COURSE PRICE: $6.00
CONTACT HOURS: 1
This course will expire or be updated on or before December 2, 2013.
ABOUT THIS COURSE
You must score 70% or better on the test and complete the course evaluation to earn a certificate of completion for this CE activity.
ACCREDITATION / APPROVAL
Wild Iris Medical Education is an approved provider for paramedic and EMT continuing education in California by the Coastal Valleys EMS Agency: CE Provider #49-0057.
This course is appropriate for EMTs, paramedics, and first responders.
Wild Iris Medical Education, Inc. provides educational activities that are free from bias. The information provided in this course is to be used for educational purposes only. It is not intended as a substitute for professional health care. See our disclosures for more information.
Copyright © 2010 Wild Iris Medical Education, Inc. All Rights Reserved.
Unless otherwise noted, the material in this course based on the report "Traumatic Brain Injury: Hope Through Research," by the National Institutes of Health, National Institutes of Neurological Disorders and Stroke. The entire text is available at http://www.ninds.nih.gov/disorders/tbi/detail_tbi.htm.
COURSE OBJECTIVE: The purpose of this course is to give healthcare providers information about the symptoms, treatment, disabilities, rehabilitation, and prevention of traumatic brain injury.
Upon completion of this course, you will be able to:
Traumatic brain injury (TBI) is a major public health problem, especially among male adolescents and young adults ages 15 to 24, and among older adults of both sexes 75 years and older. Children aged 5 and younger are also at high risk for TBI.
Perhaps the most famous TBI patient in the history of medicine was Phineas Gage. In 1848, Gage was a 25-year-old railway construction foreman working on the Rutland and Burlington Railroad in Vermont. Gage was working with explosive powder and a tamping iron when a spark caused an explosion that propelled the three-foot-long, pointed rod through his head. It penetrated his skull at the top of his head, passed through his brain, and exited the skull by his temple. Amazingly, he survived the accident with the help of physician John Harlow, who treated Gage for 73 days. Before the accident Gage was a quiet, mild-mannered man; after his injuries he became obscene, obstinate, and self-absorbed. He continued to suffer personality and behavioral problems until his death in 1861.
This computer-generated graphic shows how in 1848 a three-foot-long, pointed rod penetrated the skull of Phineas Gage, a railway construction foreman. Gage survived the accident but suffered lasting personality and behavioral problems. (Source: National Institute of Neurological Disorders and Stroke.)
In the nineteenth century, little was understood about the brain and even less was known about how to treat brain injury. Most serious injuries to the brain resulted in death due to bleeding or infection. Today, we understand a great deal more about the healthy brain and its response to trauma, although science still has much to learn about how to reverse damage resulting from head injuries.
Traumatic brain injury costs the country more than $56 billion a year, and more than 5 million Americans alive today have had a TBI that resulted 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.
Other statistics dramatically tell the story of head injury in the United States. Each year approximately:
Traumatic brain injury (also called acquired brain injury or simply head injury) occurs when a sudden trauma causes damage to the brain. The damage can be focal (confined to one area of the brain) or diffuse (involving more than one area of the brain). Traumatic brain injury 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.
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 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.
Civilians and military personnel in combat zones are also at increased risk for TBIs. The leading causes of such TBI are bullets, fragments, and blasts; falls; motor vehicle-traffic crashes; and assaults. Blasts are a leading cause of TBI for active-duty military personnel in war zones (DVBIC, 2010).
Concussion is the most minor and the most common type of TBI. Technically, a concussion is a short loss of consciousness in response to a head injury, but in common language the term has come to mean any minor injury to the head or brain.
Other injuries are more severe. As the first line of defense, the skull is particularly vulnerable to injury. Skull fractures occur when the bone of the skull cracks or breaks. A depressed skull fracture occurs when pieces of the broken skull press into the tissue of the brain. A penetrating skull fracture occurs when something pierces the skull, such as a bullet, leaving a distinct and localized injury to brain tissue.
A skull fracture can cause bruising of brain tissue called a contusion. A contusion is a distinct area of swollen brain tissue mixed with the 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 also is seen 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.
