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Traumatic Brain Injury
Traumatic brain injury (TBI), also called intracranial injury, occurs when physical trauma injures the brain. TBI is one of two subsets of acquired brain injury (ABI, brain damage that is not congenital); the other subset of ABI is non-traumatic brain injury, or injuries that do not involve external mechanical force (e.g. stroke, meningitis, insufficient oxygen). TBI is usually classified as mild, moderate, or severe, depending on the extent of loss of consciousness, loss of memory, and score on a neurological scale following the injury. TBI can result from a closed head injury or a penetrating head injury and may occur in a specific location or may be diffuse, occurring over a more widespread area. Head injury usually refers to TBI, but is broader because it can involve damage to structures other than the brain such as the scalp and skull.
TBI is a major cause of death and disability worldwide and the leading killer of people under age 45. Major causes of TBI include falls, vehicle accidents, and violence. Prevention includes using seat belts and helmets when riding bicycles or motorcycles and during some sports.
In addition to the damage caused at the moment of injury, brain trauma initiates a variety of chemical events within the brain that contribute to damage in the hours and days following the injury. This so-called "secondary injury" presents the opportunity to discover new treatments that limit the damage caused by TBI by interfering with these damaging cascades.
Imaging techniques such as computed tomography and magnetic resonance imaging are used for diagnosis. In mild cases, TBI may require little treatment; in severe ones, medications and emergency surgery may be required to lower the pressure within the skull. Physical therapy, speech therapy, and occupational therapy may be employed for rehabilitation. TBI can cause a host of physical, cognitive, emotional, and social effects. Outcome can be anything from near-complete recovery to permanent disability or death.
Classification
All traumatic brain injuries are head injuries, but head injury is not necessarily brain injury: it may involve structures within the skull and outside of it such as the skull or scalp. Similarly, all brain injuries are central nervous system (CNS) injuries, but spinal cord injuries are also considered CNS injuries.
Traumatic brain injuries are classified based on severity, location, and other injury characteristics. TBI can result from a closed or penetrating head injury; a closed (also called nonpenetrating, or blunt) injury occurs when the skull is not breached, while a penetrating head injury occurs when an object pierces the skull and breaches the dura mater, the outermost of the membranes surrounding the brain. Bone fragments may cause penetrating injuries when the skull is fractured. 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, leaving a distinct and localized traumatic injury to brain tissue.
Severity
Levels of TBI severity
GCS
PTA
LOC
Mild
13–15
<1
hour<30
minutesModerate
9–12
30 minutes–
24 hours1–24
hoursSevere
3–8
>1 day
>24
hours
Head injuries can be subdivided into mild, moderate, and severe. The Glasgow Coma Scale is the standard measure of severity of TBI in the acute setting. It is generally agreed that a TBI with GCS of 13 or above is mild, 9–12 is moderate, and 8 or below is severe.[6] One common classification system determines severity based on the duration of post-traumatic amnesia (PTA), loss of consciousness (LOC), and Glasgow Coma Score (GCS) after resuscitation according to the table at right. In a similar system, the criteria are the same as listed in the table except that trauma is only severe if unconsciousness and post-traumatic amnesia last for over a week. Other classification systems use GCS alone or PTA or LOC alone or together.
Mild TBI, commonly called concussion, is further classified based on severity. At least 16 concussion grading scales are in use for determining the severity of the injury. Duration of unconsciousness, post-traumatic amnesia, and other concussion symptoms are used to gauge severity.
Focal vs. diffuse
The damage from TBI can be focal or diffuse, confined to one area of the brain or involving more than one area, respectively. Types of injuries considered diffuse include concussion and diffuse axonal injury. The shaking that causes shaken baby syndrome results in diffuse injury. Diffuse injuries can result from sudden acceleration or deceleration of the head, and are commonly caused by rotational forces. Diffuse axonal injury involves damage to axons after forces such as rotation subject them to stress.
