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Keywords
Brain Anoxia «» Brain Hypoxia «» Concussion «» Contusion «» Depressed Skull Fractures «» Diffuse Axonal Injury «» Epidural Hematoma «» Intracerebral/Intraparenchymal Hematoma «» Penetrating Skull Fractures «» Shaken Baby Syndrome «» Skull Fractures «» Subarachnoid Hemorrhage «» Subdural Hematoma
What is traumatic brain injury?
Who is at risk?
What conditions are associated with traumatic brain injury?
What are the symptoms of traumatic brain injury?
How is traumatic brain injury diagnosed?
How is traumatic brain injury treated?
What are the consequences of traumatic brain injury?
What is traumatic brain injury?
Traumatic brain injury (TBI), also called acquired brain injury or 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 or a penetrating head injury. The former occurs when the head suddenly and violently hits an object but the object does not break through the skull, while the latter occurs when an object pierces the skull and enters brain tissue.
TBI is a major public health problem, especially among male adolescents and young adults, and among elderly people of both sexes. TBI costs the country more than $56 billion a year, and more than 5 million Americans alive today have had a TBI resulting in a permanent need for help in performing daily activities. Survivors of TBI are often left with significant cognitive, behavioral, and communicative disabilities, and some patients develop long-term medical complications, such as epilepsy. Each year in the United States approximately 1.4 million people experience a TBI, 3.6% of whom die from their head injury; about 1 million head-injured people are treated in hospital emergency rooms; and nearly 230,000 people are hospitalized for TBI and survive.
Half of all TBIs are due to accidents involving automobiles, motorcycles, bicycles, and pedestrians -- which are the major cause of TBI in people under age 75. For those 75 years of age 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 cause of the TBI plays a role in determining the patient's outcome. For example, approximately 91% of firearm TBIs (two-thirds of which may be suicidal in intent) result in death, while only 11% of TBIs from falls result in death.
What conditions are associated with traumatic brain injury?
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.
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, which involves damage to long processes (axons) that facilitate communication among the nerve cells; therefore causing loss of connections among them. 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, which is the covering around the brain. With a subdural hematoma, bleeding is confined to the area between the dura and the arachnoid membrane, which is a thin membrane between the dura and the brain. Bleeding between the arachnoid membrane and the brain is called subarachnoid hemorrhage, and hemorrhage within the brain itself is called intracerebral or intraparenchymal 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, 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, heart attack patients, or in people who suffer significant blood loss from other injuries that decrease blood flow to the brain.
What are the symptoms of traumatic brain injury?
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 for several days or weeks after the initial injury. Other symptoms of mild TBI include headache, confusion, lightheadedness, dizziness, blurred vision, 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, 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.
Severe TBI generally leads to loss of consciousness and inability to be aroused easily. Other symptoms may be present but are difficult to elicit since the patient is not conscious. A physician, through a neurologic examination, may be able to identify some signs of severe TBI, usually in the emergency room, which can help in the diagnosis and treatment of the patient.
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.
How is traumatic brain injury diagnosed?
The initial goal of healthcare professionals in the setting of traumatic injury is to stabilize the patient, which is a set of algorithms that are followed as quickly and as efficiently as possible, sometimes prior to even making a specific diagnosis of brain injury -- this is discussed in the next section.
As soon as medical personnel have stabilized the head-injured patient, they assess the patient's condition by measuring vital signs and 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 (GCS). This is a standardized 15-point test that uses three measures (eye opening, best verbal response, and best motor response) in order to determine the severity of the patient's brain injury. The eye opening part of the GCS has four scores: 4 indicates that the patient can open his/her eyes spontaneously, 3 is given if the patient can open his/her eyes on verbal command, 2 indicates that the patient opens his/her eyes only in response to painful stimuli, and 1 is given if the patient does not open his/her eyes in response to any stimulus. The best verbal response part of the test has five scores: 5 is given if the patient is oriented and can speak coherently, 4 indicates that the patient is disoriented but can speak coherently, 3 means the patient uses inappropriate words or incoherent language, 2 is given if the patient makes incomprehensible sounds, and 1 indicates that the patient gives no verbal response at all. The best motor response test has six scores: 6 means the patient can move his/her arms and legs in response to verbal commands, a score between 5 and 2 is given if the patient shows certain specific types of extremity movements in response to painful stimuli, and 1 indicates that the patient shows no movement in response to painful stimuli.
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 also 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 cross-sectional x-ray images of the skull, brain, and the spine; and can show bone fractures as well as the presence of hemorrhage, contusions, and brain tissue swelling.
Magnetic resonance imaging (MRI) may also 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 readily available in all hospitals.
How is traumatic brain injury treated?
