Traumatic brain injury ( TBI ), also known as intracranial injury , occurs when external forces injure the brain. TBI can be classified by severity, mechanism (closed or penetrating head injury), or other features (eg, occurring in certain locations or in widespread areas). Head injuries are a broader category that may involve damage to other structures such as scalp and skull. TBI can produce physical, cognitive, social, emotional, and behavioral symptoms, and results can range from complete recovery to permanent disability or death.
Causes include falls, vehicle collisions, and violence. Brain trauma occurs as a consequence of sudden acceleration or deceleration in the cranium or by a complex combination of movement and sudden impact. In addition to damage caused at the time of injury, events occurring in minutes to days after injury can cause secondary injury . These processes include changes in cerebral blood flow and pressure within the skull. Some of the imaging techniques used for diagnosis include computed tomography and magnetic resonance imaging (MRI).
Preventive measures include the use of vehicle protection technologies, such as seat belts and sport or motorcycle helmets, as well as efforts to reduce the number of collisions, such as safety education programs and traffic law enforcement. Depending on the injury, the necessary care may be minimal or may include interventions such as medication, emergency surgery or surgery several years later. Physical therapy, speech therapy, recreational therapy, occupational therapy and vision therapy can be used for rehabilitation. Counseling, employment support, and community support services can also be useful.
TBI is the leading cause of death and disability worldwide, especially in children and young adults. Men suffer traumatic brain injury more often than women. The 20th century saw developments in diagnosis and treatment that reduced mortality and improved outcomes.
Video Traumatic brain injury
Classification
Traumatic brain injury is defined as damage to the brain resulting from external mechanical forces, such as rapid acceleration or deceleration, impact, explosion waves, or penetration by projectiles. Temporary or permanent disruption of brain function and structural damage may or may not be detected by current technology.
TBI is one of two parts of the acquired brain injury (brain damage occurring after birth); another subset is a non-traumatic brain injury, which does not involve external mechanical forces (eg, stroke and infection). All traumatic brain injuries are head injuries, but the last term may also refer to injuries to other parts of the head. However, the terms head injury and brain injury are often used interchangeably. Similarly, brain injury is included in the classification of central nervous system injury and neurotrauma. In neuropsychological research literature, in general the term "traumatic brain injury" is used to refer to a non-penetrating traumatic brain injury.
TBI is usually classified based on severity, anatomical features of the injury, and mechanism (causal force). The mechanisms associated with the classification divide TBI into a closed and penetrating head injury. A closed injury (also called nonpenetrating, or blunt) occurs when the brain is not exposed. Head injuries that penetrate or open, occur when an object penetrates the skull and penetrates the dura mater, the outermost membrane that surrounds the brain.
Severity
Brain injury can be classified into mild, moderate, and severe categories. Glasgow Coma Scale (GCS), the most commonly used system to classify TBI severity, assesses a person's level of consciousness on a 3-15 scale based on verbal, motor, and eye-opening reactions to stimuli. In general, it is agreed that TBI with GCS 13 or above is mild, 9-12 moderate, and 8 or under weight. A similar system exists for small children. However, the GCS scoring system has limited ability to predict outcomes. Because of this, other classification systems as shown in the table are also used to help determine the severity. The current model developed by the Department of Defense and the Department of Veterans Affairs uses all three GCS criteria after resuscitation, post-traumatic amnesia duration (PTA), and loss of consciousness (LOC). It has also been proposed to use visible changes in neuroimaging, such as swelling, focal lesions, or diffuse injury as a method of classification. The scoring scale also exists to classify the severity of mild TBI, commonly called concussion; this uses the duration of LOC, PTA, and other concussion symptoms.
Pathological features
The system also exists to classify TBI based on its pathological features. Lesions may be extra-axial, (occurring within the skull but outside the brain) or intra-axial (occurring within the brain tissue). Damage to TBI can be focused or spread, limited to a particular area or distributed in a more general way, respectively. However, common to both types of injuries exists in certain cases.
The diffuse injury manifests with little damage to neuroimaging studies, but the lesions can be seen with post-mortem microscopy techniques, and in early 2000, researchers found that diffusion of tensor imaging (DTI), the way MRI images process that exhibits white matter, is an effective tool to display diffuse aconal injury rates. Types of perceived injuries include edema (swelling) and diffuse axonal injury, which is a widespread damage to the axon including white matter and projection to the cortex. Types of perceived spread injuries include concussion and diffuse axonal injury, extensive damage to axons in areas including white matter and cerebral hemispheres.
Focal injuries often produce symptoms associated with the functioning of damaged areas. Research shows that the most common areas have focal lesions of unexploded traumatic brain injury are the orbitofrontal cortex (the lower surface of the frontal lobe) and the anterior temporal lobe, the areas involved in social behavior, emotional regulation, smell, and decision making, resulting in social deficits/emotional and general assessment following mild TBI. Symptoms such as hemiparesis or aphasia can also occur when less common areas such as motor or language areas, respectively, are damaged.
