Traumatic brain injury

Definition

Traumatic brain injury (TBI) is the result of physical trauma to the head causing damage to the brain. This damage can be focal, or restricted to a single area of the brain, or diffuse, affecting more than one region of the brain. By definition, TBI requires that there be a head injury, or any physical assault to the head leading to injury of the scalp, skull, or brain. However, not all head trauma is associated with TBI.

Description

TBI is sometimes known as acquired brain injury. The least severe and most common type of TBI is termed a concussion, which is technically defined as a brief loss of consciousness after a head injury without any physical evidence of damage on an imaging study such as a CT or MRI scan. In common parlance, concussion may refer to any minor injury to the head or brain.

Symptoms, complaints, and neurological or behavioral changes following TBI depend on the location (s) of the brain injury and on the total volume of injured brain. Usually, TBI causes focal brain injury involving a single area of the brain where the head is struck or where an object such as a bullet enters the brain. Although damage is typically worst at the point of direct impact or entry, TBI may also cause diffuse brain injury involving several other brain regions.

Closed head injury refers to TBI in which the head is hit by or strikes an object without breaking the skull. In a penetrating head injury, an object such as a bullet fractures the skull and enters brain tissue.

Diffuse brain damage associated with closed head injury may result from back-and-forth movement of the brain against the inside of the bony skull. This is sometimes called coup-contrecoup injury. "Coup," or French for "blow," refers to the brain injury directly under the point of maximum impact to the skull. "Contrecoup," or French for "against the blow," refers to the brain injury opposite the point of maximum impact.

For example, coup-contrecoup injury may occur in a rear-end collision, with high speed stops, or with violent shaking of a baby, because the brain and skull are of different densities, and therefore travel at different speeds. The impact of the collision causes the soft, gelatinous brain tissue to jar against bony prominences on the inside of the skull.

Because of the location of these prominences and the position of the brain within the skull, the frontal lobes (behind the forehead) and temporal lobes (underlying the temples) are most susceptible to this type of diffuse damage. These lobes house major brain centers involved in speech and language, so problems with communication skills often follow closed head injuries of this type.

Depending on which areas of the brain are injured, other symptoms of closed head injury may include difficulty with concentration, memory, thinking, swallowing, walking, balance, and coordination; weakness or paralysis; changes in sensation; and alteration of the sense of smell.

Consequences of TBI can be relatively subtle or completely devastating, related to the severity and mechanism of injury. Diffuse axonal injury, or shear injury, may follow contrecoup injury even if there is no damage to the skull or obvious bleeding into the brain tissue. In this type of injury, damage to the part of the nerve that communicates with other nerves degenerates and releases harmful substances that can damage neighboring nerves.

When the skull cracks or breaks, the resulting skull fracture can cause a contusion, or an area of bruising of brain tissue associated with swelling and blood leaking from broken blood vessels. A depressed skull fracture occurs when fragments of the broken skull sink down from the skull surface and press against the surface of the brain. In a penetrating skull fracture, bone fragments enter brain tissue. Either of these types of skull fracture can cause bruising of the brain tissue, called a contusion. Contrecoup injury can also lead to brain contusion.

If the physical trauma to the head ruptures a major blood vessel, the resulting bleeding into or around the brain is called a hematoma. Bleeding between the skull and the dura, the thick, outermost layer covering the brain, is termed an epidural hematoma . When blood collects in the space between the dura and the arachnoid membrane, a more fragile covering underlying the dura, it is known as a subdural hematoma . An intracerebral hematoma involves bleeding directly into the brain tissue.

All three types of hematomas can damage the brain by putting pressure on vital brain structures. Intracerebral hematomas can cause additional damage as toxic breakdown products of the blood harm brain cells, cause swelling, or interrupt the flow of cerebrospinal fluid around the brain.

Demographics

Estimates for the number of Americans living today who have had a TBI range from between 2.5 and 6.5 million, making it a major public health problem costing the United States more than $48 billion annually. A recent review suggests that the incidence of TBI in the United States is between 180 and 250 per 100,000 population per year, with even higher incidence in Europe and South Africa.