Focal injuries are those that occur in a specific location in the brain. These localized injuries are often associated with symptoms corresponding to the part of the brain that was injured, for example manifesting in hemiparesis or other focal neurological deficits. Types of focal brain injury include intracranial hemorrhage, heavy bleeding in the skull that is not mixed with tissue, and bruising of brain tissue called a contusion. In a brain contusion, injured brain tissue is mixed with blood that has leaked from damaged blood vessels. Hemorrhage, due to rupture of a blood vessel in the head, can be extra-axial, (occurring within the skull but outside of the brain) or intra-axial (occurring within the brain tissue). 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 heavy, outermost membrane that surrounds the brain, the dura mater. With a subdural hematoma, the most common traumatic mass lesion, bleeding occurs between the dura and the arachnoid mater. A subarachnoid hemorrhage involves bleeding between the surface of the brain and the arachnoid membrane that lies just above the brain. Subarachnoid hemorrhage usually results from a tear in a blood vessel on the surface of the brain. Subarachnoid hemorrhages, common after head trauma, do not cause a mass effect because the blood is able to spread out, but they can cause blood vessels to spasm, potentially constricting enough to cause damage to the brain from insufficient blood flow. Intra-axial bleeds are further divided into intraparenchymal hemorrhage, also called intracerebral hemorrhage, which occurs within the brain tissue itself, and intraventricular hemorrhage in which bleeding occurs in the ventricular system.
Signs and symptoms
Symptoms are dependent on the type of TBI (diffuse or focal) and the part of the brain that is affected. Some symptoms are evident immediately, while others do not surface until several days, weeks, or even years after the injury. In the case of pediatric TBI children are sometimes described as having grown into their deficits years after their 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, dizziness, vomiting, nausea, lack of motor coordination, and difficulty balancing.
Unequal pupil size is a sign of a serious brain injury.
Symptoms of mild injury may remain the same or get better; worsening symptoms indicate a more severe injury. With moderate or severe TBI, the patient may have symptoms of mild injury, but may also have:
• one pupil larger than the other (anisocoria)
• a severe, persistent, or worsening headache
• seizures
• inability to awaken
• slurred speech
• weakness or numbness in the extremities
• loss of coordination
• abnormal posturing
• neurological deficit (e.g. weakness in a limb)
When the pressure within the skull (intracranial pressure) rises too high, it can cause potentially deadly brain herniation and brain death.[15] Signs of increased intracranial pressure include decreasing level of consciousness, a pupil that fails to constrict in response to light or is slow to do so, paralysis or weakness on one side of the body, and Cushing's phenomena (slow heart rate with increasing systolic blood pressure). Small children with moderate to severe TBI may show some of these signs as well as signs specific to young children, including persistent crying, inability to be consoled, and refusal to nurse or eat.
Causes
The most common cause is falls, the second is vehicle accidents, and the third is striking or being struck by something.
The most common causes of TBI include violence, transportation accidents, construction, and sports. Falls account for 28% of TBI, motor vehicle (MV) accidents for 20%, being struck by an object for 19%, violence for 11%, and non-MV bicycle accidents for 3%. TBI is the third leading injury to result from child abuse. Half of TBI incidents involve alcohol use.
Blast injuries from explosions are another cause of TBI. Traumatic brain injury is the leading cause of death and disability in war zones. Traumatic brain injury has been identified as the "signature injury" among wounded soldiers of the current military engagement in Afghanistan and Iraq; over a quarter of soldiers evaluated at the Walter Reed Army Medical Center after returning from these conflicts have TBI.
Mechanism
When the head strikes a fixed object, the coup injury occurs at the site of impact and the contrecoup injury occurs at the opposite side.
Angular, rotational, shear, and translational forces may all contribute to TBI. Compressive stress, force that causes deformation of a structure, contributes to brain contusion. Tensile stress, stretching caused by forces pulling in opposite directions along an axis of a structure, may also contribute to TBI; for example blood vessels that bridge between the brain and surrounding structures may be damaged when they are pulled as the brain accelerates at a different rate from the skull. Shear stress, opposing forces pushing in opposite directions perpendicular to the axis of a structure, can cause brain injuries such as contusions or lacerations of the brain stem. When the head is struck by or strikes something, or is rapidly accelerated or decelerated, the force from the impact sends shock waves through the skull and brain, resulting in tissue damage. Penetrating injuries, too, cause shock waves to propagate through the tissue, potentially causing cavitation and destroying a great deal of tissue along the path of a rapidly-moving projectile.
Damage may occur in the part of the brain directly under the site of impact (a coup injury), or it may occur on the side opposite the impact (a contrecoup injury), possibly because of the effects of inertia on the brain within the skull. Even in the absence of an impact, significant acceleration or deceleration of the head can cause TBI; however in most cases a combination of impact and acceleration is probably to blame.
