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Traumatic brain injury



Traumatic brain injury
Classification & external resources
ICD-10 S06.
ICD-9 800.0-801.9, 803.0-804.9, 850.0-854.1
MeSH D001930
Neuropsychology


Topics

Brain-computer interfacesBrain damage
Brain regions • Clinical neuropsychology
Cognitive neuroscience • Human brain
Neuroanatomy • Neurophysiology
Phrenology • Common misconceptions

Brain functions

arousal • attention
consciousness • decision making
executive functions • language
learning • memory
motor coordination • perception
planning • problem solving
thought

People

Arthur L. Benton• David Bohm
António DamásioKenneth Heilman
Phineas Gage • Norman Geschwind
Elkhonon Goldberg • Donald Hebb
Alexander Luria • Muriel D. Lezak •
Brenda MilnerKarl Pribram
Oliver SacksRoger Sperry• H.M.

Tests

Bender-Gestalt Test
Benton Visual Retention Test
Clinical Dementia Rating
Continuous Performance Task
Glasgow Coma Scale
Hayling and Brixton tests
Lexical decision task
Mini-mental state examination
Stroop effect
Wechsler Adult Intelligence Scale
Wisconsin card sorting task

Mind and Brain Portal
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Traumatic brain injury (TBI), traumatic injuries to the brain, also called intracranial injury, or simply head injury, occurs when a sudden trauma causes brain damage. TBI can result from a closed head injury or a penetrating head injury and is one of two subsets of acquired brain injury (ABI). The other subset is non-traumatic brain injury (e.g. stroke, meningitis, anoxia). Parts of the brain that can be damaged include the cerebral hemispheres, cerebellum, and brain stem. TBI can cause a host of physical, cognitive, emotional, and social effects.

Symptoms of a TBI can be mild, moderate, or severe, depending on the extent of the damage to the brain. Outcome can be anything from complete recovery to permanent disability or death.

Additional recommended knowledge

Contents

Epidemiology

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.[1] Children aged 5 and younger are also at high risk for TBI.[1] Males account for two thirds of childhood and adolescent head trauma patients.[2]

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 50,000 people die from head injury,[1]
  • approximately 230,000 people are hospitalized for TBI and survive,[1]
  • and approximately 80,000 of these survivors live with significant disabilities as a result of the injury.

Signs and symptoms

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:

  • headache
  • mental confusion
  • lightheadedness
  • dizziness
  • 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
  • trouble with memory, concentration, or calculation
  • 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
  • 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

Anyone with signs of moderate or severe TBI should receive immediate emergency medical attention.

Causes and risk factors

Half of all TBIs are due to transportation accidents involving automobiles, motorcycles, bicycles, and pedestrians.[1] These accidents are the major cause of TBI in people under age 75.[1]

For those aged 75 and older, falls cause the majority of TBIs.[1]

Approximately 20% of TBIs are due to violence, such as firearm assaults and child abuse, and about 3% are due to sports injuries.[1] Fully half of TBI incidents involve alcohol use.[1]

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 Iraq (see: Iraq war's signature wound: Brain injury).

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.[3]

Types

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.

A patient 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.

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 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.

Inadequate oxygen or blood flow to the brain can also cause brain injury; however these types of injury are not considered TBI because they do not involve external mechanical force. 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.

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.[4] In addition, rather than improving after being hospitalized, some 40% of TBI patients deteriorate.[5] Primary 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[6] and contribute a large amount to morbidity and mortality from TBI.[7]

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. 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.

Recent 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.[8] 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.[9]

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.[1] Complications of TBI include immediate seizures, hydrocephalus or post-traumatic ventricular enlargement, cerebrospinal fluid 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).[1]

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.[1] The condition may develop as a result of meningitis, subarachnoid hemorrhage, intracranial hematoma, or other injuries.[1] 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.[1] 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.[1] Pneumocephalus occurs when air enters the intracranial cavity and becomes trapped in the subarachnoid space.[1]

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).[1] Most of these injuries develop within a few weeks of the initial trauma and result from skull fractures or penetrating injuries.[1] Standard treatment involves antibiotics and sometimes surgery to remove the infected tissue.[1] Meningitis may be especially dangerous, with the potential to spread to the rest of the brain and nervous system.