Although TBI can affect anyone at any age, certain age groups are more vulnerable because of lifestyle and other risk factors. Males ages 15 to 24, especially those in lower socioeconomic levels, are most likely to become involved in high-speed or other risky driving, as well as physical fights and criminal activity. These behaviors increase the likelihood of TBI associated with automobile and motorcycle accidents or with violent crimes.

Infants, children under five years of age, and adults 75 years and older are also at higher risk for TBI than the general population because they are most susceptible to falls around the home. Other factors predisposing the very young and the very old to TBI include physical abuse, such as violent shaking of an infant or toddler that can result in shaken baby syndrome .

Causes and symptoms

Accidents, especially motor vehicle accidents, are the major culprit implicated in TBI. Because accidents are the leading cause of death or disability in men under age 35, and because over 70% of accidents involve injuries of the head and/or spinal cord, this is not surprising. In fact, transportation accidents involving automobiles, motorcycles, bicycles, and pedestrians account for half of all TBIs and for the majority of TBIs in individuals under the age of 75. At least half of all TBIs are associated with alcohol use. Sports injuries cause about 3% of TBIs; other accidents leading to TBI may occur at home, at work, or outdoors.

In those age 75 and older, falls are responsible for most TBIs. Other situations leading to TBI at all ages include violence, implicated in about 20% of TBIs. Firearm assaults are involved in most violent causes of TBI in young adults, whereas child abuse is the most common violent cause in infants and toddlers. In the shaken baby syndrome, a baby is shaken with enough force to cause severe countrecoup injury.

The symptoms of TBI may occur immediately or they may develop slowly over several hours, especially if there is slow bleeding into the brain or gradual swelling. Depending on the cause, mechanism, and extent of injury, the severity of immediate symptoms of TBI can be mild, moderate, or severe, ranging from mild concussion to deep coma or even death.

With concussion, the injured person may experience a brief or transient loss of consciousness, much like fainting or passing out, or merely an alteration in consciousness described as "seeing stars" or feeling dazed or "out of it." On the other hand, coma refers to a profound or deep state of unconsciousness in which the individual does not respond to the environment in any meaningful way.

When a person with TBI regains consciousness, some symptoms are immediately apparent, while others are not noticed until several days or weeks later. Symptoms which may be obvious right away after mild TBI include headache , changes in vision such as blurred vision or tired eyes, nausea, dizziness , lightheadedness, ringing in the ears, bad taste in the mouth, or altered sense of smell which is usually experienced as loss of the sense of taste.

Approximately 40% of patients with TBI develop postconcussion syndrome within days to weeks, with symptoms including headache, dizziness or a sensation of spinning (vertigo), memory problems, trouble concentrating, sleep disturbances, restlessness, irritability, depression , and anxiety. This syndrome may persist for a few weeks, especially in patients with depression, anxiety, or other psychiatric symptoms before the TBI.

With more severe injuries, there may also be immediate numbness or weakness of one or more limbs, blindness, deafness, inability to speak or understand speech, slurred speech, lethargy with difficulty staying awake, persistent vomiting, loss of coordination, disorientation, or agitation. In addition to some of these symptoms, young children with moderate to severe TBI may also experience prolonged crying and refusal to nurse or eat.

While the injured person is preoccupied with headache or pain related to other physical trauma, symptoms such as difficulty in thinking or concentrating may not be evident. Often these more subtle symptoms may appear only when the individual attempts to return to work or to other mentally challenging situations. Similarly, personality changes, depression, irritability, and other emotional and behavioral problems may initially be attributed to coping with the stress of the injury, and they may not be fully appreciated until the individual is recuperating at home.

Seizures may occur soon after a TBI or may first appear up to a year later, especially when the damage involves the temporal lobes. Other symptoms which may appear immediately or which may be noticed only while the individual is returning to usual activities are confusion, fatigue or lethargy, altered sleep patterns, and trouble with memory, concentration, attention, and finding the right words or understanding speech.

