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TRAUMATIC BRAIN
INJURY
Jassin M. Jouria, MD
Dr. Jas+ of academic medicine, and medical
author. He graduated from Ross University
School of Medicine and has completed his
clinical clerkship training in various teaching
hospitals throughout New York, including
King’s
County
Hospital
Center
and
Brookdale Medical Center, among others. Dr. Jouria has passed all USMLE medical board
exams, and has served as a test prep tutor and instructor for Kaplan. He has developed
several medical courses and curricula for a variety of educational institutions. Dr. Jouria has
also served on multiple levels in the academic field including faculty member and
Department Chair. Dr. Jouria continues to serves as a Subject Matter Expert for several
continuing education organizations covering multiple basic medical sciences. He has also
developed several continuing medical education courses covering various topics in clinical
medicine. Recently, Dr. Jouria has been contracted by the University of Miami/Jackson
Memorial Hospital’s Department of Surgery to develop an e-module training series for
trauma patient management. Dr. Jouria is currently authoring an academic textbook on
Human Anatomy & Physiology.
Abstract
Traumatic brain injury (TBI) is a major health issue that can lead to physical
and mental disability as well as morbidity. The brain anatomy and
physiology is discussed as well as the medical evaluation and diagnosis of a
TBI. Additionally, the lifelong challenge of patient quality of life and
implications to patients’ family members are a major focus with emphasis on
current and newer medial and alternative approaches of therapy to promote
improved health and wellbeing.
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Continuing Nursing Education Course Planners
William A. Cook, PhD, Director, Douglas Lawrence, MA, Webmaster,
Susan DePasquale, MSN, FPMHNP-BC, Lead Nurse Planner
Policy Statement
This activity has been planned and implemented in accordance with the
policies of NurseCe4Less.com and the continuing nursing education
requirements of the American Nurses Credentialing Center's Commission on
Accreditation for registered nurses. It is the policy of NurseCe4Less.com to
ensure objectivity, transparency, and best practice in clinical education for
all continuing nursing education (CNE) activities.
Continuing Education Credit Designation
This educational activity is credited for 5 hours. Nurses may only claim credit
commensurate with the credit awarded for completion of this course activity.
Statement of Learning Need
Identifying current research and guidelines related to traumatic brain
injuries is needed to support health providers and nurses in order to help
reduce TBI-related morbidity and improve patient care outcomes.
Assessment tools and testing to assist in the diagnosis of a TBI is needed to
appropriately develop a treatment plan and to select new technology that
supports improved care.
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Course Purpose
To provide nursing professionals with knowledge of how to care for the
patient with a TBI as well as for the needs of their family.
Target Audience
Advanced Practice Registered Nurses and Registered Nurses
(Interdisciplinary Health Team Members, including Vocational Nurses and
Medical Assistants may obtain a Certificate of Completion)
Course Author & Planning Team Conflict of Interest Disclosures
Jassin M. Jouria, MD, William S. Cook, PhD, Douglas Lawrence, MA,
Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures
Acknowledgement of Commercial Support
There is no commercial support for this course.
Activity Review Information
Reviewed by Susan DePasquale, MSN, FPMHNP-BC
Release Date: 1/29/2016
Termination Date: 1/29/2019
Please take time to complete a self-assessment of knowledge, on page 4,
sample questions before reading the article.
Opportunity to complete a self-assessment of knowledge learned will be
provided at the end of the course.
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1.
Head trauma may include an alteration in consciousness that
involves any trauma to the
a. scalp
b. skull
c. brain
d. All of the above.
2.
A majority of traumatic brain injury cases occur as the result of
a. gunshot wounds
b. transportation accidents
c. sports injuries
d. domestic violence
3.
Mild injuries typically cause all EXCEPT:
a. brief, change in mental status.
b. seizure disorder.
c. no long-term adverse affects.
d. temporary loss of consciousness.
4.
The nervous system is comprised of two regions:
a. Central Nervous System and Peripheral Nervous System
b. Central Nervous System and Autonomic Nervous System
c. Autonomic Nervous System and Peripheral Nervous System
d. Autonomic and Parasympathetic Nervous Systems.
5.
The cranial bones include the
a. frontal, temporal, occipital, parietal, lacrimal
b. foramen magnum, frontal, temporal, occipital, parietal
c. maxilla, malar, temporal, occipital, parietal
d. foramen magnum, volar, frontal, temporal, occipital
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Introduction
Traumatic brain injury has many causes, including sports injuries, violence,
vehicular accidents, and falls. Each instance is unique and outcomes can be
difficult to predict, which is why every patient with a potential traumatic
brain injury (TBI) needs to be appropriately assessed and provided with
immediate, intensive care to address his or her needs. Traumatic brain
injuries can present with a wide array of symptoms and every symptom
needs to be treated seriously. Even cases that present as mild can become
serious in a matter of seconds. Over 5 million people in the United States are
survivors of traumatic brain injuries. Many of them have long-term
disabilities as a result of their injury. Medical professionals who understand
the unique needs of TBI patients are the key to minimizing the potential
impact of these disabilities.
Health care providers must be familiar with the different causes and types of
head injury to adequately treat trauma patients. In many instances, head
injury will accompany other trauma-induced injuries. Therefore, all trauma
patients must be evaluated for head injuries, even if no signs are present.
Many head injuries will not produce immediate symptoms, even if significant
damage has occurred.1 A patient should be evaluated using standard
guidelines and diagnostic imaging, if appropriate.2 When a head injury is
detected, treatment should begin immediately to avoid further
complications.
Overview Of TBI
Head trauma involves any trauma to the scalp, skull or brain and may
include an alteration in consciousness, even if it is brief. Patients who
experience head trauma will have a range of symptoms depending on the
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type of injury, the force, the location and the severity of the injury. In some
patients, the injury will be mild and resolve over a short period of time.
However, in other patients, the trauma will produce severe injuries that have
long-term effects.
The most common causes of head trauma include:3

