Traumatic Brain Injury (TBI) - Definition and Pathophysiology - Overview, Epidemiology, Primary Injury

12/15/2016 Traumatic Brain Injury (TBI) Definition and Pathophysiology: Overview, Epidemiology, Primary Injury
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Traumatic Brain Injury (TBI) Definition and
Pathophysiology
Updated: Sep 22, 2015
Author: Segun Toyin Dawodu, JD, MD, MS, MBA, LLM, FAAPMR, FAANEM; Chief Editor: Stephen
Kishner, MD, MHA more...
OVERVIEW
Overview
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.
See Posttraumatic Stress Disorder (PTSD), a Critical Images slideshow, to help recognize the
symptoms of PTSD and to determine effective treatment options.
For excellent patient education resources, see the patient education article Concussion.
Glasgow Coma Scale
The Glasgow Coma Scale (GCS) defines the severity of a TBI within 48 hours of injury.
Eye opening
See the list below:
Spontaneous = 4
To speech = 3
To painful stimulation = 2
No response = 1
Motor response
See the list below:
Follows commands = 6
Makes localizing movements to pain = 5
Makes withdrawal movements to pain = 4
Flexor (decorticate) posturing to pain = 3
http://emedicine.medscape.com/article/326510overview 1/15
Extensor (decerebrate) posturing to pain = 2
No response = 1
Verbal response
See the list below:
Oriented to person, place, and date = 5
Converses but is disoriented = 4
Says inappropriate words = 3
Says incomprehensible sounds = 2
No response = 1
The severity of TBI according to the GCS score (within 48 h) is as follows:
Severe TBI = 38
Moderate TBI = 912
Mild TBI = 1315
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 = Confusedagitated
level V = Confusedinappropriate
level VI = Confusedappropriate
level VII = Automaticappropriate
level VIII = Purposefulappropriate
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 912 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 3point 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
A study by Thompson et al determined that in an outofhospital setting, the SMS was similar to the
GCS score for predicting TBI outcomes. [2]
Related Medscape Drugs & Diseases topics:
Classification and Complications of Traumatic Brain Injury
Neurointensive Care for Traumatic Brain Injury in Children
See Medscape's Resource Center Trauma for further information.
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 abovedefined 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 014 years, an estimated 475,000 TBIs occur each year. [6] Rates are higher
among children aged 04 years. Death and hospitalization rates are highest among black children
aged 09 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 2.56.5 million Americans live with TBIrelated 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.
Highrisk populations
Some particular segments of the populace are at increased risk of sustaining a TBI, including the
following:
Young people [7]
Lowincome 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 maletofemale mortality rate for TBI is 3.4:1. However, the causespecific 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 1530 years. The risk is highest for individuals
aged 1524 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 1524 years.
The mortality rate in patients who are elderly (65 y or older) is about 31.4 individuals per 100,000
people.
A study by Haring et al of TBI in the elderly found that between 2000 and 2010, 950,132 TBI
related hospitalizations occurred in adults aged 65 years or older in the United States, along with
107,666 TBIrelated deaths. The data, from the Nationwide Inpatient Sample, also indicated that
falls were the most common cause of injury in the elderly and occurred most often among the
oldest patients in the study. [9]
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 2030% 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 2534 years. Gunshotrelated, fatal TBIs are higher among men than
among women and are more prevalent among African Americans than they are among
whites.
Workrelated TBIs constitute an estimated 4550% 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 19982000. [10] 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 514 years.
Skull Fracture
Imaging in Skull Fractures
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. [11, 12] 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
See the list below:
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 DixHallpike 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 6080%.
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 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. [13]
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.
A study by Harish et al on the pathophysiologic differences between contusions and pericontusions
to the brain found that while contusions are characterized by inflammation, astrogliosis, petechial
hemorrhages, thrombosis, and neuronal pyknosis, pericontusions are characterized by axonal loss,
neuropil vacuole formation, edema, and dystrophic changes. Moreover, contusions were found to
be associated with immune response changes, as well as mitochondrial and synaptic dysfunction,
while pericontusions were associated with changes in the regulation of neurogenesis and
cytoskeletal architecture. The study also indicated that compared with pericontusions, contusions
lead to more severe glutathione depletion, synaptic protein loss, oxidative damage, and
mitochondrial dysfunction. [14]
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 highspeed 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). [15]
Neuropathologic findings in patients with diffuse axonal injury were graded by Gennarelli and
colleagues, as follows [16] :
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.