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's immune system 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.[1] Thrombotic-ischemic strokes are treated with anticoagulants, while surgery is the preferred treatment for hemorrhagic stroke.[1] Other types of vascular injuries include vasospasm and the formation of aneurysms.

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.[1]

Pain, especially headache, is commonly a significant complication for conscious patients in the period immediately following a TBI. 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.[1]

When a person sustains a head injury, other body parts are frequently injured as well.

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.[1]

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).[1]

Postconcussion syndrome

Within days to weeks of the head injury approximately 40% of TBI patients develop a host of troubling symptoms collectively called postconcussion syndrome (PCS).[1] 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.[1] Symptoms include headache, dizziness, memory problems, trouble concentrating, sleeping problems, restlessness, irritability, apathy, depression, and anxiety.[1] 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.[1] Treatment for PCS may include medicines for pain and psychiatric conditions, and psychotherapy and occupational therapy.

Cognitive problems

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.[1]

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.[1]

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.

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.[1] 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.[1] (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.[1]

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.[1]

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 problems

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 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 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.

Physical problems

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).[1]

About 25% of patients with brain contusions or hematomas and about 50% of patients with penetrating head injuries will develop immediate seizures, seizures that occur within the first 24 hours of the injury.[1] These immediate seizures increase the risk of early seizures - 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).[1] Generally, medical professionals use anticonvulsant medications to treat seizures in TBI patients only if the seizures persist.[1]

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.

Medical personnel 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 and response to light. 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) 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. The use of CT and MRI is standard in TBI treatment, 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).

Approximately half of severely head-injured patients will need surgery to remove or repair hematomas or contusions.[1] 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 leads to increased pressure is 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, causing 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 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 ventricles to bring the pressure down by way of an external ventricular drain (EVD).

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[10][11][12] may have been falsified[13].

Decompressive craniectomy is a last-resort surgical procedure in which part of the skull is removed in an attempt to reduce severely high ICP.[14]

Rehabilitation

Rehabilitation is an important and critical part of the recovery process for a TBI patient. During the acute stage, 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 or 'free-standing' rehabilitation hospital. Patients are best managed on an inpatient treatment unit that has a specialty focus in Brain Injury Rehabilitation. Rehabilitation programs may be reviewed and accredited for this type of specialty care by the Commission on Accreditation of Rehabilitation Facilities.

Decisions regarding when and where an individual should be treated at a particular point during the recovery process are complex and depend on many different factors including the level to which the person can be engaged actively and can participate to some degree in the rehabilitation process. Moderately to severely injured patients may receive specialized rehabilitation treatment that draws on the skills and knowledge of many specialists, involving treatment programs in the areas of physical therapy, occupational therapy, speech/language therapy, physiatry (medical specialist in physical medicine and rehabilitation), psychology, psychiatry, and social work, among others. The services and efforts of this team of healthcare professionals are generally applied to the practical concerns of and the pragmatic problems encountered by the brain injury survivor in their daily life. This treatment program is generally provided through a coordinated and self-organized process in the context of a transdisciplinary model of team healthcare delivery. This model keeps the primary focus on the overarching goal of optimizing patient function and independence through the coordinated application of discipline-specific expertise brought to bear on this issue by individual experts from various specific disciplinary backgrounds.

The overall goal of rehabilitation after a TBI is to improve the patient's ability to function at home and in society in the face of the residual effects of the injury, which may be complex and multifaceted (see Disabilities resulting from TBI section above). Therapists help the patient adapt to disabilities or change the patient's living space and conditions to make everyday activities easier and to accommodate residual impairments. Education and training for identified caregivers who will be involved in assisting the patient after discharge are also critically important components of the rehabilitation program.