Motor vehicle accidents

Firearm-related injuries

Falls

Assaults

Sports-related injuries

Recreational accidents
Traumatic Brain Injury is one of the most common trauma related injuries,
and is the most severe form of head trauma. According to the Center for
Disease Control, approximately 1.7 million traumatic brain injuries occur
each year.4 Many of these injuries occur along with other injuries. While
traumatic brain injury is considered one type of head trauma, it is
sometimes used to refer to most head injuries that a patient experiences. In
fact, some providers use the term traumatic brain injury interchangeably
with head trauma.
Traumatic brain injury is commonly referred to as either TBI, acquired brain
injury, or head injury.5 It is caused by a sudden trauma to the head that
causes damage to the brain. Depending on how the trauma occurs, the
resulting damage may be focal or it can be diffuse.6 Traumatic brain injury
can result from either a closed head injury or from a penetrating head
injury.4
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Traumatic brain injury is the direct result of a blow to the head. However,
not all forces to the head cause traumatic brain injury. Depending on a
number of factors, such as the level of impact and the type of object, the
severity of the injury may range from non-existent to severe.7 In instances
where the force actually causes some level of trauma, the injury will range
from mild to severe.4 Mild injuries typically cause a minor, or brief, change in
mental status. Mild injuries may result in a temporary loss of consciousness,
but there will be no long-term adverse affects.8 Severe injuries can result in
full, extended loss of consciousness. They may also cause short or long-term
amnesia.9 Throughout all levels of injury, TBI produces a range of functional
and sensory changes. These changes impact the patient’s movement,
thinking, sensation, language, and emotions.4
Many of the symptoms of traumatic brain injury develop over time and may
not appear for a number of days or weeks. In some rare cases, the
symptoms may not appear for months.10 Many patients with mild traumatic
brain injury will recover within a number of weeks or months, although some
symptoms may persist for longer.6 In patients who experience moderate to
severe traumatic brain injury, the recovery time is greater. In fact, many
moderate to severe TBI patients never fully recover.11 Many TBI symptoms
are life long complications. According to the Center for Disease Control
(CDC), approximately 5.3 million Americans are living with a TBI-related
disability.4
A majority of traumatic brain injury cases (approximately half) occur as the
result of transportation accidents, which includes automobiles, motorcycles,
bicycles, and pedestrian accidents. These accidents are the major cause of
TBI in people under age 75.5 For those 75 and older, falls cause the majority
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of TBIs.12 Approximately 20% of TBIs are due to violence, such as firearm
assaults and child abuse, and about 3% are due to sports injuries.10
The cause of the TBI plays a role in determining the patient’s outcome. For
example, approximately 91% of firearm TBIs (two-thirds of which may be
suicidal in intent) result in death, while only 11% of TBIs from falls result in
death.10 Civilians and military personnel in combat zones are also at
increased risk for TBIs. The leading causes of such TBI are bullets,
fragments, blasts, falls, motor vehicle-traffic crashes, and assaults. Blasts
are a leading cause of TBI for active-duty military personnel in war zones.13
Anatomy and Physiology of the Brain
The head is a complex region comprised of various components, all of which
can be injured during head trauma situations. The components of the head
and brain are outlined below.
Nervous System
The brain is part of the nervous system and operates in conjunction with
other parts of the body to provide operative functions.14 The nervous system
is comprised of two regions:

Central Nervous System (CNS)

Peripheral Nervous System (PNS)
The central nervous system houses the brain and spinal cord, while the
peripheral nervous system is comprised of spinal nerves and cranial
nerves.15 The spinal nerves branch from the spinal cord outward and the
cranial nerves branch from the brain outward. The peripheral nervous
system also houses the autonomic nervous system.14 The autonomic
nervous system controls various functions including:16
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
Breathing

Digestion

Heart rate

Secretion of hormones
Scalp15
The scalp is the soft tissue that covers the entire area of the skull. It is
comprised of five layers:

Skin

Connective tissue

Epicranial aponeurosis

Loose areolar tissue

Pericranium
The first three layers of the scalp are joined together to form one unit, but
the unit is able to move freely along the loose areolar tissue that covers the
pericranium. The pericranium adheres to the calvaria (skullcap).14
Skull16
The skull provides protection for the brain. It consists of two distinct regions:
Cranial Bones:

Foramen Magnum

Frontal

Temporal

Occipital

Parietal
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Facial Bones:

Lacrimel bone

Inferior nasal conchae

Vomer

Nasal bone

Malar

Maxilla bone

Mandible bone
A dense white fibrous membrane called the periosteum, which is very
vascular, covers the skull bone. The periosteum provides nutrition to the
bone cells through branches that it sends into the bone. These nutrients are
necessary for brain growth and repair. At the base of the skull is the
foramen magnum, which is an opening in the occipital bone through which
the spinal cord passes.17
Meninges15
The region between the brain and the skull is called the meninges. This area
is comprised of three layers of tissue. The tissue covers the brain and the
spinal cord and provides protection to both areas. The three layers of the
meninges are:

Dura mater

Arachnoid

Pia mater
The dura mater is the outermost layer of the meninges, and the pia mater is
the innermost layer. The dura mater contains two layers of membrane. The
outer layer is called the periosteum and the inner layer is the dura. The dura
lines the inside of the entire skull. It helps protect and secure the brain by
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creating small folds and compartments. The folds of the dura are called the
falx and the tentorium. The right and left side of the brain is separated by
the falx. The upper and lower parts of the brain are separated by the
tentorium.16
The arachnoid layer of the meninges is thin and delicate and contains a
number of blood vessels. It covers the entire surface of the brain. The space
between the dura and arachnoid membranes is referred to as the subdural
space.18
The pia mater is the layer of the meninges that is located closest to the
surface of the brain. The pia mater is comprised of a number of blood
vessels that branch far into the brain. The pia covers the entire surface of
the brain and follows the folds of the brain. Major arteries supply blood. The
area between the arachnoid and the pia is referred to as the subarachnoid
space, which contains cerebrospinal fluid.19
Cranial Vault (brain)
The cranial vault is the region of the head that houses the cerebrum,
cerebellum, and brainstem.14 The cranial vault is comprised of the following
components:20

Brain tissue (80%)

Cerebral Spinal Fluid (CSF) (10%)

