Traumatic Brain Injury - Injury Essay Example

Definition Traumatic brain injury (TBI) is a nondegenerative, noncongenital insult to the brain from an external mechanical force, possibly leading to permanent or temporary impairment of cognitive, physical, and psychosocial functions, with an associated diminished or altered state of consciousness. The definition of TBI has not been consistent and tends to vary according to specialties and circumstances. Often, the term brain injury is used synonymously with head injury, which may not be associated with neurologic deficits. The definition also has been problematic with variations in inclusion criteria.

Glasgow Coma Scale The Glasgow Coma Scale (GCS) defines the severity of a TBI within 48 hours of injury. * Spontaneous = 4 * To speech = 3 * To painful stimulation = 2 * No response = 1 Motor response * Follows commands = 6 * Makes localizing movements to pain = 5 * Makes withdrawal movements to pain = 4 * Flexor (decorticate) posturing to pain = 3 * Extensor (decerebrate) posturing to pain = 2 * No response = 1 Verbal response * Oriented to person, place, and date = 5 * Converses but is disoriented = 4 * Says inappropriate words = 3 * Says incomprehensible sounds = 2

Need

essay sample on "Traumatic Brain Injury"

? We will write a cheap essay sample on "Traumatic Brain Injury" specifically for you for only $12.90/page

More Injury, Concussion Essay Topics.

* No response = 1 The severity of TBI according to the GCS score (within 48 h) is as follows: * Severe TBI = 3-8 * Moderate TBI = 9-12 * Mild TBI = 13-15 Ranchos Los Amigos Scale of Cognitive Functioning The severity of deficit in cognitive functioning can be defined by the Ranchos Los Amigos Scale. * level I = No response * level II = Generalized response * level III = Localized response * level IV = Confused-agitated * level V = Confused-inappropriate * level VI = Confused-appropriate * level VII = Automatic-appropriate * level VIII = Purposeful-appropriate

TBI defined by the Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation Medicine The Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation Medicine defines mild head injury as “a traumatically induced physiologic disruption of brain function, as manifested by one of the following: * Any period of loss of consciousness (LOC), * Any loss of memory for events immediately before or after the accident, * Any alteration in mental state at the time of the accident, * Focal neurologic deficits, which may or may not be transient.

” The other criteria for defining mild TBI include the following: * GCS score greater than 12 * No abnormalities on computed tomography (CT) scan * No operative lesions * Length of hospital stay less than 48 hours The following criteria define moderate TBI: * Length of stay at least 48 hours * GCS score of 9-12 or higher * Operative intracranial lesion * Abnormal CT scan findings The National Institutes of Health Traumatic Coma Data Bank The National Institutes of Health (NIH) sponsored the Traumatic Coma Data Bank (TCDB).

[1] The TCDB revealed that severe TBI is indicated when the GCS score is below 9 within 48 hours of the injury. Simplified Motor Score (SMS) The SMS is a 3-point scale developed to address the perceived limitations of the GCS, such as its complexity and poor interrater reliability. The points are as follows: * Obeys commands = 2 points * Localizes pain = 1 point * Withdraws to pain or worse = 0 points Epidemiology Inconsistency in the definition and classification of traumatic brain injury (TBI), along with discrepancies in data collection, has made the epidemiology of TBI difficult to describe accurately.

Problems with TBI data collection include the fact many patients with mild TBI may not present to the hospital, and the ones who do present may be discharged at the emergency department (ED) without adequate documentation. Severe TBI with associated death at the scene of the accident or during transport to a hospital also may not be accounted for completely in data collection for TBI epidemiologic studies. Differences in diagnostic tools and admission criteria also may affect the above-defined severity classifications.

In the past, the use of roentgenograms to help diagnose skull fractures after head injury did not show much of any concurrent intracranial lesions. These lesions were difficult to diagnose until the advent of CT scanning, which is now the diagnostic imaging of choice in TBI cases. [3, 4] Other confounding variables in determining the epidemiology of TBI exist. The use of different definitions that may not clearly define the type of injury (see Synonyms, Key Words, and Related Terms) makes the epidemiology of TBI difficult to describe.

Another variable is the difference in findings from diagnostic imaging at different time intervals (eg, when early epidural hematoma is present, the CT scan may be normal, but if the scan is later repeated, it may show evidence of pathology). [3, 5] TBI accounts for approximately 40% of all deaths from acute injuries in the United States. Annually, 200,000 victims of TBI need hospitalization, and 1. 74 million persons sustain mild TBI requiring an office visit or temporary disability for at least 1 day. The financial cost is estimated at approximately $4 billion per year.

This estimate includes the loss of potential income of the patient and of relatives (who may need to become caregivers), the cost of acute care, and other medical expenses, such as continuous ambulatory and rehabilitation care. Mortality rate Approximately 52,000 US deaths per year result from TBI. Local factors in the United States may influence this mortality rate; it is lowest in the Midwest and Northeast and is highest in the South. The mortality rate for deaths outside of the hospital is approximately 17 per 100,000 people; it is approximately 6 per 100,000 people for patients who are hospitalized.

The initial GCS score and, therefore, the severity of the TBI help to predict the likelihood of death from the injury. The mortality rate is high in severe TBI and is low in moderate TBI. In a TCDB study, the mortality rate in severe TBI was about 33%; in another study, in Central Virginia, the mortality rate in moderate TBI was found to be 2. 5%. Among children aged 0-14 years, an estimated 475,000 TBIs occur each year. [6] Rates are higher among children aged 0-4 years. Death and hospitalization rates are highest among black children aged 0-9 years, compared with whites, in TBIs related to motor vehicle accidents (MVAs).

Prevalence and incidence The prevalence (ie, the existing cases at any given time) of TBI is not well documented, because most cases (ie, mild TBI) are not fatal, and patients may not have been hospitalized. Estimates often are based on existing disabilities. Estimates by the National Institutes of Health Consensus Development Panel on Rehabilitation of Persons with TBI showed that 2. 5-6. 5 million Americans live with TBI-related disabilities. A National Health Interview Survey estimated that annually, 1. 9 million persons sustain a skull fracture or intracranial injury, with such trauma making up approximately 1% of all injuries.