Contrecoup can cause diffuse axonal injury, also called shearing, which involves damage to individual nerve cells (neurons) and loss of connections among neurons. This can lead to a breakdown of overall communication among neurons in the brain.
Damage to a major blood vessel in the head can cause a hematoma, or heavy bleeding into or around the brain. Three types of hematomas can cause brain damage. (1) An epidural hematoma involves bleeding into the area between the skull and the dura. With a subdural hematoma, bleeding is confined to the area between the dura and the arachnoid membrane. Bleeding within the brain itself is called intracerebral hematoma.
Another insult to the brain that can cause injury is anoxia. Anoxia is a condition in which there is an absence of oxygen supply to an organ’s tissues, even if there is adequate blood flow to the tissue. Hypoxia refers to a decrease in oxygen supply rather than a complete absence of oxygen. Without oxygen, the cells of the brain die within several minutes. This type of injury is often seen in near-drowning victims, in heart attack patients, or in people who suffer significant blood loss from other injuries that decrease blood flow to the brain.
TYPES OF BLAST INJURIES
Exposure to blast events can cause a concussion or other traumatic brain injury.
Source: DVBIC, 2010.
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 become evident until several days or weeks after the injury. Difficulties experienced as a result of a closed brain blast injury may include a range of physical, emotional, cognitive, and behavioral symptoms; many of these symptoms are nonspecific, however, and occur with other conditions such as depression or combat stress.
A person with a mild TBI may remain conscious or may experience a loss of consciousness for a few seconds or minutes. The person may also feel dazed or not like himself for several days or weeks after the initial injury.
Other symptoms of mild TBI include:
Symptoms of moderate or severe TBI may show the above symptoms, but also include:
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.
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.
TBI resulting from blast exposure can be much more complex compared to TBI from other causes. It may be difficult to assess blast-related TBI and concussion in the same manner that other brain injuries are examined. A better approach may be to conduct an evaluation based on the mechanism (cause) of the injury; that is, screen all individual service members exposed to a blast for any symptoms which might be resulting from the effects of blast on the brain (DVBIC, 2010).
Primary concerns for TBI patients include ensuring 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 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 backboard and in a neck restraint. These devices immobilize the patient and prevent further injury to the head and spinal cord.
As soon as medical personnel have stabilized the head-injured patient, they assess the patient’s condition by measuring vital signs and reflexes and by performing a neurologic 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 neurologic functioning using the Glasgow Coma Scale (GCS), a standardized, 15-point test that uses three measures—eye opening, best verbal response, and best motor response—to determine the severity of the patient’s brain injury.
GLASGOW COMA SCALE
The “eye-opening” part of the Glasgow Coma Scale is scored from 4 to 1:
The “best verbal response” part of the test is scored from 5 to 1:
The “best motor response” test is scored from 6 to 1:
The results of the three tests are added up to determine the patient’s overall condition. A total score of 3 to 8 indicates a severe head injury, 9 to 12 indicates a moderate head injury, and 13 to 15 indicates a mild head injury.
Imaging tests help to determine 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.
A recent study has found that the state-of-the-art diffusion tensor imaging (DTI) can be used to reliably detect and track brain abnormalities in patients with mild traumatic brain injury (Mayer et al., 2010). Additional clinical studies of mild traumatic brain injury will also analyze the use of magnetoencephalography.
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 head and brain and can show bone fractures as well as the presence of hemorrhage, hematomas, contusions, brain tissue swelling, and tumors.
Magnetic resonance imaging (MRI) may be used after the initial assessment and treatment of the TBI patient. MRI uses magnetic fields to detect subtle changes in brain tissue content and can show more detail than x-rays or CT. Unfortunately, MRI is not ideal for routine emergency imaging of TBI patients because it is time-consuming and is not available in all hospitals.