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. Rather than improving after being hospitalized, some 40% of TBI patients deteriorate. Primary brain 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. These secondary processes can dramatically worsen the damage caused by primary injury and account for the greatest number of TBI deaths occurring in hospitals. Secondary injury events include release of inflammatory factors, damage to the blood–brain barrier, free radical overload, excessive release of the neurotransmitter glutamate, influx of calcium and sodium ions into neurons, and mitochondrial dysfunction. Injured axons in the brain's white matter may separate as a result of secondary injury. Other factors in secondary injury are ischemia (insufficient blood flow); cerebral hypoxia (insufficient oxygen in the brain); hypotension (low blood pressure); cerebral edema (swelling of the brain); changes in the blood flow to the brain; and raised intracranial pressure (the pressure within the skull). Intracranial pressure may rise due to swelling or a mass effect from a lesion such as a hemorrhage. As a result of increased intracranial pressure, cerebral perfusion pressure (the pressure of blood flow in the brain) is reduced; ischemia (insufficient blood flow to tissues) results. If intracranial pressure gets too high, it can lead to deadly brain herniation, in which parts of the brain are squeezed past structures in the skull. No medication exists to halt the progression of secondary injury, but the variety of pathological events presents opportunities for treatments that interfere with the injury; for example mechanical ventilation and fluid resuscitation seek to ensure adequate oxygen and fluid levels respectively.
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.
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.
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. Voluntary control of eye movements or blinking may be spared permitting the detection of conscious awareness and enabling the establishment of functional communication.
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.
Prevention
Helmets protect motorcycle riders from head injury and death.
Measures for preventing TBI include changes to public policy and safety laws such as speed limits, seat belt and helmet laws, and road engineering. Public education and prevention programs exist to lower the incidence of TBI. Changes to common practices are other preventative measures; for example a reduction in alcohol abuse or an increase in use of helmets during sports could also reduce the incidence of TBI. Other preventative measures include use of seat belts and child safety seats and bike, motorcycle and sports helmets. Installation of roll bars and airbags in modern vehicles has increased survival after vehicle accidents. Falls can be avoided 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; and using safety gates at the top and bottom of stairs when young children are around. Playgrounds with surfaces made of shock-absorbing material (e.g. mulch, sand) may also help prevent head injuries. Gun safety, including keeping guns unloaded and locked is another preventative measure. Recently new Head Impact Telemetry System technology is being placed in American Football helmets to measure and record impacts to the head while sending signals to the sideline.
Diagnosis
Medical personnel assess the patient's condition by measuring vital signs and reflexes and by performing a neurological examination. They assess the patient's neurological functioning by checking whether the the pupils respond normally to light by constricting and using the Glasgow Coma Scale
Imaging tests help in determining the diagnosis and prognosis and in deciding what treatments to give. Patients with mild to moderate injuries may receive skull and neck X-rays to check for bone fractures. The gold standard radiologic imaging test for TBI is a computed tomography (CT) scan, which creates a series of cross-sectional X-ray images of the head. Magnetic resonance imaging (MRI), which can show more detail than X-rays or CT, can add information about expected outcome in the long-term treatment of TBI.[6] However, MRI is not used in the emergency setting; reasons for this include the relative inefficacy in detecting bleeds and bone fractures on MRI, the length of time it takes to obtain images, the inaccessibility of the patient in the magnet, and the metal items used in emergency care that cannot be around the strong magnet. Diffuse injuries have more microscopic injury than macroscopic injury and are difficult to detect with CT and MRI, but the presence of diffuse axonal injury can be inferred when small bleeds are visible in the corpus callosum or the cerebral cortex. However, newer studies such as Diffusion Tensor Imaging are able to demonstrate the degree of white matter fiber tract injury even when the standard MRI is negative.
CT and MRI are standard in TBI diagnosis, 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). Functional magnetic resonance imaging (fMRI) and Positron emission tomography (PET) can show the neurocognitive or neurophysiologic effects of TBI. PET can show changes in cerebral blood flow and the amount of glucose used by the brain.
Neuropsychological tests and neuropsychological assessment can be performed to demonstrate the cognitive effects of the injury and to aid in recovery and rehabilitation. Tests used to determine neurological outcome include those that measure memory and amnesia, learning, motor abilities, language, attention, and ability to form concepts.