One type of focal injury, cerebral laceration, occurs when the tissue is cut or torn. Tearing like that often occurs in the orbitofrontal cortex in particular, because of bony bulge in the upper skull bone above the eye. In the same injury, cerebral contusions (bruised brain tissue), blood mixes between tissues. In contrast, intracranial hemorrhage involves bleeding that does not mix with the tissues.
Hematoma, also a focal lesion, is a collection of blood in or around the brain that can result from bleeding. Intracerebral hemorrhage, with bleeding in the brain tissue itself, is an intra-axial lesion. Extra-axial lesions include epidural hematoma, subdural hematoma, subarachnoid hemorrhage, and intraventricular hemorrhage. Epidural hematoma involves bleeding into the area between the skull and the dura mater, the outermost of the three membranes surrounding the brain. In subdural hematoma, bleeding occurs between the dura and arachnoid mater. Subarachnoid hemorrhage involves bleeding into the space between the arachnoid membrane and the pia mater. Intraventricular hemorrhage occurs when there is bleeding in the ventricle.
Maps Traumatic brain injury
Signs and symptoms
Symptoms depend on the type of TBI (diffuse or focal) and the affected part of the brain. Unconsciousness tends to last longer for people with injuries to the left side of the brain than those who suffer injuries to the right. Symptoms also depend on the severity of the injury. With mild TBI, the patient may remain conscious or may lose consciousness for a few seconds or minutes. Other symptoms of mild TBI include headache, vomiting, nausea, lack of motor coordination, dizziness, difficulty balancing, dizziness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, and changes in sleep patterns.. Cognitive and emotional symptoms include changes in behavior or mood, confusion, and problems with memory, concentration, attention, or thought. Symptoms of mild TBI can also occur in moderate and severe injuries.
A person with moderate or severe TBI may experience headaches that are not lost, vomiting or recurring nausea, seizures, inability to wake up, dilation of one or both pupils, slurred speech, aphasia, dysarthria (muscle weakness causing speech impairment) , weakness or numbness of the limbs, loss of coordination, confusion, anxiety, or agitation. The common long-term symptoms of moderate to severe TBI are appropriate social behavior changes, deficits in social assessment, and cognitive changes, especially problems with sustained attention, processing speed, and executive function. Alexithymia, lack of identifying, understanding, processing, and illustrating emotions occurs in 60.9% of individuals with TBI. Cognitive and social deficits have long-term consequences for the daily lives of people with moderate to severe TBI, but can be improved by appropriate rehabilitation.
When the pressure inside the skull (intracranial pressure, abbreviated as ICP) rises too high, it can be deadly. Signs of increased ICT include decreased levels of consciousness, paralysis or weakness on one side of the body, and enlarged pupils, which fail to narrow in response to light or slow to do so. Triad Cushing, slow heartbeat with high blood pressure and respiratory depression are the classic manifestations of ICP that increase significantly. Anisocoria, unequal pupil size, is another sign of serious TBI. Abnormal posture, the typical position of the limb caused by severe diffuse injury or high ICP, is an unpleasant sign.
Young children with moderate to severe TBI may have some of these symptoms but have difficulty communicating. Other signs seen in small children include incessant crying, inability to comfort, lethargy, refusal to nurse or eat, and irritability.
Cause
The most common causes of TBI in the US include violence, transport accidents, construction, and exercise. Motorcycles are the main cause, increasing significance in developing countries due to other causes are reduced. Estimates that between 1.6 and 3.8 million traumatic brain injury each year are the result of sporting and recreational activities in the US. In children aged two to four, falling is the most common cause of TBI, while in larger children's traffic accidents competes with falling for this position. TBI is the third most common injury resulting from child abuse. Abuse causes 19% of pediatric brain trauma cases, and mortality rates are higher among these cases. Although men are twice as likely to have TBI. Domestic violence is another cause of TBI, as are occupational and industrial accidents. Firearms and blast injuries from explosions are another cause of TBI, which is the leading cause of death and disability in war zones. According to Representative Bill Pascrell (Democrat, NJ), TBI is "the signature injury of the wars in Iraq and Afghanistan." There is a promising technology called activation of a database-guided EEG biofeedback, which has been documented to restore TBI's hearing memory capability to the performance of the control group
Mechanism
Physical strength
The type, direction, intensity, and duration of strength all contribute to the characteristics and severity of TBI. Forces that can contribute to TBI include angular, rotational, shear, and translational forces.