Approximately half of severely head-injured patients need surgery to remove or repair hematomas or contusions. Patients may also need surgery to treat injuries in other parts of the body. These patients usually go to the intensive care unit (ICU) 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 brain, there is no place within the skull for swollen tissues to expand and no adjoining tissues to absorb excess fluid. This increased pressure is called intracranial pressure (ICP).
Medical personnel measure patients’ ICP using a probe or catheter. The instrument is inserted through the skull to the subarachnoid level and is connected to a monitor that displays the patient’s ICP. If patients have high ICP, they may undergo a ventriculostomy, a procedure that drains cerebrospinal fluid (CSF) from the brain to bring the pressure down. Drugs that can be used to decrease ICP include mannitol or barbiturates, although the safety and effectiveness of the latter are unknown.
A TBI can cause problems with arousal, consciousness, awareness, alertness, and responsiveness. Generally, there are five abnormal states of consciousness that can result from a TBI: stupor, coma, persistent vegetative state, locked-in syndrome, and brain death.
Stupor is a state in which the patient is unresponsive but can be aroused briefly by a strong stimulus, such as sharp pain.
Coma is a state in which the patient is totally unconscious, unresponsive, unaware, and unarousable. Patients in a coma do not respond to external stimuli such as pain or light and do not have sleep-wake cycles. Coma results from widespread and diffuse trauma to the brain, including the cerebral hemispheres of the upper brain and the lower brain or brainstem. Coma generally is of short duration, lasting a few days to a few weeks. After this time, some patients gradually come out of the coma, some progress to a vegetative state, and others die.
Patients in a vegetative state are unconscious and unaware of their surroundings, but they continue to have a sleep-wake cycle and can have periods of alertness. Unlike coma, where the patients’ eyes are closed, patients in a vegetative state often open their eyes and may move, groan, or show reflex responses.
A vegetative state can result from diffuse injury to the cerebral hemispheres of the brain without damage to the lower brain and brainstem. Anoxia, or lack of oxygen to the brain, which is a common complication of cardiac arrest, can also bring about a vegetative state.
Many patients emerge from a vegetative state within a few weeks, but those who do not recover within 30 days are said to be in a persistent vegetative state (PVS). The chances of recovery depend on the extent of injury to the brain and the patient’s age, with younger patients having a better chance of recovery than older patients. Generally, adults have a 50% 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 are. 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 normally due to complete paralysis of the body. Unlike persistent vegetative state 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 patients can communicate through movements and blinking 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 patients do not regain motor control, but several devices are available to help them 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 results in immediate cardiac arrest and cessation of breathing.
Advances in imaging and other technologies have led to devices that help differentiate among the various 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).
Sometimes health complications occur in the period immediately following a TBI. These are not types of TBI but distinct medical problems that arise as a result of the injury. Although complications are rare, the risk increases with the severity of the trauma. Complications of TBI include:
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. 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 posttraumatic epilepsy (recurrent seizures occurring more than 1 week after the initial trauma). Generally, medical professionals use anticonvulsant medications to treat seizures in TBI patients only if the seizures persist.
Hydrocephalus or posttraumatic 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 appear later. Generally it occurs within the first year of the injury and is characterized by worsening neurologic outcome, impaired consciousness, behavioral changes, ataxia (lack of coordination or balance), incontinence, or signs of elevated ICP.
Intracranial pressure may develop as a result of meningitis, subarachnoid hemorrhage, intracranial hematoma, or other injuries. Treatment includes shunting and draining of CSF as well as any other appropriate treatment for the root cause of the condition.
Skull fractures can tear the membranes that cover the brain, leading to CSF leaks. A tear between the dura and the arachnoid membranes, called a CSF fistula, can cause CSF to leak out of the subarachnoid space into the subdural space; this is called a subdural hygroma. Cerebrospinal fluid can also leak from the nose and the ear. Tears that leak CSF from the brain cavity can also allow air and bacteria into the cavity, possibly causing infections such as meningitis. Pneumocephalus occurs when air enters the intracranial cavity and becomes trapped in the subarachnoid space.