Diagnosis

Recognizing a serious head injury, starting basic first aid, and seeking emergency medical care can help the injured person avoid disability or even death. When encountering a potential TBI, it is helpful to find out what happened from the injured person, from clues at the scene, and from any eyewitnesses. Because spinal cord injury often accompanies serious head trauma, it is prudent to assume that there is also injury to the spinal cord and to avoid moving the person until the paramedics arrive. Spinal cord injury is a challenging diagnosis; nearly one-tenth of spinal cord injuries accompanying TBI are missed initially.

Signs apparent to the observer that suggest serious head injury and mandate emergency treatment include shallow or erratic breathing or pulse; drop in blood pressure; broken bones or other obvious trauma to the skull or face such as bruising, swelling or bleeding; one pupil larger than the other; or clear or bloody fluid drainage from the nose, mouth, or ears.

Symptoms reported by the injured person that should also raise red flags include severe headache, stiff neck, vomiting, paralysis or inability to move one or more limbs, blindness, deafness, or inability to taste or smell. Other ominous developments may include initial improvement followed by worsening symptoms; deepening lethargy or unresponsiveness; personality change, irritability, or unusual behavior; or incoordination.

When emergency personnel arrive, they will stabilize the patient, evaluate the above signs and symptoms, and assess the nature and extent of other injuries, such as broken bones, spinal cord injury, or damage to other organ systems. Medical advances in early detection and treatment of associated injuries have improved the overall out-come in TBI. The initial evaluation measures vital signs such as temperature, blood pressure, pulse, and breathing rate, while the neurological examination assesses reflexes, level of consciousness, ability to move the limbs, and pupil size, symmetry, and response to light.

These neurological features are standardized using the Glasgow Coma Scale, a test scored from 1 to 15 points. Each of three measures (eye opening, best verbal response, and best motor response) is scored separately, and the combined score helps determine the severity of TBI. A total score of 3 to 8 reflects a severe TBI, 9 to 12 a moderate TBI, and 13 to 15 a mild TBI.

Imaging tests reveal the location and extent of brain injury and associated injuries and therefore help determine diagnosis and probable outcome. Sophisticated imaging tests can help differentiate the variety of unconscious states associated with TBI and can help determine their anatomical basis.

Until neck fractures or spinal instability have been ruled out with skull and neck x rays, and with head and neck computed tomography (CT) scan for more severe injuries, the patient should remain immobilized in a neck and back restraint.

By constructing a series of cross-sectional slices, or xray images through the head and brain, the CT scan can diagnose bone fractures, bleeding, hematomas, contusions, swelling of brain tissue, and blockage of the ventricular system circulating cerebrospinal fluid around the brain. In later stages after the initial injury, it may also show shrinkage of brain volume in areas where neurons have died.

Using magnetic fields to detect subtle changes in brain tissue related to differences in water content, the magnetic resonance imaging (MRI) scan shows more detail than x rays or CT. However, it takes more time than the CT and is not as readily available, making it less suited for routine emergency imaging.

For patients with seizures or for those with more subtle episodic symptoms thought possibly to be seizures, the electroencephalogram (EEG) may reveal abnormalities in the electrical activity of the brain or brain waves. Other diagnostic techniques that may be helpful include cerebral angiography , transcranial Doppler ultrasound, and single photon emission computed tomography (SPECT).

Treatment team

The first responder at the scene of TBI is usually a paramedic or emergency medical technician (EMT). In the emergency department, a trauma specialist may determine the extent of associated injuries. The neurologist is usually the primary treating physician assessing and managing the symptoms and consequences of TBI. Diagnostic technicians involved in TBI management include radiological and EEG technicians and audiologists who assess hearing.

If surgery is needed to remove blood clots or to insert a shunt to relieve increased pressure within the skull, a neurosurgeon is needed. After surgery, or for any patient with loss of consciousness, intensive care is managed by a specialized treatment team including neurologists, neurosurgeons, intensivists, respiratory therapists, and specialized nurses and technicians.