Even without impact, significant acceleration or head deceleration can lead to TBI; But in many cases the combination of impact and acceleration may be to blame. A force that involves the head striking or being hit by something, called contact or loading impact , is the cause of most focal injuries, and the movement of the brain within the skull, termed noncontact or inertial loading , usually causing widespread injury. The baby's hard shock that causes shaken baby syndrome generally manifests as a diffuse injury. In impact loading, the force sends shock waves through the skull and brain, resulting in tissue damage. Shock waves caused by penetrating wounds can also destroy tissues along the projectile path, adding to the damage caused by the missiles themselves.
Damage may occur directly below the impact site, or may occur on the opposite side of the impact (coup and contrecoup injuries, respectively). When a moving object affects the stationary head, a coup injury is typical, whereas a contrecoup injury is usually generated when a moving head strikes an immovable object.
Primary and secondary injuries
Most people who are killed by brain trauma do not die instantly but days to weeks after the event; rather than improved after hospitalization, about 40% of TBI patients worsened. Primary brain injury (damage that occurs during trauma when the tissues and blood vessels are stretched, compressed, and torn) is insufficient to explain this damage; more precisely, this is caused by a secondary injury, a complex set of cellular processes and biochemical cascades that occur in the minutes to the day after trauma. This secondary process can dramatically exacerbate damage caused by primary injury and cause the highest number of TBI deaths occurring in hospitals.
Secondary injury events include damage to the blood-brain barrier, release of factors causing inflammation, excessive free radicals, excessive release of glutamate neurotransmitters (excitotoxicity), influx of calcium and sodium ions into neurons, and mitochondrial dysfunction. Axons injured in white matter of the brain may be separated from their body cells as a result of secondary injury, potentially killing the neurons. Another factor in secondary injury is changes in blood flow to the brain; ischemia (insufficient blood flow); cerebral hypoxia (insufficient oxygen in the brain); cerebral edema (brain swelling); and increase intracranial pressure (pressure inside the skull). Intracranial pressure may increase due to swelling or mass effect of the lesion, such as bleeding. As a result, cerebral perfusion pressure (blood flow pressure in the brain) is reduced; ischemia results. When the pressure inside the skull rises too high, it can cause brain death or herniation, in which the part of the brain is squeezed by a structure in the skull. The very weak part of the skull that is susceptible to damage that causes extradural hematoma is its ptery, in which there is a central meningeal artery, which is easily damaged in a pterion fracture. Because the pawn is very weak, this type of injury can easily occur and can become secondary to trauma to other parts of the skull where the force of impaction spreads to the pterion.
Diagnosis
Diagnosis is suspected based on the state of the lesion and clinical evidence, the most prominent of which is neurological examination, eg checking whether the pupil narrows normally in response to light and establishes a Glasgow Coma Score. Neuroimaging helps in determining the diagnosis and prognosis and in deciding what treatments should be administered.
The preferred radiological test in emergency settings is computed tomography (CT): fast, accurate, and widely available. Follow-up CT scan can be done later to determine if the injury has progressed.
Magnetic resonance imaging (MRI) can show more detail than CT, and can add information about expected results in the long run. This is more useful than CT for detecting injury characteristics such as diffuse axonal injury in the long term. However, MRI is not used in emergency settings for reasons including its relative ineffectiveness in detecting bleeding and fractures, acquisition of long drawings, inaccessibility of patients in machines, and incompatibility with metallic items used in emergency care. The MRI variant since 2012 is high definition fiber tracking (HDFT).
Other techniques can be used to confirm a particular diagnosis. X-rays are still used for head trauma, but evidence shows that they are useless; head injuries are so mild that they do not need imaging or are severe enough to get a more accurate CT. Angiography can be used to detect the pathology of blood vessels when risk factors such as head penetration trauma are involved. Functional imaging can measure blood flow or brain metabolism, summarize neuronal activity in certain areas and potentially help predict outcomes. Transcranial electroencephalography and doppler can also be used. The most sensitive physical size to date is quantitative EEG, which has documented the ability of 80% to 100% in distinguishing between subjects of normal and traumatic brain injury.
Neuropsychological assessment may be undertaken to evaluate long-term cognitive sequelae and to assist in rehabilitation planning. Instruments range from brief measurements of common mental functions to complementing batteries formed from different domain-specific tests.
Prevention
Since the main cause of TBI is a vehicle accident, their prevention or improvement of their consequences can reduce the incidence and gravity of TBI. In accidents, damage can be reduced by using seat belts, child safety chairs and motorcycle helmets, and the presence of roll bars and airbags. Educational programs exist to reduce the amount of damage. In addition, changes to public policy and safety laws may be made; these include speed limits, seat belts and helmet laws, and road engineering practices.
Changes in general practice in sports have also been discussed. Increased use of helmets may reduce the incidence of TBI. Due to the possibility that repeatedly "headed" soccer ball practice can cause cumulative brain injury, the idea of ​​introducing a head protector for the player has been proposed. Improved equipment design can enhance security; Softer baseballs reduce the risk of head injury. Rules against dangerous contact types, such as "spears" in American soccer, when one player handles another head first, can also reduce the level of head injury.