That incidence of mild TBI is about 131 cases per 100,000 people, the incidence of moderate TBI is about 15 cases per 100,000 people, and the incidence of severe TBI is approximately 14 cases per 100,000 people. The inclusion of prehospital deaths increases the last figure to 21 cases per 100,000 people. Differences in rates in various parts of the United States may be attributable to differences in the methods of case verification and in the cause of injury. High-risk populations Some particular segments of the populace are at increased risk of sustaining a TBI, including the following: * Young people[7]

* Low-income individuals * Unmarried individuals * Members of ethnic minority groups * Residents of inner cities * Men[7] * Individuals with a history of substance abuse * Individuals who have suffered a previous TBI Sex Men are approximately twice as likely as women to sustain a TBI. [8] This ratio approaches parity as age increases because of the increased likelihood of TBI caused by falls, for which males and females have similar risks in later life. The male-to-female mortality rate for TBI is 3. 4:1. However, the cause-specific ratio for firearm-related injuries is 6:1, while that for injuries related to MVAs is 2.

4:1. Age Injury is the leading cause of death among Americans younger than 45 years; TBI is the major cause of death related to injury. The risk of TBI peaks when individuals are aged 15-30 years. The risk is highest for individuals aged 15-24 years. [8] Peak age is similar for males and females. Twenty percent of TBIs occur in the pediatric age group (ie, birth to 17 y). The highest mortality rate (32. 8 cases per 100,000 people) is found in persons aged 15-24 years. The mortality rate in patients who are elderly (65 y or older) is about 31. 4 individuals per 100,000 people.

Mechanism of injury Common causes of fatal injuries vary according to gender, age, race, and geographical location. Such causes are as follows: * MVAs are the leading cause of TBI in the general population, especially among whites in the United States. MVAs account for approximately 50% of all TBIs. In the United Kingdom, MVAs are the third most common cause of TBI, after falls and assaults. * Falls are the second leading cause of TBI. Falls account for 20-30% of all TBIs. In individuals aged 75 years or older, falls are the most common cause of TBI.

Very young persons also commonly sustain TBI due to falls. * Firearms are the third leading cause of TBI (12% of all TBIs) and are a leading cause of TBI among individuals aged 25-34 years. Gunshot-related, fatal TBIs are higher among men than among women and are more prevalent among African Americans than they are among whites. * Work-related TBIs constitute an estimated 45-50% of all TBIs. Incidence varies from 37 cases per 100,000 people for military employees (57% are related to transportation) to 15 cases per 100,000 people for civilians (50% are because of falls).

* While the incidence of TBIs from major causes decreased significantly following the introduction of safety measures (eg, seatbelts, helmets), the rate of TBI from gunshots has increased. * Alcohol is a major factor in many TBIs and often is associated with the leading causes of TBI. Prevention The use of helmets by cyclists has led to fewer TBIs, and the cases that do occur are less severe than they were in prehelmet days. Automobile seatbelts and child restraints also have been associated with reduced TBI morbidity and mortality rates. No data currently address the effects of air bag use on TBI mortality and morbidity rates.

Trends The incidence of TBI has been decreasing because of the introduction of preventive measures and as a result of better enforcement of drunk driving laws. The length of stay in acute hospitals and rehabilitation facilities has been declining because of the increased demand for facilities and because of the resources that are available in the community for patients who are discharged early. Update on mild TBI The National Hospital Ambulatory Medical Care Survey, published in February 2005, looked at mild TBI in the United States from 1998-2000.

[9] The survey found that the average rate of mild TBI was 503. 1 cases per 100,000 population, with peaks among males at 590 cases per 100,000 population, among Native Americans at 1026 cases per 100,000 population, among persons younger than 5 years at 1115. 2 cases per 100,000 population, and in the Midwest region of the United States at 578. 4 cases per 100,000 population. Sports and bicycles account for about 26. 4% of mild TBIs among children aged 5-14 years. Related eMedicine topics: * Skull Fracture * Skull, Fractures Previous Next Section: Epidemiology

Pathophysiology: Primary Injury Overview Traumatic brain injury (TBI) is the result of an external mechanical force applied to the cranium and the intracranial contents, leading to temporary or permanent impairments, functional disability, or psychosocial maladjustment. [10, 11] TBI can manifest clinically from concussion to coma and death. Injuries are divided into 2 subcategories: (1) primary injury, which occurs at the moment of trauma, and (2) secondary injury, which occurs immediately after trauma and produces effects that may continue for a long time.

This section focuses on primary injury, while the next section focuses on secondary injury. The physical mechanisms of brain injury are classified using the following categories: * Impact loading – Collision of the head with a solid object at a tangible speed * Impulsive loading – Sudden motion without significant physical contact * Static or quasistatic loading – Loading in which the effect of speed of occurrence may not be significant Impact loading causes TBI through a combination of contact forces and inertial forces.

Inertial force ensues when the head is set in motion with or without any contact force, leading to acceleration of the head. Contact force occurs when impact injury is delivered to the head at rest. Static or quasistatic loading is rare and occurs when a slowly moving object traps the head against a fixed rigid structure and gradually squeezes the skull, causing many comminuted fractures that may be enough to deform the brain and lead to fatal injury. Contact or inertial forces may strain the brain tissue beyond its structural tolerance, leading to injury.

Strain is the amount of tissue deformation caused by an applied mechanical force. The 3 basic types of tissue deformation are as follows: * Compressive – Tissue compression * Tensile – Tissue stretching * Shear – Tissue distortion produced when tissue slides over other tissue Types of Primary Injuries Primary injuries can manifest as focal injuries (eg, skull fractures, intracranial hematomas, lacerations, contusions, penetrating wounds), or they can be diffuse (as in diffuse axonal injury). Skull fractures * Skull fractures can be vault fractures or basilar fractures.

