Traumatic brain injury (TBI) is a major public health problem, especially among male adolescents and young adults ages 15 to 24, and among elderly people of both sexes 75 years and older. Children aged 5 and younger are also at high risk for TBI.
TBI costs the country more than $48 billion a year, and between 2.5 and 6.5 million Americans alive today have had a TBI. Survivors of TBI are often left with significant cognitive, behavioral, and communicative disabilities, and some patients develop long-term medical complications, such as epilepsy.
Other statistics dramatically tell the story of head injury in the United States. Each year:
What is a Traumatic Brain Injury?
TBI, also called acquired brain injury or simply head injury, occurs when a sudden trauma causes damage to the brain. The damage can be focal - confined to one area of the brain - or diffuse - involving more than one area of the brain. TBI can result from a closed head injury* or a penetrating head injury. A closed injury occurs when the head suddenly and violently hits an object but the object does not break through the skull. A penetrating injury occurs when an object pierces the skull and enters brain tissue.
*National Institutes of Health Consensus Development Conference Statement, October 26-28, 1998. Rehabilitation of Persons with Traumatic Brain Injury. Bethesda, MD, September 1999.
Signs and Symptoms
Symptoms of a TBI can be mild, moderate, or severe, depending on the extent of the damage to the brain. Some symptoms are evident immediately, while others do not surface until several days or weeks after the injury. A person with a mild TBI may remain conscious or may experience a loss of consciousness for a few seconds or minutes. The person may also feel dazed or not like himself for several days or weeks after the initial injury. Other symptoms of mild TBI include headache, confusion, lightheadedness, dizziness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, a change in sleep patterns, behavioral or mood changes, and trouble with memory, concentration, attention, or thinking.
A person with a moderate or severe TBI may show these same symptoms, but may also have a headache that gets worse or does not go away, repeated vomiting or nausea, convulsions or seizures, inability to awaken from sleep, dilation of one or both pupils of the eyes, slurred speech, weakness or numbness in the extremities, loss of coordination, and/or increased confusion, restlessness, or agitation. Small children with moderate to severe TBI may show some of these signs as well as signs specific to young children, such as persistent crying, inability to be consoled, and/or refusal to nurse or eat. Anyone with signs of moderate or severe TBI should receive medical attention as soon as possible.
Causes and Risk Factors
Half of all TBIs are due to transportation accidents involving automobiles, motorcycles, bicycles, and pedestrians. These accidents are the major cause of TBI in people under age 75. For those 75 and older, falls cause the majority of TBIs. Approximately 20 percent of TBIs are due to violence, such as firearm assaults and child abuse, and about 3 percent are due to sports injuries. Fully half of TBI incidents involve alcohol use.
The cause of the TBI play a role in determining the patient's outcome. For example, approximately 91 percent of firearm TBIs (two-thirds of which may be suicidal in intent) result in death, while only 11 percent of TBIs from falls result in death.
Types of TBI
Concussion is the most minor and the most common type of TBI. Technically, a concussion is a short loss of consciousness in response to a head injury, but in common language the term has come to mean any minor injury to the head or brain.
Other injuries are more severe. As the first line of defense, the skull is particularly vulnerable to injury. Skull fractures occur when the bone of 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 injury to brain tissue.
Skull fractures can cause bruising of brain tissue called a contusion. A contusion is a distinct area of swollen brain tissue mixed with blood released from broken blood vessels. A contusion can also occur in response to shaking of the brain back and forth within the confines of the skull, an injury called contrecoup. This injury often occurs in car accidents after high-speed stops and in shaken baby syndrome, a severe form of head injury that occurs when a baby is shaken forcibly enough to cause the brain to bounce against the skull. In addition, contrecoup can cause diffuse axonal injury, also called shearing, which involves damage to individual nerve cells ( neurons ) and loss of connections among neurons. This can lead to a breakdown of overall communication among neurons in the brain.
Damage to a major blood vessel in the head can cause a hematoma, or heavy bleeding into or around the brain. Three types of hematomas can cause brain damage. 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 . Bleeding within the brain itself is called intracerebral hematoma . Another insult to the brain that can cause injury is anoxia. Anoxia is a condition in which there is an absence of oxygen supply to an organ's tissues, even if there is adequate blood flow to the tissue.
Hypoxia refers to a decrease in oxygen supply rather than a complete absence of oxygen. Without oxygen, the cells of the brain die within several minutes. This type of injury is often seen in near-drowning victims, in heart attack patients, or in people who suffer significant blood loss from other injuries that decrease blood flow to the brain.
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.
As soon as medical personnel have stabilized the head injured patient, they assess the patient's condition by measuring vital signs and reflexes and by performing a neurological examination. They check the patient's temperature, blood pressure, pulse, breathing rate, and pupil size in response to light. They assess the patient's level of consciousness and neurological functioning using the Glasgow Coma Scale, a standardized, 15-point test that uses three measures - eye opening, best verbal response, and best motor response - to determine the severity of the patient's brain injury.