Waterfalls can be avoided by installing handles in the bathroom and handrails on stairs; erase tripping dangers such as throwing rugs; or installing window guards and safety gates at the top and bottom of stairs around small children. Playgrounds with shock-absorbing surfaces such as mulch or sand also prevent head injuries. Prevention of child abuse is another tactic; programs exist to prevent the baby's syndrome shaken by educating about the dangers of trembling children. Security of weapons, including keeping the weapons dismantled and locked, is another precaution. Studies of the influence of laws aimed at controlling access to weapons in the United States are insufficient to determine their effectiveness in preventing the number of deaths or injuries.
Recent clinical and laboratory studies by neurosurgeon Julian Bailes, M.D., and colleagues from West Virginia University, have produced papers showing that dietary supplementation with omega-3 DHA offers protection against biochemical brain damage that occurs after traumatic injury. Mice given DHA before induced brain injury experienced a smaller increase in two key markers for brain damage (APP and caspase-3), compared with mice given no DHA. "The potential of DHA to provide prophylactic benefits to the brain against traumatic injuries appears promising and requires further investigation The important concept of daily dietary supplementation with DHA, so that those at significant risk can be loaded to provide protection against the acute effects of TBI, have far-reaching public health implications ordinary. "
Furthermore, acetylcysteine ​​has been confirmed, in a recent double-blind placebo-controlled trial conducted by the US military, to reduce the effects of mild traumatic brain induced outbursts and neurological injuries to soldiers. Several studies in animals have also shown their efficacy in reducing damage associated with moderate traumatic brain or spinal cord injury, as well as ischemia-induced brain injury. In particular, it has been shown through several studies to significantly reduce neuronal loss and to improve the cognitive and neurological outcomes associated with this traumatic event. Acetylcysteine ​​has been used safely to treat paracetamol overdose for more than forty years and is widely used in emergency medicine.
Treatment
It is important to start emergency treatment in what is called "golden hour" after injury. People with moderate to severe injuries tend to receive treatment in an intensive care unit followed by a neurosurgery ward. Treatment depends on the patient's recovery stage. In the acute stage the primary goal of medical personnel is to stabilize the patient and focus on preventing further injury as little can be done to reverse the initial damage caused by the trauma. Rehabilitation is the main treatment for the subacute and chronic recovery stage. International clinical guidelines have been proposed with a view to guiding decisions in TBI care, as defined by the authoritative examination of the current evidence.
Acute stage
Certain facilities are equipped to handle TBI better than others; early steps include transporting patients to the appropriate care center. Both during transport and in hospitals, the main concern is ensuring proper oxygen supply, maintaining adequate blood flow to the brain, and controlling intracranial pressure (ICP), because high ICP removes the brain from the much-needed bloodstream and can cause brain herniation turn off. Other methods to prevent damage include management of other injuries and seizure prevention. Some data support the use of hyperbaric oxygen therapy to improve yield.
Neuroimaging is useful but not perfect in detecting ICP increases. A more accurate way to measure ICP is to place the catheter into the cerebral ventricle, which has the added benefit of allowing the cerebrospinal fluid to flow out, releasing pressure on the skull. The improved treatment of ICT may be as simple as tilting one's bed and straightening the head to increase blood flow through the veins of the neck. Tranquilizers, analgesics and paralytic agents are often used. Hypertonic saline may increase ICP by reducing the amount of brain water (swelling), although it is used with caution to avoid electrolyte imbalance or heart failure. Mannitol, osmotic diuretics, appear to be equally effective at reducing ICP. Some concerns; However, it has been raised about several studies conducted. Diuretics, drugs that increase the output of urine to reduce excess fluid in the system, can be used to treat high intracranial pressure, but can cause hypovolemia (insufficient blood volume). Hyperventilation (larger and/or faster breath) reduces carbon dioxide levels and causes blood vessels to contract; this reduces blood flow to the brain and reduces ICP, but potentially causes ischemia and is therefore only used in the short term. Corticosteroid administration is associated with an increased risk of death, so their routine use is not recommended.
Endotracheal intubation and mechanical ventilation can be used to ensure proper oxygen supply and provide a safe airway. Hypotension (low blood pressure), which has poor results in TBI, can be prevented by administering intravenous fluids to maintain normal blood pressure. Failure to maintain blood pressure can lead to inadequate blood flow to the brain. Blood pressure can be stored at an artificial high level under conditions controlled by norepinephrine or similar drugs; this helps to maintain cerebral perfusion. Body temperature is carefully regulated as temperature increases increase the need for brain metabolism, which potentially deprives nutrients. Convulsions are common. While they can be treated with benzodiazepines, these drugs are used with caution as they can suppress breathing and lower blood pressure. People with TBI are more susceptible to side effects and may react negatively or become very sensitive to some pharmacological agents. During maintenance monitoring continues for signs of damage such as decreased level of consciousness.