Infections within the intracranial cavity are a dangerous complication of TBI. They may occur outside of the dura, below the dura, below the arachnoid (meningitis), or within the space of the brain itself (abscess). Most of these injuries develop within a few weeks of the initial trauma and result from skull fractures or penetrating injuries. Standard treatment involves antibiotics and sometimes surgery to remove the infected tissue. Meningitis may be especially dangerous, with the potential to spread to the rest of the brain and nervous system.
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 may 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 (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 semi-consciousness 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 (cavities) adjacent to the brain. Thrombotic-ischemic strokes are treated with anticoagulants, while surgery is the preferred treatment for hemorrhagic stroke. Other types of vascular injuries include vasospasm (an exaggerated, persistent contraction of the walls of a blood vessel) and the formation of aneurysms (blood-filled sacs formed by disease-related stretching of an artery or blood vessel).
Skull fractures, especially at the base of the skull, can cause cranial nerve injuries that result in compressive cranial neuropathies. All but three of the 12 cranial nerves project out from the brainstem to the head and face. The seventh cranial nerve, called the facial nerve, is the most commonly injured cranial nerve in TBI, and damage to it can result in paralysis of facial muscles.
Pain is a common symptom of TBI and can be a significant complication for conscious patients in the period immediately following a TBI. Headache is the most common form of pain experienced by TBI patients, but other forms of pain can also be problematic. Serious complications for patients who are unconscious, in a coma, or in a vegetative state include bed or pressure sores of the skin, recurrent bladder infections, pneumonia or other life-threatening infections, and progressive multiple organ failure.
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 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 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.
Fluid and hormonal imbalances can complicate the treatment of hypermetabolism and high ICP. Hormonal problems can result from dysfunction of the pituitary, the thyroid, or other glands throughout the body. Two common hormonal complications of TBI are hypothyroidism and syndrome of inappropriate secretion of antidiuretic hormone (SIADH). SIADH is condition in which excessive secretion of antidiuretic hormone leads to a sodium deficiency in the blood and abnormally concentrated urine; symptoms include weakness, lethargy, confusion, coma, seizures, or death if left untreated.
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.
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.
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, vertigo (a sensation of spinning around or of objects spinning around the patient), memory problems, trouble concentrating, sleeping problems, restlessness, irritability, apathy, depression, and anxiety.
These symptoms may last for a few weeks after the head injury. The syndrome is more prevalent in patients who had psychiatric symptoms, such as depression or anxiety, before the injury. Treatment for PCS may include medicines for pain and psychiatric conditions, and psychotherapy and occupational therapy to develop coping skills.
Cognition is a term used to describe the processes of thinking, reasoning, problem solving, information processing, and memory. Most patients with severe TBI, if they recover consciousness, suffer from cognitive disabilities, including the loss of many higher-level mental skills. The most common cognitive impairment among severely head-injured patients is memory loss, characterized by some loss of specific memories and the partial inability to form or store new ones.
Some of these patients may experience posttraumatic 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. Traumatic brain injury patients often have difficulty with hand-eye coordination. Because of this, TBI patients may be prone to bumping into or dropping objects, or may seem generally unsteady. Traumatic brain injury patients may have difficulty driving a car, working complex machinery, or playing sports. A recent study has shown that optometric vision therapy can be a successful treatment for those with such oculomotor dysfunctions (Ciuffreda et al., 2008).
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, nonverbal signals.
In nonfluent 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 when trying to express themselves.
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 nonessential 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.
Traumatic brain injury patients may have problems with spoken language if the part of the brain that controls speech muscles is damaged. In this disorder, called dysarthria, the patient can think of the appropriate language but cannot easily speak the words because they are unable to use the muscles needed to form the words and produce the sounds. Speech is often slow, slurred, and garbled. Some may have problems with intonation or inflection, called prosodic dysfunction. An important aspect of speech, inflection conveys emotional meaning and is necessary for certain aspects of language, such as irony.
These language deficits can lead to miscommunication, confusion, and frustration for patients as well as for those interacting with them.
Most TBI patients have emotional or behavioral problems that fit under the broad category of psychiatric health. Family members of TBI patients often find that personality changes and behavioral problems are the most difficult disabilities to handle.