Once the patient has been discharged 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 assessing and treating broader psychosocial issues associated with long-term adjustment and community re-integration. Patients/clients will often have problems in the areas of general cognition, social cognition/awareness, behavior and emotional regulation that present significant challenges, in terms of being able to resume expected social roles. Often these problems are complicated by adjustment issues that emerge as the person becomes more aware of their residual deficits and faces the challenges of coming to terms with the long-term effects of the injury. Other concerns such as posttraumatic stress disorder associated with preserved remembrance of emotionally provocative circumstances of injury, may emerge and complicate the recovery process.

An additional goal of the rehabilitation program is to prevent, wherever possible, but otherwise to diagnose and treat in an efficient and effective manner, any complications (e.g. posttraumatic hydrocephalus, neuro-endocrine deficiencies, adjustment reactions, deep venous thromboembolism, etc.) that may cause additional morbidity and mortality.

Some patients may need medication for psychiatric and physical problems resulting from the TBI, and various medications are available that may lessen or moderate the problematic manifestations of the injury without directly altering the underlying pathology. Great care must be taken in prescribing medications because 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 effects.

It is important for the family caregivers to provide assistance and encouragement for the patient by being involved in the rehabilitation program. Family members may also benefit from psychotherapy and social support services. Support for caregivers becomes particularly important during the outpatient phase of care when behavioral and cognitive problems may complicate and impair the relationships that patients have with those around them. Major challenges occur in sustaining these relationships, particularly in the context of marriage, when the impact of the injury significantly alters the relationship in such a way that the resumption of an adult-level interactive relationship may be deeply undermined.

It should be noted that similar principles of rehabilitation for diffuse brain injury can be applied to individuals with brain injury of both traumatic and nontraumatic etiologies. Acquired Brain Injury (ABI) is an all-encompassing term that can be applied to the various etiologies producing global encephalopathies with diffuse and/or multi-focal brain dysfunction that is precipitated during life in a previously fully functional individual. The etiologic processes associated with ABI can be subdivided into those related to trauma and those not directly related to trauma. TBI can therefore be viewed as a particular instance of ABI caused by trauma, and the principles of rehabilitation referred to here for TBI can be readily adapted and applied to individuals with all forms of ABI, independent of specific etiology.

Caretakers of traumatically brain injured patients can often feel a great deal of emotional stress, which can reduce the quality of care. Respite care such as supported living and residential holidays, supported days out doing activities like walking, cycling, kayaking and climbing offers relief for them and a new area of brain stimulation for the patient. When dealing with caretakers, providers of respite care need to be sensitive and reassuring, and should be aware that some caretakers may have feelings of guilt or inadequacy.

Prevention

Unlike most neurological disorders, head injuries can be prevented. The Centers for Disease Control and Prevention (CDC) have suggested taking the following safety precautions for reducing the risk of suffering a TBI.[15]

  • Wearing a seatbelt when driving or riding in a car.
  • 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.
  • Keeping firearms and bullets stored in a locked cabinet when not in use.
  • 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., hardwood mulch, sand).

Famous persons with TBI

  • Muhammad Ali
  • James Brady
  • Phineas Gage
  • Chris Irwin
  • Ahad Israfil
  • Eric Lindros
  • Kurt Vonnegut
  • Bob Woodruff
  • Chris Nowinski

