Traumatic brain injury natural history, complications and prognosis
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Common complications of traumatic brain injury include:
The results of traumatic brain injury vary widely in type and duration. A head-injured patient may experience physical effects of the trauma such as headaches, movement disorders (e.g. Parkinsonism), seizures, difficulty walking, sexual dysfunction, lethargy, or coma. Cognitive symptoms include changes in judgment or ability to reason or plan, memory problems, and loss of mathematical ability. Emotional problems include mood swings, poor impulse control, agitation, low frustration threshold, self-centeredness, clinical depression, and psychotic symptoms such as hallucinations and delusions.
Natural history, Complications, and Prognosis
- If left untreated, 100% of patients with traumatic brain injury die.
- 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.
- Differentiating a patient in a persistent vegetative state from one in a minimally conscious state can be challenging but remains a critically important clinical task.
- Locked-in syndrome is a condition in which a patient is aware and awake, but cannot move or communicate due to complete paralysis of the body.
- 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 will result in immediate cardiac arrest and cessation of breathing.
- Recent studies have brought into question the nature of coma and consciousness in TBI.
- For example, a 23-year-old woman in a vegetative state after a severe brain injury due to a car accident was able to communicate with a team of British researchers at Cambridge University in England via functional magnetic resonance imaging.
- While cautious about accepting the study's results, Nicholas Schiff, a neurologist at the Weill Cornell Medical College in New York, agrees that the research was groundbreaking. "It's the first time we've ever seen something like this. It really is kind of shocking," he said.
- Hydrocephalus or post-traumatic ventricular enlargement occurs when cerebrospinal fluid (CSF) accumulates in the brain resulting in dilation of the cerebral ventricles (cavities in the brain filled with CSF) and an increase in ICP.
- This condition can develop during the acute stage of TBI or may not appear until later.
- Generally, it occurs within the first year of the injury and is characterized by worsening neurological outcome, impaired consciousness, behavioral changes, ataxia (lack of coordination or balance), incontinence, or signs of elevated ICP.
- The condition 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.
- 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. 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.
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 (hemorrhagic stroke) or through the formation of a clot at the site of injury, called a thrombus or thrombosis, blocking blood flow to the brain (ischemic stroke). Blood clots also can develop in other parts of the head. Symptoms such as headache, vomiting, seizures, paralysis on one side of the body, and semiconsciousness developing within several days of a head injury may be caused by a blood clot that forms in the tissue of one of the sinuses, or cavities, adjacent to the brain. Other types of vascular injuries include vasospasm and the formation of aneurysms.
Cranial Nerve Injuries
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 twelve cranial nerves project out from the brainstem to the head and face. Damage to the seventh cranial nerve, the most commonly injured cranial nerve in TBI can result in paralysis of facial muscles.
Pain, especially headache, is a common complication following a TBI.
Fluid and hormonal imbalances can complicate the treatment of hypermetabolism and high intracranial pressure (ICP). Hormonal problems can result from dysfunction of the pituitary, the thyroid, and other glands throughout the body. Two common hormonal complications of TBI are syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and hypothyroidism.
Trauma victims often develop hypermetabolism or an increased metabolic rate, which leads to an increase in the amount of heat the body produces. The body redirects into heat the energy needed to keep organ systems functioning, causing muscle wasting and the starvation of other tissues. The nutritional management of patients with TBI, including the provision of adequate calories, and protein through an available route of administration to balance consumption, is thus critically important in order to avoid complications related to hypermetabolism and resulting malnutrition. Provision of food through a feeding tube may be temporarily necessary to meet the nutritional needs of the patient with a severe TBI, until they are awake and able to eat and swallow safely without risking pulmonary aspiration and the development of aspiration pneumonia. Sometimes the use of parenteral feeding is necessary if the patient has associated injuries or complications that prevent direct access to the digestive system.
Disabilities Resulting from TBI
Disabilities resulting from a TBI depend upon the severity of the injury, the location of the injury, and the age and general health of the patient. Some common disabilities include problems with cognition (attention, calculation, memory, judgment, insight, and reasoning), sensory processing (sight, hearing, touch, taste, and smell), communication (language expression and understanding), social function (empathy, capacity for compassion, interpersonal social awareness and facility) and mental health (depression, anxiety, personality changes, aggression, acting out, and social inappropriateness).
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 loss of consciousness to develop the syndrome. Symptoms include headache, dizziness, memory problems, trouble concentrating, sleeping problems, restlessness, irritability, apathy, clinical 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 involves treating symptoms, for example giving medicines for pain and psychiatric conditions, and psychotherapy and occupational therapy.