Blood (within blood vessels) (10%)
The following table provides descriptions of each area of the cranial vault.15
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Region
Description
The cerebrum is the largest part of the brain and is composed of
right and left hemispheres. It performs higher functions like
interpreting touch, vision and hearing, as well as speech, reasoning,
emotions, learning, and fine control of movement.
The surface of the cerebrum has a folded appearance called the
cortex. The cortex contains about 70% of the 100 billion nerve
cells. The nerve cell bodies color the cortex grey-brown giving it the
Cerebrum
name – gray matter. Beneath the cortex is long connecting fibers
between neurons, called axons, which make up the white matter.
The folding of the cortex increases the brain’s surface area allowing
more neurons to fit inside the skull and enabling higher functions.
Each fold is called a gyrus, and each groove between folds is called
a sulcus. There are names for the folds and grooves that help
define specific brain regions.
The cerebellum is located under the cerebrum. Its function is to
Cerebellum
coordinate muscle movements, maintain posture, and balance.
The brainstem includes the midbrain, pons, and medulla. It acts as
a relay center connecting the cerebrum and cerebellum to the
spinal cord. It performs many automatic functions such as
Brainstem
breathing, heart rate, body temperature, wake and sleep cycles,
digestion, sneezing, coughing, vomiting, and swallowing.
Ten of the twelve cranial nerves originate in the brainstem.
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Right and Left Hemispheres
The brain is divided into two
hemispheres, the right
hemisphere and the left
hemisphere, which are joined by
the corpus callosum fibers.
These fibers are responsible for
delivering messages to each
hemisphere. The right
hemisphere controls the left
side of the body and the left
hemisphere controls the right
side of the body.16,21
The left hemisphere controls the
following functions:

Speech

Comprehension

Arithmetic

Writing
The right hemisphere controls the following functions:

Creativity

Spatial ability

Artistic skills

Musical skills
Injury to the cranial vault commonly produces an increase in intracranial
pressure. Ultimately, according to the Monroe-Kellie Doctrine, when the
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volume of any of the three cranial components increases, the volume of one
or both of the others must decrease or the intracranial pressure will rise.22
Intracranial volume typically increases when the patient experiences cerebral
edema, intracranial mass, or an increase in blood or cerebral spinal fluid.23
Lobes:
The right and left hemisphere is further divided into lobes by fissures. Each
hemisphere contains four lobes:24

Frontal

Temporal

Parietal

Occipital
Each of the lobes is divided into areas that control specific functions.
However, while the lobes are divided, they do not function independently.
The complexity of the cranial cavity requires consistent relationships
between the various lobes as well as between the left and right
hemispheres.14
The following table provides information on the different functions of each
lobe.16
Lobe
Frontal
Lobes
Function
The frontal lobes are the largest of the four lobes responsible for many
different functions. These include motor skills such as voluntary
movement, speech, intellectual and behavioral functions. The areas that
produce movement in parts of the body are found in the primary motor
cortex or precentral gyrus. The prefrontal cortex plays an important part
in memory, intelligence, concentration, temper and personality.
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The premotor cortex is a region found beside the primary motor cortex.
It guides eye and head movements and a person’s sense of orientation.
Broca's area, important in language production, is found in the frontal
lobe, usually on the left side.
Occipital
Lobes
These lobes are located at the back of the brain and enable humans to
receive and process visual information. They influence how humans
process colors and shapes. The occipital lobe on the right interprets
visual signals from the left visual space, while the left occipital lobe
performs the same function for the right visual space.
Parietal
Lobes
These lobes interpret simultaneously, signals received from other areas
of the brain such as vision, hearing, motor, sensory and memory. A
person’s memory and the new sensory information received, give
meaning to objects.
Temporal
Lobes
These lobes are located on each side of the brain at about ear level, and
can be divided into two parts. One part is on the bottom (ventral) of
each hemisphere, and the other part is on the side (lateral) of each
hemisphere.
An area on the right side is involved in visual memory and helps
humans recognize objects and peoples' faces. An area on the left side is
involved in verbal memory and helps humans remember and
understand language. The rear of the temporal lobe enables humans to
interpret other people’s emotions and reactions.
Vascular System
Regular and consistent blood flow is crucial to the maintenance of brain
activity. Approximately 20% of the cardiac output of blood is used for
arterial blood flow.14 The brain is responsible for the regulation of blood flow
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over various blood pressure ranges using vasodilation or vasoconstriction of
the arteries.23 Blood is supplied to the brain by two primary arteries:25

Carotid:
These arteries are responsible for providing circulation to the anterior
region of the brain. The anterior region of the brain includes the
frontal, temporal, partial, and occipital lobes. The carotid arteries
supply the brain with approximately 80% of the blood flow.

