, meaning that it is incurable and will progress in severity until the end of life. Other movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), and myoclonus (shock-like contractions of muscles).

Prevention

The Centers for Disease Control and Prevention (CDC) have suggested taking the following safety precautions for reducing the risk of suffering a TBI.

Wearing a seatbelt.
Buckling children into a child safety seat, booster seat, or seatbelt (depending on the child's age) every time the child rides in a car.
Wearing a helmet and making sure children wear helmets when

riding a bike or motorcycle;
playing a contact sport such as American football or ice hockey;
using in-line skates or riding a skateboard;
batting and running bases in baseball or softball;
riding a horse;
rock climbing;
sledding;
skiing or snowboarding.

Avoiding falls by

using a step-stool with a grab bar to reach objects on high shelves;
installing handrails on stairways;
installing window guards to keep young children from falling out of open windows;
using safety gates at the top and bottom of stairs when young children are around.

Using only playgrounds with surfaces made of shock-absorbing material (e.g. mulch, sand).

Diagnosis

Medical personnel assess the patient's condition by measuring vital signs and reflexes and by performing a neurological examination. They assess the patient's level of consciousness and neurological functioning using the Glasgow Coma Scale.

Imaging tests help in determining the diagnosis and prognosis of a TBI patient. Patients with mild to moderate injuries may receive skull and neck X-rays to check for bone fractures. For moderate to severe cases, the gold standard imaging test is a computed tomography (CT) scan, which creates a series of cross-sectional X-ray images of the head and brain and can show bone fractures as well as the presence of hemorrhage, hematomas, contusions, brain tissue swelling, and tumors. Magnetic resonance imaging (MRI), which can show more detail than X-rays or CT, may be used. Diffuse traumatic brain injury -even when severe - often shows no abnormality in standard imaging. However, 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.

CT and MRI is standard in TBI diagnosis, but other imaging and diagnostic techniques that may be used to confirm a particular diagnosis include cerebral angiography, electroencephalography (EEG), transcranial Doppler ultrasound, and single photon emission computed tomography (SPECT). The newest imaging techniques to show the neurocognitive or neurophysiologic effects on the brain due to TBI are Functional Magnetic Resonance Imaging (fMRI) and Positron emission tomography (PET). Previously listed studies are used to determine structural defects rather than functional alterations.

Treatment

Medical care usually begins when paramedics or emergency medical technicians arrive on the scene of an accident or when a TBI patient arrives at the emergency department of a hospital. Because little can be done to reverse the initial brain damage caused by trauma, medical personnel try to stabilize the patient and focus on preventing further injury. Primary concerns include insuring proper oxygen supply, maintaining adequate blood flow, and controlling blood pressure. Since many head-injured patients may also have spinal cord injuries, the patient is placed on a back-board and in a neck restraint to prevent further injury to the head and spinal cord.

Sometimes when the brain is injured swelling occurs and fluids accumulate within the brain space. When an injury occurs inside the skull-encased brain, there is no place for swollen tissues to expand and no adjoining tissues to absorb excess fluid. This leads to an increase in the pressure within the skull, called intracranial pressure (ICP). High ICP can cause delicate brain tissue to be crushed, or parts of the brain to herniate across structures within the skull, potentially leading to severe damage. Medical personnel measure a patient's ICP using a probe or catheter. The instrument is inserted through the skull to the subarachnoid level and is connected to a monitor that registers ICP. If a patient has high ICP, he or she may undergo a ventriculostomy, a procedure that drains cerebrospinal fluid (CSF) from the ventricles to bring the pressure down by way of an external ventricular drain.

Approximately half of severe head injuries require surgery to remove or repair hematomas or contusions. Patients may also need surgery to treat injuries in other parts of the body. These patients usually go to the intensive care unit after surgery. Decompressive craniectomy is a last-resort surgical procedure in which part of the skull is removed in an attempt to reduce severely high ICP.

Barbiturates can be used to decrease ICP; mannitol was thought to be useful, but it appears likely that the studies suggesting that it was of use may have been falsified.