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. Hypotension (low blood pressure), which has a devastating outcome in TBI, can be prevented by giving intravenous fluids to maintain a normal or even high blood pressure to prevent inadequate blood flow to the brain. Methods to prevent further damage to the brain include endotracheal intubation, mechanical ventilation, preventing seizures and dangerous increases in intracranial pressure, and managing other injuries such as fractures. Certain facilities are equipped to handle TBI better than others are; care involves bringing the patient to such specialist facilities.
Intracranial pressure
People with severe brain injuries are monitored for rises in intracranial pressure. Medical personnel measure a patient's ICP by placing a catheter into a ventricle of the brain. Treatment of high ICP may be as simple as straightening the head to allow blood to exit the head through the jugular vein or raising the head of the bed slightly, or it may require ventriculostomy, a procedure that drains cerebrospinal fluid (CSF) from the ventricles to bring the pressure down. Other measures to decrease dangerously high ICP include use of sedative, paralytic agents, osmotherapy (creation of a chemical gradient to maintain therapeutic concentrations of chemicals in tissues), and mild hyperventilation. Hyperventilation, ventilating the patient more than normal, decreases blood flow to the brain because the blood vessels constrict in response to the lowered carbon dioxide levels. It thus reduces ICP, but it potentially causes ischemia, and it worsens outcome if used for a long time preemptively. It is not indicated as a protective measure against high ICP.
Medication
Seizures can be prevented with benzodiazepines; however these drugs are used carefully because of their potential to depress breathing and lower blood pressure. 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 may have been falsified. Diuretics, drugs that increase urine output to reduce excessive fluid in the system, may be used to treat high intracranial pressures (those above 25 mm Hg), but carry the potential side effect of causing hypovolemia, insufficient blood volume.
Patients may need medication for psychiatric and physical problems resulting from the TBI.
TBI patients are more susceptible to side effects and may react adversely to some pharmacological agents or may be inordinately sensitive to them. This may be due, for example, to a more permeable blood-brain barrier that can result from injury.[citation needed]
Surgery
Mass lesions such as contusions or subdural, epidural, or intracerebral hematomas may need to be surgically removed. Contusions or hematomas that are causing a significant mass effect (shift of intracranial structures by more than 5 mm) are medical emergencies and need to be treated surgically. Craniotomy (removal of part of the skull) is required in about a third of severe TBIs. For intracranial hematomas, the collected blood may be removed using suction or special forceps or it may be floated off by irrigating with water. Hemorrhaging vessels are located and the bleeding is controlled. Decompressive craniectomy is a last-resort surgical procedure in which part of the skull is removed in an attempt to reduce severely high ICP.
Rehabilitation
During the acute stage of rehabilitation, moderately to severely injured people 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, they may be transferred to a subacute nursing unit of the medical center or to an independent rehabilitation hospital. Decisions regarding when and where an individual should be treated depend on factors including the level to which the person can participate in rehabilitation. Moderately to severely injured patients may receive physical therapy, occupational therapy, speech and language therapy, physiatry (physical medicine and rehabilitation), psychology, psychiatry, and social work. The goal of rehabilitation is to improve the patient's ability to function independently at home and in society. Therapists help patients adapt to disabilities or change their living conditions to accommodate impairments.
After discharge 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 treating broader psychosocial issues associated with long-term adjustment and community reintegration.[citation needed] Respite care such as supported living and residential holidays, with supported days out, offers relief for caregivers and a new area of brain stimulation for the patient.[citation needed]
TBI patients who show psychiatric or behavioral problems may be helped with medication and psychotherapy, but the effectiveness of psychotherapy may be limited by the residual neurocognitive impairment.
Prognosis
Prognosis worsens with the severity of injury, but mild TBI is more poorly defined and prognosis is not as clear with it. Most TBIs (by some estimates, almost 90%) are mild and do not cause permanent or long-term disability; however, all severity levels of TBI have the potential to cause significant, long-lasting disability. Permanent disability is thought to occur in 10% of mild injuries, 66% of moderate injuries, and 100% of severe injuries. Most mild TBI is completely resolved within three weeks, and almost all people with mild TBI are able to live independently return to the jobs they had before the injury, although a portion have mild cognitive and social impairments. Post-concussion syndrome, a set of lasting symptoms experienced after mild and other forms of TBI, can include physical, cognitive, emotional and behavioral problems such as headaches, dizziness, difficulty concentrating, and depression. A young person who receives a second concussion before symptoms from another one have healed may be 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. Over 90% of people with moderate TBI are able to live independently, although a portion require assistance in areas such as physical abilities, employment, and financial managing.