After the physical condition has stabilized, a speech therapist and/or neuropsychologist may evaluate swallowing, cognitive, and behavioral abilities and carry out appropriate rehabilitation. Other specialized therapists include the occupational therapist, who addresses sensory deficits, hand movements, and the ability to perform activities of daily living such as dressing; and the physical therapist who directs exercise and other programs to rehabilitate weakness annd loss of coordination. Vocational planners, psychologists, and psychiatrists may help the individual with TBI cope with returning to society and to gainful employment.

Treatment

Although no specific treatment may be needed for a mild head injury, it is crucial to watch the person closely for any developing symptoms over the next 24 hours. Acetaminophen or ibuprofen, available over the counter, may be used for mild headache. However, aspirin should not be given because it can increase the risk of bleeding.

If the person is sleeping, he should be awakened every two to three hours to determine alertness and orientation to name, time, and place. Immediate medical help is needed if the person becomes unusually drowsy or disoriented, develops a severe headache or stiff neck, vomits, loses consciousness, or behaves abnormally.

Treatment for moderate or severe TBI should begin as soon as possible by calling 911 and beginning emergency care until the EMT team arrives. This includes stabilizing the head and neck by placing the hands on both sides of the person's head to keep the head in line with the spine and prevent movement which could worsen spinal cord injury. Bleeding should be controlled by firmly pressing a clean cloth over the wound unless a skull fracture is suspected, in which case it should be covered with sterile gauze dressing without applying pressure. If the person is vomiting, the head, neck, and body should be rolled to the side as one unit to prevent choking without further injuring the spine.

Although the initial brain damage caused by trauma is often irreversible, the goal is to stabilize the patient and prevent further injury. To achieve these goals, the treatment team must insure adequate oxygen supply to the brain and the rest of the body, maintain blood flow to the brain, control blood pressure, stabilize the airway, assist in breathing or perform CPR if necessary, and treat associated injuries.

About half of severely head-injured patients require neurosurgery for hematomas or contusions. Swelling of the injured brain may cause increased pressure within the closed skull cavity, known as increased intracranial pressure (ICP). ICP can be measured with a intraventricular probe or catheter inserted through the skull into the fluid-filled chambers (ventricles) within the brain. Placement of the ICP catheter is usually guided by CT scan. If ICP is elevated, ventriculostomy may be needed. This procedure drains cerebrospinal fluid from the brain and reduces ICP. Drugs that may decrease ICP include mannitol and barbiturates.

A recent review suggests that using intraventricular catheters coated with antibiotics reduces the risk for infection. Keeping the patient's body temperature low (hypothermia) also improves outcome after moderate to severe TBI. Increasing the level of oxygen in the blood beyond normal concentrations is also being explored as a treatment option for improving brain metabolism in TBI. Large, multicenter trials of these and other treatments, such as early surgery to relieve increased ICP, are still needed, and the quest continues for a therapy that could prevent nerve cell death in TBI.

Although some patients need medication for psychiatric and physical problems resulting from the TBI, prescribing drugs may be problematic because TBI patients are more sensitive to side effects.

Both in the immediate and later stages of TBI, rehabilitation is vital to optimal recovery of ability to function at home and in society. The Consensus Development Conference on Rehabilitation of Persons with TBI, held by the National Institutes of Health in 1998, recommended individualized rehabilitation based on specific strengths and abilities.

Problems with orientation, thinking, and communication should be addressed early, often during the hospital stay. The focus is typically on improving alertness, attention, orientation, speech understanding, and swallowing problems.

As the patient improves, rehabilitation should be modified accordingly. The panel suggested that physical therapy, occupational therapy, speech/language therapy, physiatry (physical medicine), psychology/psychiatry, and social support should all play a role in TBI rehabilitation. Appropriate settings for rehabilitation may include the home, the hospital outpatient department, inpatient rehabilitation centers, comprehensive day programs, supportive living programs, independent living centers, and school-based programs. Families should become involved in rehabilitation, in modifying the home environment if needed, and in psychotherapy or counseling as indicated.