Vertebral Arteries:
The vertebral arteries are responsible for the posterior circulation of
the brain. These arteries join together and form the basilar artery.
The vertebral arteries provide approximately 20% of the blood flow to
the brain.
While the anterior and posterior circulation function independent of each
other, they often communicate with each other using communicating
arteries that come together to form the Circle of Willis.18 The Circle of Willis
responds to decreased arterial flow by establishing a protective mechanism.
It shunts blood from the anterior to posterior regions of the brain, or vice
versa. This protective measure helps delay the deteriorating neurological
signs and symptoms that are often present in patients.15
The following table provides an overview of the different arterial regions and
functions.14
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Anterior Circulation
Anterior Cerebral
Supplies most medial portions of frontal lobe and superior medial
Artery (ACA)
parietal lobes.
Anterior
Connects the anterior cerebral arteries at their closest juncture.
Communicating
Artery (AcomA)
Internal Carotid
Ascends through the base of the skull to give rise to the anterior
Artery (ICA)
and middle cerebral arteries, and connects with the posterior half of
the circle of Willis via the posterior communicating artery.
Middle Cerebral
Trifurcates off the ICA and supplies the lateral aspects of the
Artery (MCA)
temporal, frontal and parietal lobes.
Posterior Circulation
Posterior
Connects to the anterior circle of Willis with the posterior cerebral
Communicating
artery of vertebral-basilar circulation posteriorly.
Artery (PcomA)
Posterior Cerebral
Supplies the occipital lobe and the inferior portion of the temporal
Artery (PCA)
lobe. A branch supplies the choroid plexus.
Basilar Artery
Formed by the junction of the two vertebral arteries, it terminates
(BA)
as a bifurcation into the posterior and cerebral arteries supplying
the brainstem.
Vertebral Artery
The vertebrals emerge from the posterior base of the skull
(VA)
(Foramen Magnum) and merge to form the basilar artery supplying
the brainstem.
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Cranial Nerves
The brain includes twelve cranial nerves that control specific bodily
functions.26 The following is a list of the cranial nerves and the functions that
they control:27

Olfactory: Smell

Optic: Visual fields and ability to see

Oculomotor: Eye movements and eyelid opening

Trochlear: Eye movements

Trigeminal: Facial sensation

Abducens: Eye movements

Facial: Eyelid closing, facial expression, and taste sensation

Auditory/vestibular: Hearing and sense of balance

Glossopharyngeal: Taste sensation and swallowing

Vagus: Swallowing and taste sensation

Accessory: Control of neck and shoulder muscles

Hypoglossal: Tongue movement
Hypothalamus
The hypothalamus is directly responsible for sending messages to the
pituitary gland.15 The structure itself is very small, but it contains a number
of nerve connections that make communication between the hypothalamus
and the pituitary gland possible.28 The hypothalamus receives information
from the autonomic nervous system and is responsible for the following
functions:14

Eating

Sexual behavior

Sleeping

Body temperature regulation
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
Emotions

Hormone secretion

Movement
Brain Stem
The brainstem is the part of the brain that connects the brain to the spinal
cord. It is located in front of the cerebellum.23 The brainstem is comprised of
three components:16

Midbrain – responsible for ocular motion

Pons – responsible for coordinating eye and facial movements, facial
sensations, hearing, and balance

Medulla Oblongata – controls breathing, blood pressure, heart
rhythms, and swallowing
The pons and the brainstem transmit messages from the cortex to the spinal
cord and are responsible for maintaining the basic life functions.29 If this
area of the brainstem is damaged or destroyed, it can cause brain death in
the patient.30 Humans require these basic functions to survive and if
transmission is interrupted, survival is not possible.20
The midbrain, pons, medulla and part of the thalamus contain the reticular
activating system. This system is responsible for controlling wakefulness as
well as attentiveness and the regulation of sleep patterns.14
The brainstem contains ten of the twelve cranial nerves that control the
following:16

Hearing

Eye movement
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
Facial sensations

Taste

Swallowing

Movements of the face, neck, shoulder and tongue muscles
Brain Cells
The two types of cells contained within the brain are the neurons and glial
cells. They are sometimes referred to as the neuroglia and glia. There are
approximately 50% more glial cells than neurons.31 The primary job of the
neuron is to send and receive nerve impulses and signals.32 The glial cells
are responsible for the following:14