Brain Contusion Imaging
Emergent Management of Subarachnoid Hemorrhage [Emergency Medicine]
Subarachnoid Hemorrhage [Neurology]
Subarachnoid Hemorrhage Surgery [Neurosurgery]
Imaging in Subarachnoid Hemorrhage [Radiology]
Diffuse Axonal Injury Imaging
Penetrating Head Trauma
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 [17] :
Excitatory amino acids
Excitatory amino acids (EAAs), including glutamate and aspartate, are significantly elevated after a
TBI. [18]
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 NmethylD
aspartate receptor agonists, which also contribute to increased calcium influx, EAAs may decrease
highenergy phosphate stores (adenosine 5'triphosphate, or ATP) or increase free radical
production.
EAAs can cause astrocytic swellings via volumeactivated 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 TBIinduced stimulation of the sympathoadrenomedullary axis and
serotonergic system (with associated depression in glucose utilization [19] ), 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. [20]
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 abovementioned neurochemical transmitters and by
increased ICP. Disruption of the bloodbrain 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. [21] 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.
Chronic traumatic encephalopathy
Persons with a history of repetitive brain trauma, including boxers and football players, are at risk
for developing chronic traumatic encephalopathy (CTE), a progressive degenerative disease.
Degenerative changes, which can begin months to decades after the patient’s last brain trauma,
include atrophy of the cerebral hemispheres, medial temporal lobe, thalamus, mammillary bodies,
and brainstem. The condition is also characterized by ventricular dilatation and by fenestration of
the cavum septum pellucidum, as well as the accumulation of phosphorylated tau in the brain, with
deposits of the protein being found in the sulci and in perivascular areas of the cerebral cortex.
Symptoms of CTE include memory loss, confusion, impaired judgment, reduced impulse control,
aggression, explosive anger, depression, and progressive dementia. [22, 23, 24, 25]
According to a report from the US Department of Veterans Affairs and Boston University, 87 of 91
deceased former players for the National Football League (NFL) (96%) who donated their brains
for study were found to have CTE (although the donors had, prior to death, expressed concern that
they might have CTE and so may have had a higher proportion of the disease than does the
overall population of former NFL players). [26, 27]
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Contributor Information and Disclosures
Author
Segun Toyin Dawodu, JD, MD, MS, MBA, LLM, FAAPMR, FAANEM Attending Interventional
Physiatrist, Wellspan Health
Segun Toyin Dawodu, JD, MD, MS, MBA, LLM, FAAPMR, FAANEM is a member of the following
medical societies: American College of Sports Medicine, American Academy of Physical Medicine
and Rehabilitation, Royal College of Surgeons of England, American Association of
Neuromuscular and Electrodiagnostic Medicine, American Medical Association, American Medical
Informatics Association, Association of Academic Physiatrists, International Society of Physical and
Rehabilitation Medicine
Disclosure: Nothing to disclose.
Specialty Editor Board
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical
Center College of Pharmacy; EditorinChief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Richard Salcido, MD Chairman, Erdman Professor of Rehabilitation, Department of Physical
Medicine and Rehabilitation, University of Pennsylvania School of Medicine
Richard Salcido, MD is a member of the following medical societies: American Academy of Pain
Medicine, American Academy of Physical Medicine and Rehabilitation, American Association for
Physician Leadership, American Medical Association, Academy of Spinal Cord Injury Professionals
Chief Editor
Stephen Kishner, MD, MHA Professor of Clinical Medicine, Physical Medicine and Rehabilitation
Residency Program Director, Louisiana State University School of Medicine in New Orleans
Stephen Kishner, MD, MHA is a member of the following medical societies: American Academy of
Physical Medicine and Rehabilitation, American Association of Neuromuscular and
Electrodiagnostic Medicine
Additional Contributors
Rajesh R Yadav, MD Associate Professor, Section of Physical Medicine and Rehabilitation, MD
Anderson Cancer Center, University of Texas Medical School at Houston
Rajesh R Yadav, MD is a member of the following medical societies: American Academy of
Physical Medicine and Rehabilitation
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