Referral for neuropsychological testing and neuropsychological assessment can prove of great benefit to those suffering from TBI to demonstrate the cognitive areas of their brain that have been affected and to aid in the recovery and rehabilitation processes.

For patients who survive the initial complications of TBI, a number of therapies have been and are being investigated. Many of these therapies have not been validated in large clinical trials, but some, such as hypothermia, have shown promise for subsets of the population. The research community is also pursuing new ideas involving nanotechnology and stem cells.

Rehabilitation

During the acute stage of rehabilitation, moderately to severely injured patients may receive treatment and care in an intensive care unit of a hospital followed by movement to a step-down unit or to a neurosurgical ward. Once medically stable, the patient may be transferred to a subacute unit of the medical center, to a long-term acute care (LTAC) facility, to a rehabilitation inpatient treatment unit contained within the acute trauma center, or to an independent off-site rehabilitation hospital. Some inpatient treatment units have a specialty focus in brain injury rehabilitation.

Decisions regarding when and where an individual should be treated depend on factors including the level to which the person can participate in rehabilitation. Moderately to severely injured patients may receive physical therapy, occupational therapy, speech and language therapy, physiatry (physical medicine and rehabilitation), psychology, psychiatry, and social work. The goal of rehabilitation is to improve the patient's ability to function independently at home and in society. Therapists help the patient adapt to disabilities or change the patient's living conditions to accommodate impairments. Education and training for caregivers are also critical.

After discharge from the inpatient rehabilitation treatment unit, the outpatient phase of care begins and goals often will shift from assisting the person to achieve independence in basic routines of daily living to treating broader psychosocial issues associated with long-term adjustment and community reintegration. Common problems include those in areas including cognition, social awareness, and behavior and emotional regulation; these are often complicated by difficulty adjusting to deficits. Other concerns such as post-traumatic stress disorder may emerge and complicate recovery.

An additional goal of the rehabilitation program is to prevent, or failing that, to diagnose and treat TBI complications. Another type of treatment that can help to improve mental function and skills after a TBI is neurocognitive rehabilitation.

Some patients may need medication for psychiatric and physical problems resulting from the TBI. TBI patients are more susceptible to side effects and may react adversely to some pharmacological agents or may be inordinately sensitive to them, for example, due to a more permeable blood-brain barrier that may result from injury.

Involvement of caregivers in the rehabilitation program may assist and encourage the patient. Family members may also benefit from psychotherapy and social support services. Caregivers often feel a great deal of emotional stress, which can reduce the quality of their care. Support for caregivers becomes particularly important during the outpatient phase of care when behavioral and cognitive problems may complicate patients' relationships, particularly in marriage. Respite care such as supported living and residential holidays, with supported days out, offers relief for caregivers and a new area of brain stimulation for the patient.

Epidemiology

The incidence of TBI varies by age, gender, region and other factors. For example, the yearly incidence in the U.S. is estimated to be about 1.8 to 2.5 per 1000 people, but the incidence is thought to be higher in Europe and South Africa.

The age groups most at risk for TBI are children ages five to nine and adults over age 80. Children age five and younger are also at high risk for TBI. Men suffer twice as many TBIs as women do and have a fourfold risk of fatal head injury. Males also account for two thirds of childhood and adolescent head trauma patients.

Each year in the United States:

about two million people suffer a TBI
about 500,000 people are hospitalized for TBI
approximately 270,000 people experience a moderate or severe TBI,
approximately 60,000 new cases of epilepsy occur as a result of head trauma,
approximately 50,000 people die from head injury,
and approximately 80,000 of these survivors live with chronic disabilities as a result of the injury.

The likelihood of the occurrence of disabilities varies with the severity of the head injury: permanent disability is thought to occur in 10% of mild injuries, 66% of moderate injuries, and 100% of severe injuries.

Firearms are the most common cause of fatal TBI, followed by vehicle accidents and then falls (see chart at right). Of deaths from firearms, 75% are considered to be suicides.