Provide nutrition

Provide support

Maintain homeostasis

Form myelin

Facilitate signal transmission in the nervous system
Cerebrospinal Fluid (CSF)
Cerebrospinal fluid is a clear, watery substance that surrounds the brain and
the spinal cord. It provides a cushion that helps protect the brain and spinal
cord from injury.27 The fluid constantly circulates throughout the various
channels around and within the spinal cord and brain. It is absorbed and
replenished on a continuous basis.16 The fluid is produced within the
ventricles, which are hollow channels within the brain.33 The chorois plexus
is the ventricle structure that is responsible for the majority of cerebrospinal
fluid. Typically, the amount of CSF that is produced is balanced with the
amount that is absorbed.15
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Ventricles
There are four cavities that comprise the ventricular system. The four
cavities are referred to as ventricles.34 They are connected by a series of
holes that are referred to as foramen, as well as tubes.15 The cerebral
hemisphere contains two ventricles referred to as the lateral ventricles.
Their job is to communicate with the third ventricle using a separate opening
that is called the Foramen of Munro.35 The third ventricle serves as the
center of the brain, with walls comprised of the thalamus and the
hypothalamus.14 The Aqueduct of Sylvius is a long tube that connects the
third ventricle to the fourth ventricle.28
Other Parts of the Brain
Limbic System:
The limbic system includes the hypothalamus, the thalamus, the amygdala,
and the hippocampus. All of these components are involved in hormone and
emotional regulation.20
Pineal Gland:
The pineal gland is attached to the posterior region of the third ventricle.
There is no concrete understanding of the exact role of the pineal gland.
However, there is some indication that it plays a role in sexual maturation.16
Pituitary Gland:
The pituitary gland is located at the base of the brain within the region
known as the pituitary fossa or sella turcica. This area is located behind the
nose.14 The pituitary gland controls the secretion of hormones and is
responsible for the control and coordination of the following activities:32
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
Growth and development

The function of various body organs (i.e., kidneys, breasts and uterus)

The function of other glands (i.e., thyroid, gonads, and adrenal glands)
Due to the fact that the pituitary gland is responsible for controlling hormone
secretion, it is often referred to as the “Master Gland.”20
Thalamus:23
The thalamus is comprised of the basal ganglia as well as four components:

Hypothalamus

Epythalamus

Ventral thalamus

Dorsal thalamus
The thalamus is responsible for transmitting all information to and from the
cortex. The primary information that is transmitted by the thalamus
includes:16

Pain sensation

Attention

Alertness
Types Of TBI
The injuries sustained during head trauma are complex as they are impacted
by a number of factors, including the type of trauma, the amount of force,
the region, and the region injured. Since the head and brain involve a
number of different structures that operate both independent of and with
each other, injuries can range from mild to severe. Injuries can affect more
than one area of the brain, which can cause complex injuries. Head injuries
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are caused when an object strikes the head and transfers force to the brain
tissue. The type of trauma is either blunt or penetrating.
Blunt trauma produces a closed head injury, while penetrating trauma
produces an open injury.10 When a patient experiences blunt trauma, one of
the following types of force will occur:36

