TBI is a major public health problem, especially among males 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.
Each year in the United States:
approximately 1 million head-injured people are treated in hospital emergency rooms,
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 230,000 people are hospitalized for TBI and survive,
approximately 80,000 of these survivors live with significant disabilities as a result of the injury, and
approximately 70,000 people die from head injury.
Signs and Symptoms of TBI
Some symptoms are evident immediately, while others do not surface until several days or weeks after the 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:
- mental confusion,
- double vision, 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
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,
- inability to awaken,
- dilation (widening) of one or both pupils,
- slurred speech,
- weakness or numbness in the extremities,
- loss of coordination, and/or
increased confusion, restlessness, or agitation
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, and/or
- refusal to nurse or eat.
Causes of and risk factors for TBI
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 % of TBIs are due to violence, such as firearm assaults and child abuse, and about 3 % are due to sports injuries. Fully half of TBI incidents involve alcohol use.
The damage from TBI can be focal, confined to one area of the brain, or diffuse, involving more than one area of the brain. Diffuse trauma to the brain is frequently associated with concussion (a shaking of the brain in response to sudden motion of the head), diffuse 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.
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.
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 traumatic injury to brain tissue. Skull fractures can cause cerebral contusion.
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, and ischemia is inadequate blood supply, as is seen in cases in which the brain swells. In any of these cases, without adequate oxygen, a biochemical cascade called the ischemic cascade is unleashed, and the cells of the brain can die within several minutes. This type of injury is often seen in near-drowning victims, in heart attack patients (particularly those who have suffered a cardiac arrest, or in people who suffer significant blood loss from other injuries that then causes a decrease in blood flow to the brain due to circulatory (hypovolemic) shock.
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. Anoxia, or lack of oxygen to the brain, which is a common complication of cardiac arrest, can also bring about a vegetative state.
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.
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.
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 (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 % of TBI patients develop a host of troubling symptoms collectively called postconcussion 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, 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.
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.
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 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.
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.
TBI patients have been described as the "walking wounded"owing to psychological problems. 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 organic 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, although the effectiveness of psychotherapy may be limited by the residual neurocognitive impairment. Technological improvements and excellent 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 than by their residual physical disabilities.
Other Long-Term Problems Associated With TBI
Other long-term problems that can develop after a TBI 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.
A Window of hope after Research/Studies
- A 23 year old woman in a vegetative state was able to communicate with a team of British researchers at Cambridge University in England led by Neurologist Adrian Owen via functional magnetic resonance imaging (FMRI)(scan). Some researchers were cautious but note that the research was groundbreaking. "It's the first time we've ever seen something like this. It really is kind of shocking," said Nicholas Schiff, a neurologist at the Weill Cornell Medical College in New York.
- Brain injury patient While Wallis showed few outward signs of consciousness, his brain was methodically rebuilding the white-matter infrastructure necessary for him to interact with the outside world, researchers reported Monday in the Journal of Clinical Investigation.Using PET scans and an advanced imaging technique called diffusion tensor imaging, the researchers examined Wallis' brain after he regained full consciousness and found that cells in the relatively undamaged areas had formed new axons, the long nerve fibers that transmit messages between neurons.
Label for the figure on the top left side: Coronal MRI, brain (level: insert line D): AH-ant horn, BC-body caudate n, CC-corpus cal, CT-corticospinal tr, F-fornix, IH-inf horn, INC-int capsule, IR-intercerb v, L1-putamen, L2-ext seg gl pall, L3-int seg gl pall, MCA-mid cereb a, P-pons, SCA-sup cer a, SN-subst n, T-thalamus, TT-tent cereb.