Clinical trials

The National Institute of Neurological Disorders and Stroke (NINDS) supports research on the biological mechanisms of brain injury, strategies to limit brain damage following head trauma, and treatments of TBI that may improve long-term recovery. Research areas include mechanisms of diffuse axonal injury; the role of calcium entry into damaged nerves causing cell death and brain swelling; the toxic effects of glutamate and other nerve chemicals causing excessive nerve excitability; natural processes of brain repair after TBI; the therapeutic use of cyclosporin A or hypothermia to decrease cell death and nerve swelling; and the use of stem cells to repair or replace damaged brain tissue.

NINDS-supported clinical research focuses on enhancing the ability of the brain to adapt to deficits after TBI; improving rehabilitation programs for TBI-related disabilities; and developing treatments for use in the first hours after TBI. Early treatments being investigated include hypothermia for severe TBI in children, magnesium sulfate to protect nerve cells after TBI, and lowering ICP and increasing blood flow to the brain.

To address the specific problems in thinking and communication following TBI, the NINDS is designing new evaluation tools for children, developing computer programs to help rehabilitate children with TBI, and determining the effects of various medications on recovery of speech, language, and cognitive abilities.

The NINDS website (www.clinicaltrials.gov/ct/action/GetStudy) lists specific contact information for ongoing trials. These include hypothermia to treat severe brain injury, open to subjects age 16 to 45 years with nonpenetrating brain injury with a post-resuscitation Glasgow Coma Score less than 8 (contact Emmy R. Miller, PhD, RN, 713-500-6145).

The Prospective Memory in Children with Traumatic Brain Injury study is open to children age 12-18 years, with a post-resuscitation Glasgow Coma Scale score of either 13 to 15 or 3 to 8. Contact information is Stephen R. Mc-Cauley, PhD, 713-798-7479, mccauley@bcm.tmc.edu.

The Measuring Head Impacts in Sports study will test a new device to measure the speed of head impact in football players. The study is open to college football players, age 18–24 years. Contact information is Rick Greenwald, PhD, RGreenwald@simbex.com.

A trial sponsored by Avanir Pharmaceuticals will be testing the safety of the drug AVP-923 in the treatment of uncontrolled laughter and crying associated with TBI as well as with other conditions. Study subjects must be age 18–75 years without any history of major psychiatric disturbance. Contact information varies by state and is available on the website; for Arizona it is Louis DiCave, 602-406-6292, ldicave@chw.edu.

Prognosis

Although the symptoms of minor head injuries often resolve on their own, more than 500,000 head injuries each year are severe enough to require hospitalization; 200,000 are fatal; and 200,000 require institutionalization or other close supervision. Each year in the United States, head injury causes one million head-injured people to be treated in hospital emergency rooms, 270,000 to have moderate or severe TBI, 70,000 to die, and 60,000 to develop epilepsy .

Outcome varies with cause: 91% of TBIs caused by firearms, two-thirds of which may represent suicide attempts, are fatal, compared with only 11% of TBIs from falls. Low Glasgow Coma Scale scores predict a worse outcome from TBI than do high scores.

The Swedish Council on Technology Assessment in Health Care concluded that of 1,000 patients arriving at the hospital with mild head injury, one will die, nine will require surgery or other intervention, and about 80 will have abnormal findings on brain CT and will probably need to be hospitalized.

Immediate complications of TBI may include seizures, enlargement of the fluid-filled chambers within the brain (hydrocephalus or post-traumatic ventricular enlargement), leaks of cerebrospinal fluid, infection, injury to blood vessels or to the nerves supplying the head and neck, pain, bed sores, failure of multiple organ systems, and trauma to other areas of the body.

About one-quarter of patients with brain contusions or hematomas and about half of those with penetrating head injuries develop seizures within the first 24 hours of the injury. Those that do are at increased risk of seizures occurring within one week after TBI.

Hydrocephalus usually occurs within the first year of TBI, and it is associated with deteriorating neurological outcome, impaired consciousness, behavioral changes, poor coordination or balance, loss of bowel and bladder control, or signs of increased ICP.