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 to the brain and the rest of the body, maintaining adequate blood flow, and controlling blood pressure. Emergency medical personnel may have to open the patient's airway or perform other procedures to make sure the patient is breathing. They may also perform cardiopulmonary resuscitation (CPR) to help the heart pump blood to the body, and they may treat other injuries to control or stop bleeding. Because many head-injured patients may also have spinal cord injuries, medical professionals take great care in moving and transporting the patient. Ideally, the patient is placed on a back-board and in a neck restraint. These devices immobilize the patient and prevent further injury to the head and spinal cord. Following this initial stabilization phase, the diagnostic measures, mentioned in the previous section, are conducted.
Approximately half of severely head-injured patients will need surgery to remove or repair hematomas or contusions of the brain, in addition to surgery for treatment of injuries to other parts of the body.
Sometimes after head injury, excess fluids accumulate within the brain and swelling occurs. But since there is no place for the skull-encased brain to expand and no adjoining tissues to absorb excess fluid, elevated pressures can build up inside of the brain, a phenomenon called elevated intracranial pressure (ICP) or intracranial hypertension. In such cases a probe or catheter is surgically inserted through the skull and into the brain; and connected to a monitor that registers the patient's ICP. This instrument is termed an ICP monitor or ventriculostomy drain (the latter also known as external ventricular drain -- EVD), depending on the specific type of probe/catheter that is used. If a patient has high ICP, he/she may require various measures that decrease the elevated pressures which include drainage of cerebrospinal fluid (CSF) from the brain (using EVD), administration of mannitol or barbiturates, management of the patient's ventilatory status to decrease the amount of carbon dioxide within the blood stream (which triggers a reflex mechanism that brains ICP down), or surgery to remove dead brain tissue or to remove the skull in order to provide more room for the brain and decrease ICP. If the skull needs to be removed due to uncontrollably high ICP, it is generally kept in a sterile location or implanted under the skin in the patient's abdominal wall, so that it can be replaced at a later date when the patient has recovered from their brain injury and the brain swelling has subsided.
Rehabilitation is an important 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. Once stable, the patient may be transferred to a subacute unit of the medical center or to an independent rehabilitation hospital. At this point, patients follow many diverse paths toward recovery because there are a wide variety of options for rehabilitation. TBI patients receive an individualized rehabilitation program based upon the patient's strengths and capacities and services are modified over time to adapt to the patient's changing needs.
Moderately to severely injured patients receive rehabilitation treatment that draws on the skills of many specialists which involves individually-tailored treatment programs in the areas of physical therapy, occupational therapy, speech/language therapy, physiatry (physical medicine), psychology/psychiatry, and social support. Medical personnel who provide this care include rehabilitation nurses, psychologists, speech/language pathologists, physical and occupational therapists, physiatrists (physical medicine specialists), social workers, and a team coordinator or administrator.
The overall goal of rehabilitation after a TBI is to improve the patient's ability to function at home and in society. Therapists help the patient adapt to disabilities or change the patient's living space, called environmental modification, to make everyday activities easier.
Some patients may need medication for psychiatric and physical problems resulting from the TBI. 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. It is important for the family to provide social support for the patient by being involved in the rehabilitation program. Family members may also benefit from psychotherapy.
It is important for TBI patients and their families to select the most appropriate setting for rehabilitation. There are several options, including home-based rehabilitation, hospital outpatient rehabilitation, inpatient rehabilitation centers, comprehensive day programs at rehabilitation centers, supportive living programs, independent living centers, club-house programs, school-based programs for children, and others. The TBI patient, the family, and the rehabilitation team members should work together to find the best place for the patient to recover.
Other treatments that may be rendered to the TBI patient involve the specific consequences or complication that may arise as a result of the injury and are discussed in the next section.
What are the consequences of traumatic brain injury?
Traumatic brain injury can lead to short-term and long-term consequences. Sometimes distinct health complications occur in the period immediately following a TBI as a result of the injury. Although such complications tend to be relatively rare, the risk increases with the severity of the trauma. These include immediate seizures, hydrocephalus, cerebrospinal fluid (CSF) leaks, infections, vascular injuries, cranial nerve injuries, pain, bed sores, and multiple organ system failure in unconscious patients.
About 25 percent of patients with brain contusions or hematomas and about 50 percent of patients with penetrating head injuries will develop seizures that occur within the first 24 hours of the injury. 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, which are recurrent seizures occurring more than 1 week after the initial trauma. Generally, medical professionals use anticonvulsant medications to prevent seizures in TBI patients in the initial phase and only continue these medication over the long term if the seizures persist.