* Hematoma, cranial nerve damage, and increased brain injury may be associated with skull fractures. * Vault fractures tend to be linear and may extend into the sinuses. Injuries also can be stellate, closed, or open fractures. Closed fractures do not permit communication with the outside environment, while the open fractures do. Fractures are defined as depressed or nondepressed, depending on whether or not the fragments are displaced inwardly. A simple fracture is defined as having 1 bone fragment; a compound fracture exists when there are 2 or more bone fragments.

* Basal skull fractures often are caused by dissipated force and may be associated with injuries to the cranial nerves and discharges from the ear, nose, and throat. Auditory/vestibular dysfunction Impact force to the temporal region may not cause a fracture but may lead to possible conductive or sensorineural hearing loss. Conductive hearing loss results from a defect in the conduction of sound, which may occur as a result of tympanic perforation, hemotympanum, or ossicular (ie, malleus, incus, stapes) disruption. Sensorineural hearing loss may be secondary to defect in the inner ear (eg, acute cochlear concussion, perilymphatic fistula).

Benign paroxysmal positional vertigo can occur when calcium carbonate crystals become dislodged from the macula of the utricle and move into the posterior semicircular canal. In such cases, vertigo can provoked by any sudden change in head position. The diagnostic test for this condition is the Dix-Hallpike maneuver. Intracranial hemorrhages Several types of intracranial hemorrhages can occur, including the following: * Epidural hematoma occurs from impact loading to the skull with associated laceration of the dural arteries or veins, often by fractured bones and sometimes by diploic veins in the skull’s marrow.

More often, a tear in the middle meningeal artery causes this type of hematoma. When hematoma occurs from laceration of an artery, blood collection can cause rapid neurologic deterioration. * Subdural hematoma tends to occur in patients with injuries to the cortical veins or pial artery in severe TBI. The associated mortality rate is high, approximately 60-80%. * Intracerebral hemorrhages occur within the cerebral parenchyma secondary to lacerations or to contusion of the brain, with injury to larger, deeper cerebral vessels occurring with extensive cortical contusion.

* Intraventricular hemorrhage tends to occur in the presence of very severe TBI and is, therefore, associated with an unfavorable prognosis. * Subarachnoid hemorrhage may occur in cases of TBI in a manner other than secondary to ruptured aneurysms, being caused instead by lacerations of the superficial microvessels in the subarachnoid hemorrhage may occur in cases of TBI in a manner other than secondary to ruptured aneurysms, being caused instead by lacerations of the superficial microvessels in the subarachnoid space.

If not associated with another brain pathology, this type of hemorrhage could be benign. Traumatic subarachnoid hemorrhage may lead to a communicating hydrocephalus if blood products obstruct the arachnoid villi or in the event of a noncommunicating hydrocephalus secondary to a blood clot obstructing the third or fourth ventricle. * Coup and contrecoup contusions * A combination of vascular and tissue damage leads to cerebral contusion.

[12] * Coup contusions occur at the area of direct impact to the skull and occur because of the creation of negative pressure when the skull, distorted at the site of impact, returns to its normal shape. * Contrecoup contusions are similar to coup contusions but are located opposite the site of direct impact. Cavitation in the brain, from negative pressure due to translational acceleration impacts from inertial loading, may cause contrecoup contusions as the skull and dura matter start to accelerate before the brain on initial impact.

* The amount of energy dissipated at the site of direct impact determines whether the ensuing contusion is of the coup or contrecoup type. Most of the energy of impact from a small, hard object tends to dissipate at the impact site, leading to a coup contusion. In contrast, impact from a larger object causes less injury at the impact site, because energy is dissipated at the beginning or end of the head motion, leading to a contrecoup contusion. * Concussions * Concussion is caused by deformity of the deep structures of the brain,

leading to widespread neurologic dysfunction that can result in impaired consciousness or coma. Concussion is considered a mild form of diffuse axonal injury. * Diffuse axonal injury * Diffuse axonal injury is characterized by extensive, generalized damage to the white matter of the brain. Strains of the tentorium and falx during high-speed acceleration/deceleration produced by lateral motions of the head may cause the injuries. Diffuse axonal injury also could occur as a result of ischemia.

[5] In addition, primary blast exposure can lead to some axonal injury, which can be detected using diffusion tensor imaging (DTI). [13] * Neuropathologic findings in patients with diffuse axonal injury were graded by Gennarelli and colleagues, as follows[14] : * Grade 1 – Axonal injury mainly in parasagittal white matter of the cerebral hemispheres * Grade 2 – As in Grade 1, plus lesions in the corpus callosum * Grade 3 – As in Grade 2, plus a focal lesion in the cerebral peduncle * Penetrating head injuries

* Gunshot wounds and missile/nonmissile projectiles cause many penetrating head injuries. The energy dissipated on entry is equal to 1/2 mass x velocity squared. Therefore, high velocity missiles tend to cause the most profound damage. * Related eMedicine topics: * Brain, Contusion * Subarachnoid Hemorrhage [Emergency Medicine] * Subarachnoid Hemorrhage [Neurology] * Subarachnoid Hemorrhage [Neurosurgery] * Subarachnoid Hemorrhage [Radiology] * Diffuse Axonal Injury * Penetrating Head Trauma * Previous * Next Section: Epidemiology

* Pathophysiology: Secondary Injury * Secondary types of traumatic brain injury (TBI) are attributable to further cellular damage from the effects of primary injuries. Secondary injuries may develop over a period of hours or days following the initial traumatic assault. * Secondary brain injury is mediated through the following neurochemical mediators[15] : * Excitatory amino acids * Excitatory amino acids (EAAs), including glutamate and aspartate, are significantly elevated after a TBI. [16] * EAAs can cause cell swelling, vacuolization, and neuronal death.