Traumatic brain injury can lead to serious complications of complications that include cardiac arrhythmias and neurogenic lung edema. This condition should be treated adequately and stable as part of core care.
Surgery can be performed on mass lesions or to remove objects that have penetrated the brain. Mass lesions such as bruises or hematomas cause significant mass effects (shift of intracranial structures) are considered emergencies and removed surgically. For intracranial hematoma, the collected blood may be removed using suction or forceps or may be floated with water. The surgeon looks for a blood vessel bleeding and tries to control the bleeding. In penetrating the brain injury, the damaged tissue is operated by debrided, and a craniotomy may be required. The craniotomy, in which the skull part is removed, may be necessary to remove the cracked skull fragments or objects embedded in the brain. Decompressive craniectomy (DC) is performed routinely within a very short time after TBI during surgery to treat a hematoma; skull part is removed temporarily (DC primer). DC performing hours or days after TBI to control high intracranial pressure (secondary DC) has not been shown to improve outcomes in some trials and may be associated with severe side effects.
Chronic stage
After being medically stable, people may be transferred to a subacute rehabilitation unit at a medical center or to an independent rehabilitation hospital. Rehabilitation aims to improve the functioning of independent at home and in the community and to help adapt to disability and has demonstrated its effectiveness in general, when performed by a team of health professionals specializing in head trauma. As for everyone with a neurological deficit, a multidisciplinary approach is the key to optimizing results. Physiotherapists or neurologists tend to be the key medical staff involved, but depending on the person, other medical specialists can also help. Allied health professions such as physiotherapy, speech and language therapy, cognitive rehabilitation therapy, and occupational therapy will be essential for assessing function and designing rehabilitation activities for everyone. Treatment of neuropsychiatric symptoms such as emotional stress and clinical depression may involve mental health experts such as therapists, psychologists, and psychiatrists, while neurologists can help evaluate and manage cognitive deficits.
After discharge from an inpatient rehabilitation unit, care may be given to outpatients. Community-based rehabilitation will be needed for the vast majority of people, including vocational rehabilitation; this supportive work is in line with the demands of the job on the worker's abilities. Persons with TBI who can not live independently or with a family may require care at a supported living facility such as a group home. Adequate care, including day centers and recreational facilities for people with disabilities, offers break times for carers, and activities for people with TBI.
Pharmacological treatments can help manage psychiatric or behavioral problems. Drugs are also used to control post-traumatic epilepsy; but the use of anti-epileptic prevention is not recommended. In cases where the person is bedridden due to consciousness reduction, having to stay in a wheelchair because of mobility problems, or having other problems that greatly affect the ability of self-care, nurturing and nursing is essential. The most effective study documenting the intervention approach is database activation that guides the EEG biofeedback approach, which has shown significant improvements in the retention capabilities of TBI subjects that are far superior to traditional approaches (strategy, computers, treatment interventions). The 2.61 standard deviation gains have been documented. TBI hearing memory capability is superior to the control group after treatment.
Prognosis
The prognosis worsens with the severity of the injury. Most TBI are mild and do not cause permanent or long-term disability; however, all the severity of TBI has the potential to cause significant and lasting disability. Permanent disability is estimated to occur in 10% minor injuries, 66% of moderate injuries, and 100% serious injury. Most mild TBIs are completely resolved within three weeks, and almost everyone with mild TBI can live independently and return to work they have before the injury, although some have mild cognitive and social disorders. Over 90% of people with moderate TBI can live independently, although some need help in areas such as physical ability, employment, and financial management. Most people with severe severe head injuries die or recover sufficiently to live independently; middle ground less common. Coma, being closely related to severity, is a strong predictor of poor outcomes.
Prognosis differs depending on the severity and location of the lesion, and access to specific acute management. Subarachnoid hemorrhage is about twice that of mortality. Subdural hematomas are associated with poor outcomes and increased mortality, while people with epidural hematomas are expected to have good results if they receive surgery quickly. Axonal injury diffuses can be associated with coma when severe, and poor outcomes. After the acute stage, the prognosis is strongly influenced by the involvement of patients in activities that promote recovery, which for most patients requires access to specialized intensive rehabilitation services. Measurement of Functional Independence is a way of tracking progress and independence levels during rehabilitation.
Medical complications are associated with a poor prognosis. Examples are hypotension (low blood pressure), hypoxia (low blood oxygen saturation), lower cerebral perfusion pressure and longer time spent with high intracranial pressure. Patient characteristics also affect prognosis. Factors suspected to deteriorate include substance abuse such as illicit drugs and alcohol and ages over sixty or under two years (in children, younger age at the time of injury may be associated with slower recovery of some abilities). Other influences that may affect the recovery include pre-injury intellectual ability, coping strategies, personality traits, family environment, social support systems and financial circumstances.