Most patients with severe TBI who 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 activities. Recovery from cognitive deficits is greatest within the first six 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. 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. TBI patients may have problems with spoken language if the part of the brain that controls speech muscles is damaged. In this disorder, called dysarthria, the patient can think of the appropriate language, but cannot easily speak the words because they are unable to use the muscles needed to form the words and produce the sounds. Speech is often slow, slurred, and garbled. Some may have problems with intonation or inflection, called prosodic dysfunction.
Alzheimer's disease (AD) is a progressive, neurodegenerative disease characterized by dementia, memory loss, and deteriorating cognitive abilities. Research suggests an association between head injury in early adulthood and the development of AD later in life; the more severe the head injury, the greater the risk of developing AD. 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.)
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.
Many TBI patients have sensory problems, especially problems with vision. Patients may not be able to register what they are seeing or may be slow to recognize objects. Also, TBI patients often have difficulty with hand-eye coordination. Because of this, TBI patients may seem clumsy or unsteady. Other sensory deficits may include problems with hearing, smell, taste, or touch. Some TBI patients develop tinnitus, a ringing or roaring in the ears. A person with damage to the part of the brain that processes taste or smell may develop a persistent bitter taste in the mouth or perceive a persistent noxious smell. Damage to the part of the brain that controls the sense of touch may cause a TBI patient to develop persistent skin tingling, itching, or pain. These conditions are rare and hard to treat.
Emotional and Behavioral Problems
Most TBI patients have emotional or behavioral problems that fit under the broad category of psychiatric health. Family members of TBI patients often find that personality changes and behavioral problems are the most difficult disabilities to handle. Psychiatric problems that may 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. Problem behaviors may include aggression and violence, impulsivity, disinhibition, acting out, noncompliance, social inappropriateness, emotional outbursts, childish behavior, impaired self-control, impaired self-awareness, inability to take responsibility or accept criticism, egocentrism, inappropriate sexual activity, and alcohol or drug abuse or addiction. Some patients' personality problems may be so severe that they are diagnosed with an organic personality disorder, a psychiatric condition characterized by many of these problems. 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, because attitudes and behaviors that are appropriate for a child or teenager become inappropriate in adulthood. TBI patients who show psychiatric or behavioral problems may be helped with medication and psychotherapy, although the effectiveness of psychotherapy may be limited by the residual neurocognitive impairment. Technological improvements and emergency care have diminished the incidence of devastating TBI while increasing the numbers of patients with mild or moderate TBI. Such patients are more adversely affected by their emotional problems than by their residual physical disabilities.
Parkinson's disease and other motor problems as a result of TBI are rare but can occur. Parkinson's disease may develop years after TBI as a result of damage to the basal ganglia. Symptoms of Parkinson's disease include tremor or trembling, rigidity or stiffness, slow movement (bradykinesia), inability to move (akinesia), shuffling walk, and stooped posture. Despite many scientific advances in recent years, Parkinson's disease remains a chronic and progressive disorder, meaning that it is incurable and will progress in severity until the end of life. Other movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), and myoclonus (shock-like contractions of muscles).
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 post-traumatic epilepsy (recurrent post-traumatic 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.
The immediate effect after TBI is a cascade of molecular responses which includes ion imbalances. There will be an increased extracellular potassium and intracellular calcium, increase of glutamate and aspartate release from the neurons which results in blood-brain barrier compromise ultimately leading to inflammation and degeneration. Primary brain volume declines by 10% in the first 6 months after injury which equals to decades of ageing.
- Traumatic brain injury is a frequent cause of major long-term disability in individuals surviving head injuries sustained in war zones.
- This is becoming an issue of growing concern in modern warfare, in which rapid deployment of acute interventions is effective in saving the lives of combatants with significant head injuries. Traumatic brain injury has been identified as the "signature injury" among wounded soldiers of the current military engagement in Iraq.
- The 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.
- "Vegetative patient 'communicates': A patient in a vegetative state can communicate just through using her thoughts, according to research". BBC News. September 7, 2006. Retrieved 2007-09-26.
- Stein R (September 8, 2006). "Vegetative patient's brain active in test: Unprecedented experiment shows response to instructions to imagine playing tennis". San Francisco Chronicle. Retrieved 2007-09-26.
- Harris, Taylor C et al. “The Shrinking Brain: Cerebral Atrophy Following Traumatic Brain Injury.” Annals of biomedical engineering vol. 47,9 (2019): 1941-1959. doi:10.1007/s10439-018-02148-2
- Iraq war's signature wound: Brain injury. Discover Magazine.
- Hoge CW, McGurk D, Thomas DL, Cox AL, Engel CC, Castro CA (2008). "Mild Traumatic Brain Injury in U.S. Soldiers Returning from Iraq". The New England Journal of Medicine. 358 (5): 453–463.
- Tolias C and Sgouros S (February 4, 2005). "Initial Evaluation and Management of CNS Injury". eMedicine.com. Retrieved 2007-12-16.