* EAAs can cause an influx of chloride and sodium, leading to acute neuronal swelling. EAAs can also cause an influx of calcium, which is linked to delayed damage. Along with N-methyl-D-aspartate receptor agonists, which also contribute to increased calcium influx, EAAs may decrease high-energy phosphate stores (adenosine 5′-triphosphate, or ATP) or increase free radical production. * EAAs can cause astrocytic swellings via volume-activated anion channels (VRACs). Tamoxifen is a potent inhibitor of VRACs and potentially could be of therapeutic value. * Endogenous opioid peptides

* These may contribute to the exacerbation of neurologic damage by modulating the presynaptic release of EAA neurotransmitters. * Activation of the muscarinic cholinergic systems in the rostral pons mediates behavioral suppression, which often is observed in TBI, as well as LOC. * Heightened metabolism in the injured brain is stimulated by an increase in the circulating levels of catecholamines from TBI-induced stimulation of the sympathoadrenomedullary axis and serotonergic system (with associated depression in glucose utilization[17] ), contributing to further brain injury.

* Other biochemical processes leading to a greater severity of injury include an increase in extracellular potassium, leading to edema; an increase in cytokines, contributing to inflammation; and a decrease in intracellular magnesium, contributing to calcium influx. * Based on the effect on astrocytes, which are the cells that exhibit hypertrophic and hyperplastic responses to central nervous system (CNS) injury, increased production of protein kinase B/Akt with activation of P2 purinergic receptors has been implicated in neuronal survival in TBIs. [18] * Increased intracranial pressure (ICP)

* The severity of a TBI tends to increase due to heightened ICP, especially if the pressure exceeds 40 mm Hg. Increased pressure also can lead to cerebral hypoxia, cerebral ischemia, cerebral edema, hydrocephalus, and brain herniation. * Cerebral edema * Edema may be caused by the effects of the above-mentioned neurochemical transmitters and by increased ICP. Disruption of the blood-brain barrier, with impairment of vasomotor autoregulation leading to dilatation of cerebral blood vessels, also contributes. * Hydrocephalus * The communicating type of hydrocephalus is more common in TBI than is the noncommunicating type.

The communicating type frequently results from the presence of blood products that cause obstruction of the flow of the cerebral spinal fluid (CSF) in the subarachnoid space and the absorption of CSF through the arachnoid villi. The noncommunicating type of hydrocephalus is often caused by blood clot obstruction of blood flow at the interventricular foramen, third ventricle, cerebral aqueduct, or fourth ventricle. * Brain herniation * Supratentorial herniation is attributable to direct mechanical compression by an accumulating mass or to increased intracranial pressure.

[19] The following types of supratentorial herniation are recognized: * Subfalcine herniation – The cingulate gyrus of the frontal lobe is pushed beneath the falx cerebri when an expanding mass lesion causes a medial shift of the ipsilateral hemisphere. This is the most common type of herniation. * Central transtentorial herniation – This type of injury is characterized by the displacement of the basal nuclei and cerebral hemispheres downward while the diencephalon and adjacent midbrain are pushed through the tentorial notch.

* Uncal herniation – This type of injury involves the displacement of the medial edge of the uncus and the hippocampal gyrus medially and over the ipsilateral edge of the tentorium cerebelli foramen, causing compression of the midbrain; the ipsilateral or contralateral third nerve may be stretched or compressed. * Cerebellar herniation – This injury is marked by an infratentorial herniation in which the tonsil of the cerebellum is pushed through the foramen magnum and compresses the medulla, leading to bradycardia and respiratory arrest. hemorrhage may occur in cases of TBI in a manner other than secondary to

ruptured aneurysms, being caused instead by lacerations of the superficial microvessels in the subarachnoid space. If not associated with another brain pathology, this type of hemorrhage could be benign. Traumatic subarachnoid hemorrhage may lead to a communicating hydrocephalus if blood products obstruct the arachnoid villi or in the event of a noncommunicating hydrocephalus secondary to a blood clot obstructing the third or fourth ventricle. * Coup and contrecoup contusions * A combination of vascular and tissue damage leads to cerebral contusion.

[12] * Coup contusions occur at the area of direct impact to the skull and occur because of the creation of negative pressure when the skull, distorted at the site of impact, returns to its normal shape. * Contrecoup contusions are similar to coup contusions but are located opposite the site of direct impact. Cavitation in the brain, from negative pressure due to translational acceleration impacts from inertial loading, may cause contrecoup contusions as the skull and dura matter start to accelerate before the brain on initial impact.

* The amount of energy dissipated at the site of direct impact determines whether the ensuing contusion is of the coup or contrecoup type. Most of the energy of impact from a small, hard object tends to dissipate at the impact site, leading to a coup contusion. In contrast, impact from a larger object causes less injury at the impact site, because energy is dissipated at the beginning or end of the head motion, leading to a contrecoup contusion. * Concussions * Concussion is caused by deformity of the deep structures of the brain, leading to widespread neurologic dysfunction that can result in impaired consciousness or coma.

Concussion is considered a mild form of diffuse axonal injury. * Diffuse axonal injury * Diffuse axonal injury is characterized by extensive, generalized damage to the white matter of the brain. Strains of the tentorium and falx during high-speed acceleration/deceleration produced by lateral motions of the head may cause the injuries. Diffuse axonal injury also could occur as a result of ischemia. [5] In addition, primary blast exposure can lead to some axonal injury, which can be detected using diffusion tensor imaging (DTI). [13]

* Neuropathologic findings in patients with diffuse axonal injury were graded by Gennarelli and colleagues, as follows[14] : * Grade 1 – Axonal injury mainly in parasagittal white matter of the cerebral hemispheres * Grade 2 – As in Grade 1, plus lesions in the corpus callosum * Grade 3 – As in Grade 2, plus a focal lesion in the cerebral peduncle * Penetrating head injuries * Gunshot wounds and missile/nonmissile projectiles cause many penetrating head injuries. The energy dissipated on entry is equal to 1/2 mass x velocity squared. Therefore, high velocity missiles tend to cause the most profound damage.