References

  1. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an Traumatic Brain Injury: Hope Through Research. NINDS. Publication date February 2002. NIH Publication No. 02-2478. Prepared by: Office of Communications and Public Liaison, National Institute of Neurological Disorders and Stroke, National Institutes of Health
  2. ^ Necajauskaite, O; Endziniene M, Jureniene K (2005). "The prevalence, course and clinical features of post-concussion syndrome in children". Medicina (Kaunas) 41 (6): 457-464. PMID 15998982. Retrieved on 2007-01-25.
  3. ^ Tolias C and Sgouros S (February 4, 2005). Initial Evaluation and Management of CNS Injury. eMedicine.com. Retrieved on 2007-12-16.
  4. ^ Sauaia A, Moore FA, Moore EE, Moser KS, Brennan R, Read RA, and Pons PT. 1995. Epidemiology of trauma deaths: a reassessment. Journal of Trauma, Volume 38, Issue 2, Pages 185-193. PMID 7869433
  5. ^ Narayan RK, Michel ME, Ansell B, Baethmann A, Biegon A, Bracken MB, Bullock MR, Choi SC, Clifton GL, Contant CF, Coplin WM, Dietrich WD, Ghajar J, Grady SM, Grossman RG, Hall ED, Heetderks W, Hovda DA, Jallo J, Katz RL, Knoller N, Kochanek PM, Maas AI, Majde J, Marion DW, Marmarou A, Marshall LF, McIntosh TK, Miller E, Mohberg N, Muizelaar JP, Pitts LH, Quinn P, Riesenfeld G, Robertson CS, Strauss KI, Teasdale G, Temkin N, Tuma R, Wade C, Walker MD, Weinrich M, Whyte J, Wilberger J, Young AB, Yurkewicz L. 2002. Clinical trials in head injury. Journal of Neurotrauma, Volume 19, Issue 5, Pages 503-557. PMID 12042091
  6. ^ Xiong Y, Lee CP, and Peterson PL. 2001. Mitochondrial dysfunction following traumatic brain injury. In Head Trauma: Basic, Preclinical, and Clinical Directions. Miller LP and Hayes RL, eds. Co-edited by Newcomb JK. 2001, John Wiley and Sons, Inc. New York. Pages 257-280.
  7. ^ Sullivan PG, Rabchevsky AG, Hicks RR, Gibson TR, Fletcher-Turner A, and Scheff SW. 2000. Dose-response curve and optimal dosing regimen of cyclosporin A after traumatic brain injury in rats. Neuroscience, Volume 101, Issue 2, Pages 289-295. PMID 11074152
  8. ^ Vegetative patient 'communicates': A patient in a vegetative state can communicate just through using her thoughts, according to research.. BBC News (September 7, 2006). Retrieved on 2007-09-26.
  9. ^ Stein R (September 8, 2006). Vegetative patient's brain active in test: Unprecedented experiment shows response to instructions to imagine playing tennis. San Francisco Chronicle. Retrieved on 2007-09-26.
  10. ^ Cruz J, Minoja G, Okuchi K. (2001) Improving clinical outcomes from acute subdural hematomas with the emergency preoperative administration of high doses of mannitol: a randomized trial. Neurosurgery. Volume 49, Issue 4, Pages 864-871. PMID 11564247
  11. ^ Cruz J, Minoja G, Okuchi K. (2002) Major clinical and physiological benefits of early high doses of mannitol for intraparenchymal temporal lobe hemorrhages with abnormal pupillary widening: a randomized trial. Neurosurgery. Volume 51, Issue 3, Pages 628-637; discussion 637-638. PMID 12188940
  12. ^ Cruz J, Minoja G, Okuchi K, Facco E. (2004) Successful use of the new high-dose mannitol treatment in patients with Glasgow Coma Scale scores of 3 and bilateral abnormal pupillary widening: a randomized trial. Journal of Neurosurgery. Volume 100, Issue 3, Pages 376-383. PMID 15035271
  13. ^ Roberts I, Smith R, Evans S. (2007) Doubts over head injury studies. BMJ. Volume 334, Issue 7590, Pages 392-394. PMID 17322250
  14. ^ Aarabi B, Hesdorffer DC, Ahn ES, Aresco C, Scalea TM, and Eisenberg HM. (2006) Outcome following decompressive craniectomy for malignant swelling due to severe head injury. Journal of Neurosurgery. Volume 104, Issue 4, Pages 469-479. PMID 16619648. Retrieved on [2007-01-21]]
  15. ^ CDC, Department of Health and Human Services.

See also

 
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Traumatic_brain_injury". A list of authors is available in Wikipedia.
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