Life satisfaction has been known to decline for individuals with TBI soon after trauma, but evidence has shown that the role of life, age, and symptoms of depression affects the trajectory of life satisfaction over time.
Complications
Increased neurological function usually occurs for two years or more after trauma. Over the years, it is believed that recovery occurred most rapidly during the first six months, but there is no evidence to support this. This may be related to services that are generally withdrawn after this period, rather than the physiological limitations for further progress. Children recover better in the immediate time frame and increase for longer periods.
Complications are different medical problems that may arise as a result of TBI. The results of traumatic brain injury vary in type and duration; they include physical, cognitive, emotional, and behavioral complications. TBI can cause prolonged or permanent effects on consciousness, such as coma, brain death, a sedentary vegetative state (in which patients can not attain a state of alertness to interact with their environment), and a minimum conscious state (where the patient shows minimal signs of being aware self or the environment). Lie still for a long time can cause complications including pressure sores, pneumonia or other infections, multiple progressive organ failure, and deep venous thrombosis, which can cause pulmonary embolism. Infections that may follow skull fractures and penetrating injuries include meningitis and abscesses. Complications involving blood vessels include vasospasm, in which the vessels constrict and restrict blood flow, formation of aneurysms, where the vessel sides weaken and the balloon out, and stroke.
Movement disorders that can develop after TBI include tremor, ataxia (uncoordinated muscle movement), myoclonus (muscle contraction as shock), and loss of range of movement and control (especially with loss of repertoire movement). The risk of post-traumatic seizures increases with the severity of the trauma (picture on the right) and is especially increased with certain types of brain trauma such as cerebral contusions or hematoma. People with early seizures, occurring within weeks of injury, have an increased risk of post-traumatic epilepsy (recurrent seizures that occur more than a week after initial trauma). People may lose or experience vision, hearing, or olfactory changes.
Hormonal disorders can occur secondary to hypopituitarism, occurring immediately or years after injury in 10 to 15% of TBI patients. The development of diabetes insipidus or acute electrolyte abnormality after injury indicates the need for increased endocrinology. Signs and symptoms of hypopituitarism may develop and screen for adults with mild TBI and mild TBI with imaging abnormalities. Children with moderate to severe head injury may also develop hypopituitarism. Screening should be 3 to 6 months, and 12 months after the injury, but problems can occur further.
Cognitive deficits that may follow TBI include attention disorder; disturbing insights, ratings, and thoughts; reducing processing speed; distractibility; and deficits in executive functions such as abstract reasoning, planning, problem solving, and multitasking. Memory loss, the most common cognitive impairment among head injured persons, occurs in 20-79% of people with closed head trauma, depending on severity. People suffering from TBI may also have difficulty in understanding or producing spoken or written language, or with more subtle aspects of communication such as body language. Post-concussion syndrome, a series of long-lasting symptoms after mild TBI, may include physical, cognitive, emotional and behavioral problems such as headaches, dizziness, difficulty concentrating, and depression. Some TBIs may have a cumulative effect. A young boy who receives a second concussion before symptoms of another have healed may be at risk for developing a very rare but deadly condition called a second-impact syndrome, in which the brain swells recklessly even after a mild blow, with debilitating or lethal results. About one in five career boxers is affected by chronic traumatic brain injury (CTBI), which causes cognitive, behavioral, and physical disorders. Dementia pugilistica, a severe form of CTBI, affects mainly the boxer's career years after a boxing career. It generally manifests as dementia, memory problems, and parkinsonism (tremor and lack of coordination).
TBI can cause emotional, social, or behavioral problems and personality changes. These may include emotional instability, depression, anxiety, hypomania, mania, apathy, irritability, problems with social judgment, and impaired conversational skills. TBI appears to be a predisposition of survivors to psychiatric disorders including obsessive compulsive disorder, substance abuse, dysthymia, clinical depression, bipolar disorder, and anxiety disorders. In patients suffering from depression after TBI, suicidal ideas are not uncommon; the suicide rate among these people increased 2- to 3-fold. Social and behavioral symptoms that may follow TBI include disinhibition, inability to control anger, impulsivity, lack of initiative, inappropriate sexual activity, social as well as social withdrawal, and changes in personality.
TBI also has a major impact on the functioning of the family system Family members of care and TBI victims often significantly alter their family roles and responsibilities after injury, creating significant changes and tensions in the family system. Common challenges identified by families recovering from TBI include: frustration and impatience with each other, loss of life and previous relationships, difficulty setting reasonable goals, inability to effectively solve problems as family, increase stress levels and household tensions, change in emotional dynamics. , and an overwhelming desire to return to pre-injury status. In addition, families may exhibit less effective functions in various areas including coping, problem solving and communication. The psychoeducation and counseling model has proven effective in minimizing family disruption
Epidemiology
TBI is the leading cause of death and disability worldwide and presents major social, economic and health problems worldwide. This is the number one cause of a coma, it plays a major role in trauma-related disability, and is a major cause of brain damage in children and young adults. In Europe it is responsible for years of disability more than any other cause. It also plays an important role in half of traumatized deaths.