* Related eMedicine topics: * Brain, Contusion * Subarachnoid Hemorrhage [Emergency Medicine] * Subarachnoid Hemorrhage [Neurology] * Subarachnoid Hemorrhage [Neurosurgery] * Subarachnoid Hemorrhage [Radiology] * Diffuse Axonal Injury * Penetrating Head Trauma * Pathophysiology: Secondary Injury * Secondary types of traumatic brain injury (TBI) are attributable to further cellular damage from the effects of primary injuries. Secondary injuries may develop over a period of hours or days following the initial traumatic assault. * Secondary brain injury is mediated through the following neurochemical mediators[15] : * Excitatory amino acids

* Excitatory amino acids (EAAs), including glutamate and aspartate, are significantly elevated after a TBI. [16] * EAAs can cause cell swelling, vacuolization, and neuronal death. * EAAs can cause an influx of chloride and sodium, leading to acute neuronal swelling. EAAs can also cause an influx of calcium, which is linked to delayed damage. Along with N-methyl-D-aspartate receptor agonists, which also contribute to increased calcium influx, EAAs may decrease high-energy phosphate stores (adenosine 5′-triphosphate, or ATP) or increase free radical production.

* EAAs can cause astrocytic swellings via volume-activated anion channels (VRACs). Tamoxifen is a potent inhibitor of VRACs and potentially could be of therapeutic value. * Endogenous opioid peptides * These may contribute to the exacerbation of neurologic damage by modulating the presynaptic release of EAA neurotransmitters. * Activation of the muscarinic cholinergic systems in the rostral pons mediates behavioral suppression, which often is observed in TBI, as well as LOC.

* Heightened metabolism in the injured brain is stimulated by an increase in the circulating levels of catecholamines from TBI-induced stimulation of the sympathoadrenomedullary axis and serotonergic system (with associated depression in glucose utilization[17] ), contributing to further brain injury. * Other biochemical processes leading to a greater severity of injury include an increase in extracellular potassium, leading to edema; an increase in cytokines, contributing to inflammation; and a decrease in intracellular magnesium, contributing to calcium influx.

* Based on the effect on astrocytes, which are the cells that exhibit hypertrophic and hyperplastic responses to central nervous system (CNS) injury, increased production of protein kinase B/Akt with activation of P2 purinergic receptors has been implicated in neuronal survival in TBIs. [18] * Increased intracranial pressure (ICP) * The severity of a TBI tends to increase due to heightened ICP, especially if the pressure exceeds 40 mm Hg. Increased pressure also can lead to cerebral hypoxia, cerebral ischemia, cerebral edema, hydrocephalus, and brain herniation. * Cerebral edema

* Edema may be caused by the effects of the above-mentioned neurochemical transmitters and by increased ICP. Disruption of the blood-brain barrier, with impairment of vasomotor autoregulation leading to dilatation of cerebral blood vessels, also contributes. * Hydrocephalus * The communicating type of hydrocephalus is more common in TBI than is the noncommunicating type. The communicating type frequently results from the presence of blood products that cause obstruction of the flow of the cerebral spinal fluid (CSF) in the subarachnoid space and the absorption of CSF through the arachnoid villi.

The noncommunicating type of hydrocephalus is often caused by blood clot obstruction of blood flow at the interventricular foramen, third ventricle, cerebral aqueduct, or fourth ventricle. * Brain herniation * Supratentorial herniation is attributable to direct mechanical compression by an accumulating mass or to increased intracranial pressure. [19] The following types of supratentorial herniation are recognized: * Subfalcine herniation – The cingulate gyrus of the frontal lobe is pushed beneath the falx cerebri when an expanding mass lesion causes a medial shift of the ipsilateral hemisphere.

This is the most common type of herniation. * Central transtentorial herniation – This type of injury is characterized by the displacement of the basal nuclei and cerebral hemispheres downward while the diencephalon and adjacent midbrain are pushed through the tentorial notch. * Uncal herniation – This type of injury involves the displacement of the medial edge of the uncus and the hippocampal gyrus medially and over the ipsilateral edge of the tentorium cerebelli foramen, causing compression of the midbrain; the ipsilateral or contralateral third nerve may be stretched or compressed.

* Cerebellar herniation – This injury is marked by an infratentorial herniation in which the tonsil of the cerebellum is pushed through the foramen magnum and compresses the medulla, leading to bradycardia and respiratory arrest. (Dawodu, Segun. “tramatic brain injury. ” . N. p. , 10 2011. Web. 3 Dec 2012. ) Abstract Pupillary abnormalities are commonly seen in patients presenting with severe traumatic brain injury (TBI).

The objectives of this study were to determine the underlying condition responsible, the natural history of recovery of third nerve palsy and the ultimate clinical outcome in 60 patients admitted to a regional neurosurgical centre with a diagnosis of TBI and unilateral or bilateral fixed, dilated pupils (FDP). In approximately three-quarters of cases, some form of road traffic incident was the mechanism of injury. In patients presenting with a unilateral FDP, the CT-defined condition was most commonly diffuse brain injury (49%) with no obvious lateralising condition.

In 34% of cases CT demonstrated a lateralising condition ipsilateral to the side of the FDP and in 9% cases the FDP was contralateral to the side of the CT abnormality. Of those patients who survived an FDP, 72% were left with some form of ophthalmological deficit. Most patients with bilateral FDP did not survive (88%); however, of those who did survive, none was left in a persistent vegetative state or with any ophthalmological sequelae. A FDP is a grave prognostic sign following TBI commonly resulting in long term ophthalmological sequelae; however, a favourable outcome is still attainable.

(“Fixed, Dilated Pupils Following Traumatic Brain Injury: Historical Perspectives, Causes and Ophthalmological Sequelae. ” (http://link. springer. com/chapter/10. 1007/978-3-7091-0956-4_57? LI=true. N. p. , n. d. Web. 3 Dec 2012. ) Percentage on traumatic brain injury causes * Falls-35% * Struck by / against motor vehicle 17. 3% * Events-16. 5% * Assaults-10% (http://link. springer. com/chapter/10. 1007/978-3-7091-0956-4_57? LI=true. N. p. , n. d. Web. 3 Dec 2012. ) What are the effects of a traumatic brain injury? * What are the mental health-related effects of TBI that I need to be aware of? * What can I do about the effects of TBI?