Long-term survivors of TBI may suffer from persistent problems with behavior, thinking, and communication disabilities, as well as epilepsy; loss of sensation, hearing, vision, taste, or smell; ringing in the ears (tinnitus), coordination problems, and/or paralysis. Recovery from cognitive deficits is most dramatic within the first six months after TBI, and less apparent subsequently.

Memory loss is especially common in severely head-injured patients, with loss of some specific memories and partial inability to form or store new memories. Antero-grade post-traumatic amnesia refers to impaired memory of events that occurred after TBI, while retrograde post-traumatic amnesia refers to impaired memory of events that occurred before the TBI.

Personality changes and behavioral problems may include depression, anxiety, irritability, anger, apathy, paranoia, frustration, agitation, mood swings, aggression, impulsive behaviors or "acting out," social inappropriateness, temper tantrums, difficulty accepting responsibility, and alcohol or drug abuse.

Following TBI, patients may be at increased risk of other long-term problems such as Parkinson's disease , Alzheimer's disease , "punch-drunk" syndrome (dementia pugilistica), and post-traumatic dementia.

Because of all the above problems, some patients may have difficulty returning to work following TBI, as well as problems with school, driving, sports, housework, and social relationships.

Special concerns

Unlike most other devastating neurological diseases, TBI can be prevented. Practical measures to decrease risk include wearing seatbelts, using child safety seats, wearing helmets for biking and other sports, safely storing firearms and bullets; using step-stools, grab bars, handrails, window guards, and other safety devices; making playground surfaces from shock-absorbing material; and not drinking and driving.

Because TBI follows trauma, it is often associated with injuries to other parts of the body, which require immediate and specialized care. Complications may include lung or heart dysfunction following blunt chest trauma, limb fractures, gastrointestinal dysfunction, fluid and hormonal imbalances, nerve injuries, deep vein thrombosis, excessive blood clotting, and infections.

Resources

PERIODICALS

Arzaga, D., V. Shaw, and A. T. Vasile. "Dual Diagnoses: The Person with a Spinal Cord Injury and a Concomitant Brain Injury." Spinal Cord Injury Nursing 20, no. 2 (Summer 2003): 86-92.

Bruns, J. Jr, and W. A. Hauser. "The Epidemiology of Traumatic Brain Injury: A Review." Epilepsia 44, Supplement 10 (2003): 2-10.

Chisholm, J., and B. Bruce. "Unintentional Traumatic Brain Injury in Children: The Lived Experience." Axone 23, no. 1 (September 2001): 12-17.

Geijerstam, J. L., and M. Britton. "Mild Head Injury—Mortality and Complication Rate: Meta-analysis of Findings in a Systematic Literature Review." Acta Neurochirugica (Wien) 145, no. 10 (October 2003): 843-50.

Gunnarsson, T., and M. G. Fehlings. "Acute Neurosurgical Management of Traumatic Brain Injury and Spinal Cord Injury." Current Opinion in Neurology 16, no. 6 (December 2003): 717-23.

Krotz, M., U. Linsenmaier, K. G. Kanz, K. J. Pfeifer, W. Mutschler, and M. Reiser. "Evaluation of Minimally Invasive Percutaneous CT-Controlled Ventriculostomy in Patients with Severe Head Trauma." European Radiology (November 6, 2003).

Reitan, R. M., and D. Wolfson. "The Two Faces of Mild Head Injury." Archives of Clinical Neuropsychology 14, no. 2 (February 1999): 191-202.

WEBSITES

National Institute of Neurological Disorders and Stroke. NIH Neurological Institute. <http://www.ninds.nih.gov/health_and_medical/pubs/TBI.htm#research>.

National Institute on Deafness and Other Communication Disorders. National Institutes of Health. <http://www.nidcd.nih.gov/health/voice/tbrain.asp>.

U.S. National Library of Medicine. <http://www.nlm.nih.gov/medlineplus/ency/articl/000028.htm>.

Clinical Trials. <http://www.clinicaltrials.gov/ct/action/GetStudy>.

Laurie Barclay