Psychiatric problems that may surface include depression, apathy, anxiety, irritability, anger, paranoia, confusion, frustration, agitation, insomnia or other sleep problems, and mood swings. Problem behaviors may include aggression and violence, impulsivity, disinhibition, acting out, noncompliance, social inappropriateness, emotional outbursts, childish behavior, impaired self-control, impaired self-awareness, inability to take responsibility or accept criticism, egocentrism, inappropriate sexual activity, and alcohol or drug abuse/addiction.
Some patients’ personality problems may be so severe that they are diagnosed with borderline personality disorder, a psychiatric condition characterized by many of the problems mentioned above. Sometimes TBI patients suffer from developmental stagnation, meaning that they fail to mature emotionally, socially, or psychologically after the trauma. This is a serious problem for children and young adults who suffer from a TBI. Attitudes and behaviors that are appropriate for a child or teenager become inappropriate in adulthood. Many TBI patients who show psychiatric or behavioral problems can be helped with medication and psychotherapy.
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, chronic traumatic encephalopathy, ALS, dementia pugilistica, and posttraumatic dementia.
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).
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. (ApoE4 is a naturally occurring protein that helps transport cholesterol through the bloodstream.)
Epidemiological evidence suggests that TBI contributes to nerve-degenerative diseases such as amyotrophic lateral sclerosis (ALS, or Lou Gehrig’s disease) and chronic traumatic encephalopathy (CTE). Recent research conducted through autopsies of athletes has for the first time provided pathological evidence of an association between repeated blows to the head and the long-term development of such motor neuron diseases (McKee et al., 2010). These findings suggest that war veterans with repeated blast-related TBIs may be similarly at risk of long-term problems.
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.
The symptoms of posttraumatic dementia are very similar to those of dementia pugilistica, except that posttraumatic dementia is caused by a single, severe TBI that results in a coma.
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 a hospital ICU. 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.
It is recommended that moderately to severely injured patients receive rehabilitation treatment that draws on the skills of many specialists. This 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 specialists, such as 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, using environmental modification, help the patient adapt to disabilities or change the patient’s living space 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 pharmacologic 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 also important for TBI patients and their families to select the most appropriate setting for rehabilitation. There are many 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.
Unlike most neurologic disorders, head injuries can be prevented. The Centers for Disease Control and Prevention (CDC) have issued the following safety tips for reducing the risk of suffering a TBI:
Brain Injury Association of America, Inc.
National Institutes of Health
North American Brain Injury Society
Ciuffreda KJ, Rutner D, Kapoor N, Suchoff IB, Craig S, & Han ME. (2008). Vision therapy for oculomotor dysfunctions in acquired brain injury: A retrospective analysis. Optometry, 79(1), 18–22.
Defense and Veterans Brain Injury Center (DVBIC). (2010). Blast injuries. Retrieved November 2, 2010, from http://www.dvbic.org/TBI---The-Military/Blast-Injuries.aspx.
Mayer AR, et al. (2010). A prospective diffusion tensor imaging study in mild traumatic brain injury. Neurology, 74, 643–650.
McKee AC, Gavett BE, Stern RA, Nowinski CJ, Cantu RC, Kowall NW, Perl DP, et al. (2010). TDP-43 proteinopathy and motor neuron disease in chronic traumatic encephalopathy. J Neuropathol Exp Neurol, 69(9), 918–929.
National Center for Injury Prevention and Control (NCIPC). (2006). Heads up: Preventing brain injuries. Retrieved October 2010 from http://www.cdc.gov/ncipc/pub-res/tbi_toolkit/patients/preventing.htm.
National Institute of Neurological Disorders and Stroke (NINDS). (2002). Traumatic Brain Injury: Hope Through Research. Retrieved July 27, 2010 from http://ninds.nih.gov/disorder/tbi/detail_.htm.
EMS-CEU.com is a Wild Iris Medical Education Website
Copyright © Wild Iris Medical Education, Inc.
Forest Photograph © Jon Klein