* What can I do to manage the effects of TBI? * Take the next step – Make the connection. * Explore these resources for more information about TBI in Veterans. Traumatic brain injury (TBI) can occur when something outside the body hits the head with significant force. Whether it is a head hitting the windshield during a car accident, an impact from a fall, head injuries received during sports or other recreational activities , or trauma from a nearby blast or explosion, TBI can cause changes in a person’s ability to think, control emotions, walk, or speak, and can also affect sense of sight or hearing.

TBI can be mild to severe. Mild traumatic brain injury refers to brief changes in or loss of consciousness. Severe traumatic brain injury refers to longer periods of unconsciousness and memory loss around the event. While it may be easier to diagnose moderate to severe TBI, changes caused by any TBI could significantly affect many areas of a person’s life. TBI can result in changes in a person’s physical functioning, thinking abilities or cognitive function, and behavioral effects and they are often interrelated. These effects sometimes cause other difficulties such as sleeping problems, depression, and anxiety.

Physical effects may include: “I was having trouble seeing. Everything was blurry, the headaches were non-stop, I couldn’t get measurements and I was confused all the time. All of these were symptoms of a brain injury—we just didn’t know it yet. ” * Headaches * Difficulty speaking * Blurry eyesight * Trouble hearing * Loss of energy * Change in sense of taste or smell * Dizziness or trouble with balance Cognitive effects may include: * Difficulty concentrating * Trouble with attention * Forgetfulness * Difficulty making decisions * Repeating things Behavioral effects may include:

* Becoming angry easily * Getting frustrated easily * Acting without thinking ( “Coping with TBI to improve quality of life. ” Effects of Traumatic Brain Injury. make the connection . Web. 4 Dec 2012. ) How is TBI diagnosed? The speech-language pathologist (SLP) works with the person and his or her family/caregivers as part of a team that may also include: * doctors * nurses * neuropsychologists * occupational therapists * physical therapists * social workers * employers * teachers The team works together to evaluate the person and develop an appropriate treatment plan.

The SLP completes a formal evaluation of speech and language skills. An oral motor evaluation checks the strength and coordination of the muscles that control speech. Understanding and use of grammar (syntax) and vocabulary (semantics), as well as reading and writing, are evaluated. Social communication skills (pragmatic language) are evaluated with formal tests and the role-playing of various communication scenarios. The person may be asked to discuss stories and the points of view of various characters. Does he or she understand how the characters are feeling, and why they are reacting a certain way?

Can he or she explain how different characters’ actions affect what happens in the story? The person may be asked to interpret/explain jokes, sarcastic comments, or absurdities in stories/pictures (e. g. , what is strange about a person using an umbrella on a sunny day? ). The SLP will assess cognitive-communication skills. Is the person aware of his or her surroundings? Does the person know his or her name, the date, where he or she is, what happened to him or her (orientation)? Recent memory skills are assessed, such as whether the main details in a short story are retained. Executive functioning is evaluated.

The SLP assesses the patient’s ability to plan, organize, and attend to details (e. g. , completing all of the steps for brushing teeth). The SLP may read an incomplete story and ask for a logical beginning, middle, or conclusion. The person may be asked to provide solutions to problems (reasoning and problem solving; e. g. , “What would you do if you locked your keys in your car? How can this problem be avoided in the future? “). For more information about when to refer someone for a cognitive-communication evaluation, see Cognitive-Communication Referral Guidelines for Adults.

If problems are observed, the SLP will evaluate swallowing and make recommendations regarding management and treatment. The focus of this evaluation will be to ensure that the individual is able to swallow safely and receive adequate nutrition. Additional swallowing tests may be recommended as a result of this evaluation. If necessary, the SLP may also evaluate the benefit of a communication aid or device to express basic needs and ideas. To contact a speech-language pathologist, visit ASHA’s Find a Professional. What other organizations have information about TBI?

This list is not exhaustive, and inclusion does not imply endorsement of the organization or the content of the Web site by ASHA. * The Brain Injury Association * The Brain Injury Information Network * Head Injury Hotline (a nonprofit clearinghouse founded and operated by a head injury activist since 1985) * WETA’s Brainline. oHow is TBI diagnosed? * The speech-language pathologist (SLP) works with the person and his or her family/caregivers as part of a team that may also include: * doctors * nurses * neuropsychologists * occupational therapists

* physical therapists * social workers * employers * teachers * The team works together to evaluate the person and develop an appropriate treatment plan. * The SLP completes a formal evaluation of speech and language skills. An oral motor evaluation checks the strength and coordination of the muscles that control speech. Understanding and use of grammar (syntax) and vocabulary (semantics), as well as reading and writing, are evaluated. * Social communication skills (pragmatic language) are evaluated with formal tests and the role-playing of various communication scenarios.

The person may be asked to discuss stories and the points of view of various characters. Does he or she understand how the characters are feeling, and why they are reacting a certain way? Can he or she explain how different characters’ actions affect what happens in the story? The person may be asked to interpret/explain jokes, sarcastic comments, or absurdities in stories/pictures (e. g. , what is strange about a person using an umbrella on a sunny day? ). * The SLP will assess cognitive-communication skills. Is the person aware of his or her surroundings?

Does the person know his or her name, the date, where he or she is, what happened to him or her (orientation)? Recent memory skills are assessed, such as whether the main details in a short story are retained. Executive functioning is evaluated. The SLP assesses the patient’s ability to plan, organize, and attend to details (e. g. , completing all of the steps for brushing teeth). The SLP may read an incomplete story and ask for a logical beginning, middle, or conclusion. The person may be asked to provide solutions to problems (reasoning and problem solving; e. g.

, “What would you do if you locked your keys in your car? How can this problem be avoided in the future? “). * For more information about when to refer someone for a cognitive-communication evaluation, see Cognitive-Communication Referral Guidelines for Adults. * If problems are observed, the SLP will evaluate swallowing and make recommendations regarding management and treatment. The focus of this evaluation will be to ensure that the individual is able to swallow safely and receive adequate nutrition. Additional swallowing tests may be recommended as a result of this evaluation.