Hydrocephalus 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, lack of coordination or balance, and incontinence. The condition may develop as a result of meningitis, subarachnoid hemorrhage, intracranial hematoma, or other injuries suffered as a result of the trauma. Treatment includes short term drainage of the CSF using EVD or permanent shunting of CSF if the condition persists, as well as 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 (outermost covering of the brain) and the arachnoid membrane (the covering layer immediately beneath the dura) can cause CSF to leak out of the subarachnoid space into the subdural space, which is called a subdural hygroma. CSF can also leak from the nose and the ear if fractures in the skull lead to communication from these cavities to the inside of the skull.
Tears in the dura that let CSF out of the brain cavity can also allow bacteria to travel into the brain, possibly causing infections within the intracranial cavity, such as meningitis or an abscess. These are dangerous complications of TBI and usually develop within a few days to weeks of the initial trauma. 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.
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, such as stroke. This can be either through bleeding from the artery (hemorrhagic stroke) or through the formation of a blood clot at the site of injury which blocks 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 semi-consciousness developing within several days of a head injury may be an indication that a stroke is occurring. Ischemic strokes are generally treated with anticoagulants, while surgery is the preferred treatment for certain hemorrhagic stroke. Other types of vascular injuries include vasospasm and the formation of aneurysms, which are further explained in Cerebral Aneurysms.
Skull fractures at the base of the skull can cause injury to cranial nerves (nerves that exit the brain and travel through holes in the skull to the head and face). The seventh cranial nerve, called the facial nerve, is the most commonly injured 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 injury. Headache is the most common form of pain experienced by TBI patients, but other forms of pain can also be problematic.
Most TBI patients have injuries to other parts of the body in addition to the head and brain. Physicians call this polytrauma. These injuries require immediate and specialized care and can complicate treatment of and recovery from the TBI. Other medical complications that may accompany a TBI include pulmonary (lung) dysfunction; cardiovascular (heart) dysfunction from blunt chest trauma; gastrointestinal dysfunction; fluid and hormonal imbalances; and other isolated complications, such as fractures, nerve injuries, deep vein thrombosis, excessive blood clotting, and infections.
Trauma victims often develop hypermetabolism or an increased metabolic rate, which leads to an increase in the amount of heat that 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.
Complications related to pulmonary dysfunction can include neurogenic pulmonary edema (excess fluid in lung tissue), aspiration pneumonia (pneumonia caused by foreign matter in the lungs), and fat and blood clots in the blood vessels of the lungs.
Fluid and hormonal imbalances can complicate the treatment of hypermetabolism and high 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.
Blunt trauma to the chest can also cause cardiovascular problems, including damage to blood vessels and internal bleeding, and problems with heart rate and blood flow. Blunt trauma to the abdomen can cause damage to or dysfunction of the stomach, large or small intestines, and pancreas. A serious and common complication of TBI is erosive gastritis, or inflammation and degeneration of stomach tissue. This syndrome can cause bacterial growth in the stomach, increasing the risk of aspiration pneumonia. Standard care of TBI patients includes administration of prophylactic gastric acid inhibitors to prevent the buildup of stomach acids and bacteria.
A TBI can also 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 completely 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% chance and children a 60% 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.
With the development over the last half-century of assistive devices that can artificially maintain blood flow and breathing, the term brain death has come into use. 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.
Advances in imaging and other technologies have led to devices that help differentiate among the variety of unconscious states. For example, an imaging test that shows activity in the brainstem but little or no activity in the upper brain would lead a physician to a diagnosis of vegetative state and exclude diagnoses of brain death and locked-in syndrome. On the other hand, an imaging test that shows activity in the upper brain with little activity in the brainstem would confirm a diagnosis of locked-in syndrome, while invalidating a diagnosis of brain death or vegetative state. 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).
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, and social inappropriateness).
Within days to weeks of the head injury approximately 40% 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. 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 before the injury, such as depression or anxiety. Treatment for PCS may include medicines for pain and psychiatric conditions, as well as 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. 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 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, such 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. Inflection is an important aspect of speech which 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, non-compliance, 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. 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.
In addition to the immediate post-injury complications, 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) 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.
Parkinson's disease (PD) and other movement disorders as a result of TBI are rare but can occur. PD may develop years after TBI as a result of damage to the basal ganglia, which a portion of the brain that helps to control movement. Symptoms of PD 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, PD remains 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 (DP), also called chronic traumatic encephalopathy, primarily affects career boxers. The most common symptoms of the condition are dementia and Parkinson's disease-type symptoms caused by repetitive blows to the head over a long period of time. Symptoms begin anywhere between 6 and 40 years after the start of a boxing career, with an average onset of about 16 years. Post-traumatic dementia is a condition that share many similarities with DP, except that the former is also characterized by long-term memory problems and is caused by a single, severe TBI that results in a coma.