Findings at the frequency of each severity vary by definition and method used in the study. A World Health Organization study estimated that between 70 and 90% of head injuries received mild care, and a US study found that moderate and severe injuries each accounted for 10% of TBI, with the rest being mild.
TBI incidence varies by age, sex, region and other factors. The incidence and prevalence findings in epidemiological studies vary based on factors such as severity included, whether deaths were included, whether the study was restricted to hospitalized people, and the location of the study. The mild incidence of mild TBI is difficult to determine, but perhaps 100-600 people per 100,000.
Mortality
In the US, the case-fatality rate is estimated to be 21% by 30 days after TBI. A study of Iraqi War soldiers found that severe TBI carries 30-50% mortality. Death declines due to improved care and systems for managing trauma in a society rich enough to provide emergency services and modern neurosurgery. A small proportion of those who died after being hospitalized with TBI fell from almost half in 1970 to about a quarter at the beginning of the 21st century. This decline in mortality has led to an increase in the number of people living with disabilities resulting from TBI.
Biological, clinical, and demographic factors contribute to the possibility that injury will be fatal. In addition, the results depend heavily on the cause of head injury. In the US, patients with associated TBI have an 89% survival rate, while only 9% of patients with TBI associated with firearms survive. In the US, firearms are the most common cause of fatal TBI, followed by vehicle accidents and then falls. Of the deaths from firearms, 75% were considered suicides.
TBI incidence is increasing globally, primarily due to increased use of motor vehicles in low- and middle-income countries. In developing countries, car use has increased faster than the safety infrastructure can be introduced. In contrast, vehicle safety legislation has lowered TBI rates in high-income countries, which have seen a decline in traffic-related TBI since the 1970s. Every year in the United States, about two million people suffer from TBI, about 675,000 injuries are seen in the emergency department, and about 500,000 patients are hospitalized. The annual incidence of TBI is estimated to be 180-250 per 100,000 people in the US, 281 per 100,000 in France, 361 per 100,000 in South Africa, 322 per 100,000 in Australia, and 430 per 100,000 in the UK. In the EU, the annual aggregate incidence of inpatient and TBI deaths is estimated at 235 per 100,000.
Demographics
TBI is present in 85% of children who are injured traumatically, either alone or with other injuries. The largest number of TBI occurs in people aged 15-24 years. Since TBI is more common in young people, the cost to society is very high because of the loss of productive years to death and disability. The age groups most at risk for TBI are children ages five to nine and adults over the age of 80, and rates of death and hospitalization are highest because TBI resides in people over age 65. The incidence of TBI associated with falling in the country First-World Countries increases with age of population; thus the average age of people with head injuries has increased.
Regardless of age, TBI rates are higher in males. Men suffer from TBI twice as much as women and have four fatal head injury risks, and men are responsible for two-thirds of childhood and teenage head trauma. However, when matched for injury severity, women appear to be worse than men.
Socioeconomic status also appears to affect TBI rates; people with low levels of education and employment and low socioeconomic status are at greater risk.
History
Head injuries are present in ancient myths that may have existed before recorded history. The skulls found in combat graves with holes drilled above the fracture line suggest that trepanation may have been used to treat TBI in ancient times. Ancient Mesopotamia knows about head injuries and some of its effects, including seizures, paralysis, and loss of vision, hearing or speech. The Edwin Smith Papyrus, written around 1650-1550 BC, describes various head injuries and symptoms and classifies them based on their presentation and tractility. Ancient Greek physicians including Hippocrates understood the brain as the center of thought, probably because of their experience with head trauma.
The medieval and Renaissance surgeons continued the practice of trepanation for head injuries. In the Middle Ages, doctors further described the symptoms of head injury and the term concussion became more widespread. Symptoms of a concussion were first described systematically in the 16th century by Berengario da Carpi.
It was first suggested in the 18th century that intracranial pressure rather than skull damage was the cause of pathology after TBI. This hypothesis was confirmed around the end of the 19th century, and opened the skull to remove the pressure then proposed as a treatment.
In the 19th century it was noted that TBI is related to the development of psychosis. At that time there was a debate around whether post-concussion syndrome was caused by a disruption of brain tissue or psychological factors. The debate continues today.
Perhaps the first reported case of personality change after a brain injury is Phineas Gage, who survived an accident in which a large iron rod is pushed through his head, destroying one or both frontal lobes; many cases of personality changes after brain injury have been reported since then.