Glasgow Coma Scale
The eye opening part of the Glasgow Coma Scale has four scores:
The best verbal response part of the test has five scores:
The best motor response test has six scores:
The results of the three tests are added up to determine the patient's overall condition. A total score of 3 to 8 indicates a severe head injury, 9 to 12 indicates a moderate head injury, and 13 to 15 indicates a mild head injury.
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 or spinal instability. The patient should remain immobilized in a neck and back restraint until medical personnel are certain that there is no risk of spinal cord injury. For moderate to severe cases, the gold standard imaging test is a computed tomography (CT) scan. The CT scan creates a series of crosssectional 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) may be used after the initial assessment and treatment of the TBI patient. MRI uses magnetic fields to detect subtle changes in brain tissue content and can show more detail than X-rays or CT. Unfortunately, MRI is not ideal for routine emergency imaging of TBI patients because it is time-consuming and is not available in all hospitals.
Approximately half of severely head-injured patients will need 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.
Sometimes when the brain is injured swelling occurs and fluids accumulate within the brain space. It is normal for bodily injuries to cause swelling and disruptions in fluid balance. But 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 increased pressure is called intracranial pressure (ICP) .
Medical personnel measure patients. 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 the patient's ICP. If a patient has high ICP, he or she may undergo a ventriculostomy , a procedure that drains cerebrospinal fluid (CSF) from the brain to bring the pressure down. Drugs that can be used to decrease ICP include mannitol or barbiturates, although the safety and effectiveness of the latter are unknown.
How Does a TBI Affect Consciousness?
A TBI can cause problems with arousal, consciousness, awareness, alertness, and responsiveness. Generally, there are five abnormal states of consciousness that can result from a TBI: stupor, coma, persistent vegetative 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 coma do not respond to external stimuli, such as pain or light, and do not have sleep-wake cycles. Coma results from widespread and diffuse trauma to the brain, including the cerebral hemispheres of the upper brain and the lower brain or brainstem. Coma generally is of short duration, lasting a few days to a few weeks. After this time, some patients gradually come out of the coma, some progress to a vegetative state, and others die.
Patients in a vegetative state are unconscious and unaware of their surroundings, but they continue to have a sleep-wake cycle and can have periods of alertness. Unlike coma, where the patients eyes are closed, patients in a vegetative state often open their eyes and may move, groan, or show reflex responses. A vegetative state can result from diffuse injury to the cerebral hemispheres of the brain without damage to the lower brain and brainstem. Anoxia, or lack of oxygen to the brain, which is a common complication of cardiac arrest, can also bring about a vegetative state.
Many patients emerge from a vegetative state within a few weeks, but those who do not recover within 30 days are said to be in a persistent vegetative state (PVS). The chances of recovery depend on the extent of injury to the brain and the patient's age, with younger patients having a better chance of recovery than older patients. Generally adults have a 50 percent chance and children a 60 percent chance of recovering consciousness from a PVS within the first 6 months. After a year, the chances that a PVS patient will regain consciousness are very low and most patients who do recover consciousness experience significant disability. The longer a patient is in a PVS, the more severe the resulting disabilities will be. Rehabilitation can contribute to recovery, but many patients never progress to the point of being able to take care of themselves.
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.
Unlike PVS, in which the upper portions of the brain are damaged and the lower portions are spared, locked-in syndrome is caused by damage to specific portions of the lower brain and brainstem with no damage to the upper brain. Most locked-in syndrome patients can communicate through movements and blinking of their eyes, which are not affected by the paralysis. Some patients may have the ability to move certain facial muscles as well. The majority of locked-in syndrome patients do not regain motor control, but several devices are available to help patients communicate.
Post-Injury Complications Sometimes, health complications 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. Although complications are rare, the risk increases with the severity of the trauma. Complications of TBI include immediate seizures, hydrocephalus or post-traumatic ventricular enlargement, CSF leaks, infections, vascular injuries, cranial nerve injuries, pain, bed sores, multiple organ system failure in unconscious patients, and polytrauma (trauma to other parts of the body in addition to the brain).
About 25 percent of patients with brain contusions or hematomas and about 50 percent of patients with penetrating head injuries will develop immediate seizures, seizures that occur within the first 24 hours of the injury. These immediate seizures increase the risk of early seizure - defined as seizures occurring within 1 week after injury - but do not seem to be linked to the development of post-traumatic epilepsy (recurrent seizures occurring more than 1 week after the initial trauma). Generally, medical professionals use anticonvulsant medications to treat seizures in TBI patients only if the seizures persist.
Hydrocephalus or post-traumatic ventricular enlargement occurs when 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 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 air and bacteria into the cavity, possibly 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, below the dura, below the arachnoid (meningitis), or within the space of 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 cause cranial nerve injuries that result in compressive cranial neuropathies. All but three of the 12 cranial nerves project out from the brainstem to the head and face. The seventh cranial nerve, called the facial nerve, is the most commonly injured cranial nerve in TBI and damage to it can result in paralysis of facial muscles.