Other factors thought to worsen the prognosis include abuse of substances including illicit drugs and alcohol and age over sixty or under two years (in children, younger age at time of injury may be associated with a slower recovery of some abilities). Glasgow Coma Score at the time of resuscitation after the injury is an important factor in eventual outcome: the lower the score, the worse the outcome, and when the score is 3 (the lowest score), the prognosis is usually dismal. The most important predictor of the three categories is the motor score, but low scores in any of the categories is significantly correlated with poor outcome. An abnormal pupil response to light, excessive pupil dilation, and absence of pupil reflexes called oculocephalic or oculovestibular responses are also significantly correlated with a worse outcome. Lower cerebral perfusion pressures and longer times spent with high intracranial pressures (above 20 mm Hg) are also associated with worse outcomes. Scores greater than 40 on the Injury Severity Scale also correlate significantly with worse outcome. Subdural hematoma is associated with worse neurological outcome and increased mortality, while people with epidural hematoma and are expected to make a good outcome if they can receive surgery quickly. People with TBI who have GCS higher than nine, no lesions visible on CT scan, and no evidence of alcohol intoxication, low blood oxygen, or shock are tentatively expected to have a good outcome.
Complications
In the period immediately following a TBI, health complications may occur; these are not types of TBI, but are distinct medical problems that arise as a result of the injury. The risk of complications increases with the severity of the trauma.\ Serious complications for patients who are unconscious, in a coma, or in a vegetative state include pressure sores of the skin, pneumonia or other infections, and progressive multiple organ failure. Being unconscious and lying still for long periods can cause blood clots to form (deep venous thrombosis), which can cause pulmonary embolism.
The results of traumatic brain injury vary widely in type and duration. Even mild traumatic brain injury can result in disabilities that interfere with social interactions, employment, and everyday living. Head trauma can cause problems a variety of problems including physical, cognitive, emotional, and behavioral ones.
Physical
The relative risk of PTS increases with the severity of injury.
Complications of TBI include hydrocephalus (post-traumatic ventricular enlargement), cerebrospinal fluid leaks, infections, vascular injuries, and cranial nerve injuries. Pain, especially headache, is a common complication following a TBI.
As many as 50% of patients with penetrating head injuries will develop post-traumatic seizures. The risk of seizures is elevated with other types of brain trauma such as cerebral contusions or hematomas, and it increases with severity of trauma (image at right). People with early seizures, those occurring within a week of injury, have an increased risk of post-traumatic epilepsy (recurrent seizures occurring more than a week after the initial trauma). Generally, medical professionals use anticonvulsant medications to treat seizures in TBI patients within the first week of injury only and after that only if the seizures persist.
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, inability to move, shuffling walk, and stooped posture. Parkinson's disease is 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).
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. CSF can also leak from the nose and the ear. These tears that let CSF out of the brain cavity can also allow bacteria into the cavity, potentially 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 mater, below the dura, below the arachnoid (meningitis), or within 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.
Hydrocephalus or post-traumatic ventricular enlargement occurs when cerebrospinal fluid (CSF) accumulates in the brain, resulting in dilation of the cerebral ventricles 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.
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 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 or through the formation of a blood clot at the site of injury, blocking blood flow to the brain. Blood clots also can develop in other parts of the head. Other types of vascular injuries include vasospasm and the formation of aneurysms.
Fluid and hormonal imbalances can complicate treatment. 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.
Cognitive
Cognitive deficits that can follow TBI include impaired attention; disrupted insight, judgement, and thought; reduced processing speed; distractibility; and deficits in executive functions such as abstract reasoning, planning, problem-solving, and multitasking. Most patients with severe TBI who recover consciousness suffer from cognitive disabilities, including the loss of many higher level mental skills. Memory loss, the most common cognitive impairment among head-injured patients, occurs in 20–79% of people with closed head trauma, depending on severity. Post-traumatic amnesia (PTA), a confusional state with impaired memory, is characterized by loss of specific memories or the partial inability to form or store new ones.
Patients with mild to moderate head injuries who experience cognitive deficits may become easily confused or distracted and have problems with concentration and attention. They may also have problems with higher level, executive functions, such as planning, organizing, abstract reasoning, problem solving, and making judgments, which may make it difficult to resume pre-injury activities. Recovery from cognitive deficits is greatest within the first six months after the injury and more gradual after that.