* If necessary, the SLP may also evaluate the benefit of a communication aid or device to express basic needs and ideas. * To contact a speech-language pathologist, visit ASHA’s Find a Professional. * What other organizations have information about TBI? * This list is not exhaustive, and inclusion does not imply endorsement of the organization or the content of the Web site by ASHA. * The Brain Injury Association * The Brain Injury Information Network * Head Injury Hotline (a nonprofit clearinghouse founded and operated by a head injury activist since 1985) * WETA’s Brainline. org

( “traumatic brain injury . ” http://www. asha. org/. N. p.. Web. 4 Dec 2012. ) In the United States, nearly 1. 5 million individuals suffer traumatic brain injury (TBI) each year, 13,000 children receive services for TBI in the public schools, and it is estimated that nearly 5. 3 million people live with TBI-related disabilities. Adolescents and young adults age 15–24 have the highest incidence of TBI, typically associated with motor vehicle accidents. Older adults over the age of 65 and children under the age of 5 have the next highest incidence of TBI, most commonly resulting from falls.

Males are nearly twice as likely to experience a TBI than females, and individuals with TBI are three times more likely to incur a subsequent TBI. The financial consequences of TBI are staggering. It is estimated that over $48 billion is spent in the United States alone on acute medical and rehabilitation services each year for the treatment of TBI. For acute care, the average length of stay is 22 days, and the average cost is $98,000 per patient. For inpatient rehabilitation, the average length of stay is 32 days, and the average cost is $43,000 per patient. Evidence-Based Practice Guidelines

Recently, a national trend of referencing research evidence to support clinical decision making for the management of medical conditions has surfaced. Consistent with this movement, the Academy of Neurologic Communication Disorders and Sciences—in conjunction with ASHA’s Special Interest Division 2, Neurophysiology and Neurogenic Speech and Language Disorders—established committees of experts to develop evidence-based practice guidelines (EBPGs). The guidelines cover the management of dysarthria, aphasia, dementia, apraxia of speech, and cognitive-communication disorders following traumatic brain injury.

The committee developing the EBPGs for TBI identified several assumptions about the nature and management of cognitive-communication disorders following TBI (see sidebar on page 7). In addition, the committee delineated five modules for organizing the research evidence, including remediation of attention, memory, social skills, and metacognition/executive function, as well as assessment tools and procedures. Technical reports on EBPGs for each module will be compiled. To date the EBPG-TBI committee has submitted two reports that will be published in the Journal of Medical Speech-Language Pathology.

A few reports from other EBPG committees have already appeared in that journal. Family Involvement Family involvement is important in all stages of recovery and rehabilitation. In the early stages of care, the family should be encouraged to participate in the development of the treatment plan with the rehabilitation team. The family may be instructed to assist with specific treatment activities and to promote carryover. Family education is an ongoing process with the primary goal of developing the skills necessary to assist the individual with TBI at home and in the community.

The rehabilitation team also assists the family in planning for the future and becoming an advocate for the individua l with TBI. Caring for a person with a TBI can be an overwhelming responsibility. Many families and caregivers are unaware of the medical, financial, or social implications of brain injury and are uncertain how or where to find information. Although there are many sources that can be consulted, the Internet is often a good place to start. Many Web sites offer links to specific information regarding regional and local resources that may provide answers to questions families may not think to ask.

Culturally and Linguistically Diverse Populations TBI occurs in all culturally and linguistically diverse populations. Cultural competence is integral to serving these populations. Cultural competence is the consonant set of behaviors, attitudes, and policies within an individual or organization that allows that person or group to interact effectively with individuals from different cultural backgrounds. The ability to function adeptly and actively in cross-cultural contexts is critical to delivering meaningful services to culturally and linguistically diverse populations.

Clinicians must evaluate the individual’s cultural and linguistic context, selecting and implementing TBI assessments and intervention programs that are culturally relevant and meaningful. It is equally important for clinicians to understand how the cultural and linguistic background of individuals with TBI influences their feelings about health and health care. Clinicians also need to examine their own biases and value system and be aware of how their beliefs influence interactions with individuals with TBI.

By identifying and addressing the cultural and linguistic factors that may hinder or foster intervention, clinicians can increase the chances for the success of services (see sidebar above). Through cultural competence, clinicians can provide better care for individuals with TBI from unique cultural backgrounds, laying the foundations for better outcomes. School Re-Entry Many children with TBI return to school and often experience difficulty learning new information, understanding abstract material, learning in the

presence of distractions, and organizing information. In addition, their impaired social and pragmatic skills affect relationships with peers, teachers, and family members. Transitional planning must carefully address these issues to promote the student’s academic success, which will determine future social and vocational competency. Successful re-entry to school involves collaboration among the student, the parents, and staff from the school and medical facility in developing and conducting assessment and intervention procedures.

Ongoing, authentic assessments of students with TBI are critical to providing effective intervention. The nature of the SLP’s intervention in the educational setting depends on the learning needs of the student. For students with less severe injuries, the clinician may provide services through consultation and offering instructional strategies to family members, classroom teachers, and support staff. A pullout or classroom-based program may be appropriate for students with more intensive cognitive-communicative needs.

Along with the remediation of other cognitive abilities, effective intervention must address communication and social skills, necessitating the participation of family, peers, and teachers in functional situations. Community Reintegration Returning to the community following a TBI can be challenging. The literature emphasizes that persistent cognitive impairments frequently impede successful community reintegration. Even those individuals who make significant gains in rehabilitation may experience difficulty when returning to premorbid activities.

Community reintegration should emphasize a multidisciplinary approach, which also includes peers and family, in the attempt to close the gap between treatment activities and functional competence in the individual’s natural environment. The primary focus of community reintegration should be on what the individual with TBI needs to achieve for returning to work, school, and avocational interests (see sidebar above). Ongoing assessment of progress and modification of goals is critical to the success of any community reintegration program. (Youse, K. M. , Le, K. N. , Cannizzaro, M. S. & Coelho, C.