The 20th century saw technological advances that improved care and diagnosis such as the development of imaging tools including CT and MRI, and, in the 21st century, the diffusion of tensor imaging (DTI). The introduction of intracranial pressure monitoring in the 1950s has been credited with starting a "modern era" of head injuries. Until the 20th century, high rates of TBI death and rehabilitation were rare; improvements in care undertaken during World War I reduced mortality rates and enabled rehabilitation. Facilities dedicated to the rehabilitation of TBI were probably first established during World War I. The explosives used in World War I caused numerous blast injuries; a large amount of TBI that allows researchers to learn about the localization of brain function. The wounds associated with the explosion are now a common problem in returning veterans from Iraq & amp; Afghanistan; research has shown that such symptoms of TBI are largely similar to those of TBI involving a physical blow to the head.
In the 1970s, TBI awareness as a public health problem increased, and much progress has been made since then in brain trauma studies, such as the discovery of primary and secondary brain injury. The 1990s saw the development and dissemination of standard guidelines for TBI treatment, with protocols for various problems such as medication and intracranial pressure management. Research since the early 1990s has improved the survival of TBI; the decade was known as the "Decade of the Brain" for the advances made in brain research.
Direction of research
Drugs
No drugs were approved to stop the progression of the initial injury for secondary injury. Pathological events present opportunities to find treatments that interfere with the damage process. The neuroprotection method to reduce secondary injury, has been an interesting subject to follow TBI. However, trials to test agents that can stop this cellular mechanism have largely failed. For example, interest arises in cooling the injured brain; However, the Cochrane 2014 review did not find enough evidence to see if it was useful or not. Maintaining a normal temperature in the period immediately after TBI appears useful. One review found that lower temperatures are usually useful in adults but not children. While two other reviews found it seemed to be useless.
In addition, drugs such as NMDA receptor antagonists to stop the neurochemical cascade such as excitotoxicity show promise in animal experiments but fail in clinical trials. This failure may be due to factors including errors in the experimental design or in the inadequacy of a single agent to prevent the composition of the injury process involved in secondary injury.
Other research topics include investigations of mannitol, dexamethasone, progesterone, xenon, barbiturates, magnesium, calcium channel blockers, PPAR-? agonists, curcuminoids, ethanol, NMDA antagonists, caffeine.
Procedures
In addition to the traditional imaging modalities, there are several tools that help to monitor brain injury and facilitate research. Microdialysis allows extracellular fluid sampling for metabolite analysis that may indicate brain ischemia or metabolism, such as glucose, glycerol, and glutamate. The intraparenchymal brain oxygen monitoring system (either Licox or Neurovent-PTO) is used routinely in neurointensive care in the US. A non-invasive model called CerOx is being developed.
Research is also planned to clarify factors that correlate with outcomes in TBI and to determine in which cases it is best to perform CT scans and surgical procedures.
Hyperbaric oxygen therapy (HBO) has been evaluated in addition to treatment after TBI. The systematic review findings of Cochrane 2012 do not justify the routine use of hyperbaric oxygen therapy to treat people who are recovering from traumatic brain injury. The review also reports that only a small number of randomized controlled trials have been conducted at the time of review, many of which have poor methodological and reporting problems. HBO for controversial TBI with further evidence is needed to determine if it has a role.
Psychological
In 2010, the use of predictive visual tracking measurements to identify mild traumatic brain injury is being studied. In a visual tracking test, a head mounted display unit with eye tracking capability indicates the object is moving in a regular pattern. People without brain injury can track moving objects with smooth pursue motions and correct trajectories. This test requires attention and working memory which is a difficult function for people with mild traumatic brain injury. The question being studied, is whether the results for people with brain injury will show a visual-tracking error of relative relative to a moving target.
References
Text cited
- Boake C, Diller L (2005). "History of rehabilitation for traumatic brain injury". At WM High, Sander AM, Struchen MA, Hart KA. Rehabilitation for Traumatic Brain Injury . Oxford [Oxfordshire]: Oxford University Press. ISBNÃ, 0-19-517355-4
- Granacher RA (2007). Brain Injury Traumatic: Methods for Clinical & amp; Assessment of Forensic Neuropsychiatric, Second Edition . Boca Raton: CRC. ISBNÃ, 0-8493-8138-X
- LaPlaca MC, Simon CM, Prado GR, Cullen DR (2007). "CNS biomechanical injury and experimental model". In Weber JT. Neurotrauma: New Insights into Pathology and Treatment . Amsterdam: Academic Press. ISBNÃ, 0-444-53017-7
- "Introduction". At Marion DW. Traumatic Brain Injury . Stuttgart: Thieme. ISBNÃ, 0-86577-727-6
The original version of this article contains text from the public domain NINDS on TBI
External links
- Brain injury in Curlie (based on DMOZ)
- Brain Injury Hub - practical information and advice for parents and family members of children with acquired brain injury
- Center for Brain and Veterans' Brain Injuries - US Department of Defense Military Health System Center for traumatic brain injury
Source of the article : Wikipedia
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