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. 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, head-injured people who have a particular form of the protein apolipoprotein E (apoE4, a naturally occurring protein that helps transport cholesterol through the bloodstream) fall into this increased risk category.
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. 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. 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.
Communication
Language and communication problems are common disabilities in TBI patients. Some may experience aphasia, difficulty with understanding and producing spoken and written language; or they may have difficulty with the more subtle aspects of communication, such as body language and emotional, non-verbal signals. Problems with spoken language may occur 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.
Sensory
TBI patients may have sensory problems, especially problems with vision; they 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, causing them to seem clumsy or unsteady. Other sensory deficits include problems with hearing, smell, taste, or touch. Tinnitus, a ringing or roaring in the ears, may also occur. A person with damage to the part of the brain that processes taste or smell may perceive a persistent bitter taste or 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 difficult to treat.
Emotional and behavioral
TBI may cause emotional or behavioral problems and changes in personality. Emotional symptoms that can follow TBI include emotional instability, depression, anxiety, hypomania, mania, apathy, irritability, and anger. TBI appears to predispose a person to psychiatric disorders including obsessive compulsive disorder, alcohol or substance abuse or substance dependence, dysthymia, clinical depression, bipolar disorder, phobias, panic disorder, and schizophrenia. The prevalence of all psychiatric illnesses is 49% in moderate to severe TBI and 34% in mild TBI within a year of injury, compared with 18% of controls. People with TBI continue to be at greater risk for psychiatric problems than others even years after an injury. Problems that may persist for one half year to two years after the injury may include irritability, suicidal ideation, insomnia, and loss of the ability to experience pleasure from previously enjoyable experiences. Other problems include apathy, anxiety, anger, paranoia, confusion, frustration, agitation, and mood swings. About one quarter of people with TBI suffer from clinical depression, and about 9% suffer mania.
Behavioral symptoms that can follow TBI include disinhibition, inability to control anger, impulsiveness, lack of initiative, inappropriate sexual activity, and changes in personality. Other problem behaviors include violence, acting out, social inappropriateness, emotional outbursts, impaired self-awareness, inability to take responsibility or accept criticism, egocentrism, and alcohol or drug abuse or addiction.[citation needed] Sometimes people with TBI fail to mature emotionally, socially, or psychologically after the trauma. Different behavioral problems are characteristic of the location of injury; for instance, frontal lobe injuries often result in disinhibition and inappropriate or childish behavior, and temporal lobe injuries often cause irritability and aggression.
Epidemiology
TBI plays the leading role in disability and death due to physical trauma and plays a significant role in half of deaths due to trauma.
Incidence
The incidence of TBI varies by age, gender, region and other factors. For example, he yearly incidence in the US is estimated to be about 1.8–2.5 per 1000 people, but the incidence is thought to be higher in Europe and South Africa. The annual incidence of mild TBI is difficult to determine but may be 1–6 people per 1000.
Each year in the United States about two million people suffer a TBI and about 500,000 are hospitalized for TBI. In developing countries, the incidence of TBI has risen as automobile use (and therefore the number of vehicle accidents) has increased faster than safety infrastructure could be introduced. In contrast, high-income countries have seen decreases in traffic-related TBI since the 1970s.
Demographics
TBI is the leading killer of people under age 45. TBI, the leading cause of death and a major cause of disability for children worldwide, is present in 85% of traumatically injured children, either alone or with other injuries. The age groups most at risk for TBI are children ages five to nine and adults over age 80. The highest rates of death and hospitalization due to TBI are in people over age 65. However, the greatest number of TBIs occur in people aged 15–24. Regardless of age, TBI rates are higher in males. Men suffer twice as many TBIs as women do and have a fourfold risk of fatal head injury. Males also account for two thirds of childhood and adolescent head trauma patients.
Mortality
Causes of TBI fatalities
The mortality rate is estimated to be 21% 30 days after TBI. Severe TBI carries a mortality (death rate) of 30–50%. The mortality rate has declined due to improved treatments and systems for managing trauma. This decline in mortality has led to a concomitant increase in the number of people living with disabilities that result from TBI. The fraction of those who die after being hospitalized with TBI fell from almost half in the 1970s to about a quarter at the beginning of the 21st century.
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. Firearms are the most common cause of fatal TBI, followed by vehicle accidents and then falls (see chart at right). Of deaths from firearms, 75% are considered to be suicides.