Pain is a common symptom of TBI and can be a significant complication for conscious patients in the period immediately following a TBI. Headache is the most common form of pain experienced by TBI patients, but other forms of pain can also be problematic. Serious complications for patients who are unconscious, in a coma, or in a vegetative state include bed or pressure sores of the skin, recurrent bladder infections, pneumonia or other life-threatening infections, and progressive multiple organ failure.
What Disabilities Can Result From a 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 (thinking, memory, and reasoning), sensory processing (sight, hearing, touch, taste, and smell), communication (expression and understanding), and behavior or mental health (depression, anxiety, personality changes, aggression, acting out, and social inappropriateness).
Within days to weeks of the head injury approximately 40 percent of TBI patients develop a host of troubling symptoms collectively called post-concussion syndrome (PCS). A patient need not have suffered a concussion or loss of consciousness to develop the syndrome and many patients with mild TBI suffer from PCS. Symptoms include headache, dizziness, vertigo (a sensation of spinning around or of objects spinning around the patient), memory problems, trouble concentrating, sleeping problems, restlessness, irritability, apathy, depression, and anxiety. These symptoms may last for a few weeks after the head injury. The syndrome is more prevalent in patients who had psychiatric symptoms, such as depression or anxiety, before the injury. Treatment for PCS may include medicines for pain and psychiatric conditions, and psychotherapy and occupational therapy to develop coping skills.
Cognition is a term used to describe the processes of thinking, reasoning, problem solving, information processing, and memory. Most patients with severe TBI, if they recover consciousness, suffer from cognitive disabilities, including the loss of many higher level mental skills. The most common cognitive impairment among severely head-injured patients is memory loss, characterized by some loss of specific memories and 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.
Many patients with mild to moderate head injuries who experience cognitive deficits become easily confused or distracted and have problems with concentration and attention. They also have problems with higher level, so-called executive functions, such as planning, organizing, abstract reasoning, problem solving, and making judgments, which may make it difficult to resume pre-injury work-related activities. Recovery from cognitive deficits is greatest within the first 6 months after the injury and more gradual after that.
The most common cognitive impairment among severely head-injured patients is memory loss, characterized by some loss of specific memories and the partial inability to form or store new ones.
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 effect, causing cognitive deficits equal to a moderate or severe injury.
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 be prone to bumping into or dropping objects, or may seem generally unsteady. TBI patients may have difficulty driving a car, working complex machinery, or playing sports. 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. Although rare, these conditions are hard to treat.
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.
In non-fluent aphasia, also called Broca's aphasia or motor aphasia, TBI patients often have trouble recalling words and speaking in complete sentences. They may speak in broken phrases and pause frequently. Most patients are aware of these deficits and may become extremely frustrated. Patients with fluent aphasia, also called Wernicke's aphasia or sensory aphasia, display little meaning in their speech, even though they speak in complete sentences and use correct grammar. Instead, they speak in flowing gibberish, drawing out their sentences with non-essential and invented words. Many patients with fluent aphasia are unaware that they make little sense and become angry with others for not understanding them. Patients with global aphasia have extensive damage to the portions of the brain responsible for language and often suffer severe communication disabilities.
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. An important aspect of speech, inflection conveys emotional meaning and is necessary for certain aspects of language, such as irony.
These language deficits can lead to miscommunication, confusion, and frustration for the patient as well as those interacting with him or her.
Most TBI patients have emotional or behavioral problems that fit under the broad category of psychiatric health. Family members of TBI patients often find that personality changes and behavioral problems are the most difficult disabilities to handle. Psychiatric problems that may surface include depression, apathy, anxiety, irritability, anger, paranoia, confusion, frustration, agitation, insomnia or other sleep problems, and mood swings. Problem behaviors may include aggression and violence, impulsivity, disinhibition, acting out, noncompliance, social inappropriateness, emotional outbursts, childish behavior, impaired self-control, impaired self-awareness, inability to take responsibility or accept criticism, egocentrism, inappropriate sexual activity, and alcohol or drug abuse/addiction. Some patients' personality problems may be so severe that they are diagnosed with borderline personality disorder, a psychiatric condition characterized by many of the problems mentioned above. 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. Attitudes and behaviors that are appropriate for a child or teenager become inappropriate in adulthood. Many TBI patients who show psychiatric or behavioral problems can be helped with medication and psychotherapy.
Are There Other Long-Term Problems Associated With a TBI?
In addition to the immediate post-injury complications discussed on page 13, other long-term problems can develop after a TBI. These include Parkinson's disease and other motor problems, Alzheimer's disease, dementia pugilistica, and post-traumatic dementia.
Alzheimer's disease (AD) - AD is a progressive, neurodegenerative disease characterized by dementia, memory loss, and deteriorating cognitive abilities. Recent 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.)
Parkinson's disease and other motor problems - Movement disorders 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).
Dementia pugilistica - Also called chronic traumatic encephalopathy, dementia pugilistica 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 - 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.
Source: The National Institute of Neurological Disorders and Stroke,
National Institutes of Health,
Bethesda, MD 20892