A. (2002, June 25). Traumatic Brain Injury : A Primer for Professionals. The ASHA Leader. ) Strategies for Community Reintegration Community/Family Environment * Assess family’s ability to facilitate cognitive remediation in the home * Provide clear demonstrations and multiple opportunities for the individual with TBI and family to practice new skills * Increase opportunities for socialization and recreation to reestablish social networks * Allow the individual with TBI to systematically assume greater responsibility for planning and completing activities Work Environment

* Conduct assessment in the actual place of employment * Evaluate social and physical obstacles * Use a job coach to facilitate success on the job * Integrate adaptation and compensatory strategies Working With Culturally and Linguistically Diverse Groups * Identify the cultural and linguistic background of the individual with TBI * Learn about the culture, beliefs, and values of the individual with TBI and how these affect attitudes toward injury and management of health * Use culturally relevant and meaningful assessment and intervention tools.

* Seek thoughts and feelings of family members and involve them in clinical decision-making and intervention process * Create and distribute culturally appropriate materials to promote awareness of TBI and available resources in the community * Use interpreters and translators with appropriate training * Conduct ongoing advocacy and outreach on TBI through community/cultural centers * Conduct cultural competence assessment Managing Cognitive-Communication Disorders Following TBI 1. Management of cognitive-communication disorders is an integral part of SLPs’ scope of practice.

SLPs are uniquely trained to manage these disorders with clinical knowledge in the interaction between cognition and communication. 2. Managing cognitive-communication disorders is an interdisciplinary endeavor. 3. Cognitive-communication intervention does not include communication intervention for aphasia or motor-speech disorders following TBI. 4. There are many approaches to cognitive-communication intervention—behavioral approaches, skill training, process-specific approaches, and multi-modal approaches. 5.

Numerous service delivery models exist—in-patient medical rehabilitation, long-term care, outpatient care, job coaching, school-based services, day-treatment, transitional living programs, or individual and group therapy. 6. Improvements in impairments may or may not facilitate a change in an individual’s activity or participation level and vice versa. 7. The ultimate goal of cognitive-communication intervention is to achieve the highest level of communicative participation in everyday living. TBI Prevention

Motor Vehicles * Using a seatbelt in combination with an airbag reduces the risk of head injury by 81%, compared to 60% for seatbelts alone * Children should ride in age and size appropriate car seats; learn to use car seats properly (www. safekids. org) * Children under the age of 12 years should never ride in the front seat of a car equipped with an airbag * Never drink and drive—41% of individuals with TBI test positive for alcohol at time of injury Bicycles * Always wear a helmet, even on short rides

* Wearing reflective clothing allows riders to be seen at dusk or at night * Bicycles should have a headlight and reflectors * Children should ride on sidewalks or paths until they are at least 10 years old or show the ability to follow basic rules of the road Motorcycles * Wearing a motorcycle helmet reduces the risk of a brain injury by 67% * Obey speed limits—40% of motorcyclists who die in crashes are speeding * Turn headlight on every time you ride * Don’t carry passengers until you are skilled at driving in all kinds of conditions * Take a motorcycle safety course—call 800-446-9227

Playground Safety * Supervise children at all times * Children should always play on equipment that is age appropriate * Choose playgrounds with soft under-surfaces that will cushion a fall * Make sure there is fencing between the playground and the street * Check playground equipment to be certain it is in good repair Preventing Falls Among Older Adults * Begin an exercise program to increase strength and balance * Use non-slip mats in the bathtub and on shower floors * Remove things that can be easily tripped over * Improve lighting in the home

* Wear shoes with good support and non-slip soles Stages of Recovery 1. Coma: unresponsive; eyes closed 2. Vegetative state: no cognitive responses; gross wakefulness; sleep-wake cycles 3. Minimally conscious state: purposeful wakefulness; responds to some commands 4. Confusional state: recovered speech; amnesic (PTA); severe attentional deficits; agitated; hypoaroused; possible labile behavior 5. Postconfusional, evolving independence: resolution of PTA; cognitive improvement; achieving independence in daily self-care; improving social interaction; developing independence at home 6.

Social competence, community re-entry: recovering cognitive abilities; goal-directed behaviors; social skills; personality; developing independence in the community; returning to academic or vocational pursuits Reprinted with permission from: Sohlberg, M. M. , & Mateer, C. A. (2001). Cognitive rehabilitation: An integrative neuropsychological approach. NY: Guilford Press. Severity Classification| GCS Score| Duration of Coma| Length of PTA| Severe| 3–8| Over 6 hours| Over 24 hours| Moderate| 9–12| Less than 6 hours| 1–24 hours| Mild| 13–15| 20 minutes or less| 60 minutes or less| Reprinted with permission from: Sohlberg, M.

M, & Mateer, C. A. (2001). Cognitive rehabilitation: An integrative neuropsychological approach. NY: Guilford Press. Improving Cognitive-Communicative and Social Skills Cognitive-Communicative * Present new material in an organized and sequential manner with clear explanations, using visual aids or other teaching aids * Provide repetitions and multiple opportunities for practicing new skills * Encourage responsiveness and allow adequate time for the client to respond * Use alternative or augmentative communication where appropriate and functional * Focus on attention and memory skills

* Promote the use of higher level thinking (i. e. , problem-solving, reasoning) Social Skills * Allow the client to participate in the selection and prioritization of target skills * Facilitate acquisition and understanding of client’s social knowledge * Create awareness of social settings, social interactions, and corresponding appropriate modes of behavior and communication * Educate and train family members how to best interact with client * Focus on self-monitoring and self-evaluating behavior and performance * Use role-playing and scripting to practice social interactions .

(Youse, K. M. , Le, K. N. , Cannizzaro, M. S. & Coelho, C. A. (2002, June 25). Traumatic Brain Injury : A Primer for Professionals. The ASHA Leader. )

Haven't found the Essay You Want?

Get your custom essay sample

For Only $13/page