Deceleration

Acceleration

Acceleration-deceleration

Rotational

Deformation
The following is an explanation of the different injuries that can occur as a
result of the forces listed above:37
Deceleration forces occur when the head hits an immovable object
such as the forehead hitting the windshield. This causes the skull to
decelerate rapidly. The brain moves slower than the skull causing the
brain tissue to collide with skull. As the brain moves over the bony
prominences, it can stretch, shear or tear the tissue. Acceleration
injuries can occur when an object hits the head and the skull and the
brain are set in motion.
Acceleration-deceleration forces occur due to the rapid changes in
velocity of the brain within the cranial vault. Rotational forces occur
from the twisting of the head usually after impact. The degree of injury
depends upon the speed and direction the brain is rotated. Rotational
forces affect white matter tissue of the brain.
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The most common areas affected include the corpus collosum and the
brain stem. Deformation forces occur when the velocity of the impact
changes the shape of the skull and compresses the brain tissue. The
brain tissue is cushioned within the cranial vault by cerebrospinal fluid,
one of the protective mechanisms of the brain. Direct injury to the
brain tissue can occur as contusions, lacerations, necrosis and
hematomas with coup and contrecoup injuries.
Coup injuries occur at the site of impact and the contrecoup injury
occurs at the opposite side or at the rebound site of impact. Bi-polar
injuries may occur from front to back or side to side. Quadra-polar
injuries involve all sides of the brain — front, back, and each side. The
most common area of impact of a coup injury is the occipital lobe and
the contrecoup injury is the frontal lobe.
When a patient experiences a penetrating injury, the object causing the
injury breaks through the scalp and skull and penetrates the brain.
Typically, the penetrating object will cause tissue lacerations, contusions and
hemorrhages, along with a range of secondary injuries.38 The injury will
range in severity depending on a number of factors including size, shape,
speed and location of entry. Gunshot wounds and stab wounds are especially
problematic and both have a high incidence of mortality.19
There are two classifications of brain injury:10

Primary – This type of injury occurs as a direct result of the trauma.

Secondary – These injuries often develop over a period of time
(typically between several hours and five days).
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Initial treatment will focus on repairing any primary injuries, while later
treatment will transition to minimizing potential secondary injuries.6 When a
patient experiences a head trauma, he or she will often incur both primary
and secondary injuries.32 The following table provides information on both
types of injury.37
Injury
Description
Type
Primary
Primary injuries are a result of acceleration-deceleration and rotational
Injuries
forces occurring at the time of impact. These cause coup (initial impact
site) and contrecoup (rebound site of impact) injuries. The forces exerted
on the brain tissue may result in shearing, tensile or compressive stresses.
They can lead to ruptured blood vessels causing hemorrhage, hematomas,
and/or contusions. Injuries include lacerations, bone fractures, contusions,
hematomas and diffuse axonal injuries.
Secondary
Injuries
Secondary injuries occur after the initial traumatic injury and are a
consequence of the primary injury. A pathological cascade occurs due to
the biochemical changes in cellular structure. These changes lead to cell
death and further secondary injuries such as hypoxia, hypotension,
hypercarbia, hyperexcitation, cerebral edema, pathologic changes
associated with increased intracranial pressure, late bleeding and
expanding intracranial lesions.
Open versus Closed Injuries
Head injuries can be either open or closed. With a closed injury, the patient
experiences trauma in the absence of skull penetration.3 With an open
injury, the patient’s skull is penetrated.28 Open and closed head injuries
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cause different symptoms and must be treated differently. The following
information provides the distinctions between the two types of injuries.
Signs and Symptoms of Closed Injury:39

Altered or decreasing mental status — the best indicator of a brain
injury

Irregular breathing pattern

Obvious signs of a mechanism of injury — contusions, lacerations, or
hematomas to the scalp or deformity to the skull

Blood or cerebrospinal fluid leaking from the ears or nose

Bruising around the eyes (raccoon eyes)

Bruising behind the ears, or mastoid process (Battle’s sign)

Loss of movement or sensation

Nausea and/or vomiting (vomiting may be forceful or repeated)

Unequal pupil size (dilated) that does not react to light (fixed) with
altered mental status

Possible seizures

Unresponsiveness
Signs and Symptoms of Open Injury:40

Obvious results of the mechanism of injury — contusions, lacerations,
or hematomas to the scalp

Deformity to the skull or obvious penetrating injury

A soft area or depression detected during palpation

Brain tissue exposed through an open wound

Bleeding from an open bone injury
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Diffuse versus Focal Injuries
Brain injuries are either diffuse or focal. In focal injuries, the damage occurs
throughout various areas of the brain. The damage is microscopic and
widespread and it often occurs as the result of force that is exerted on the
brain tissues.41 The force causes damage to the axons, which are the parts
of the brain that communicate with each other and initiate nerve cell
responses.42
Focal brain injuries are confined to one specific region of the brain. They
cause localized damage and are easily identifiable.43
Types of Diffuse Injuries:10

concussion

brain edema

diffuse axonal injury
Types of Focal Injuries:5

contusion

intracranial hematoma

extradural hematoma

subdural hematoma

intracerebral hematoma (ICH )

subarachnoid hemorrhage (SAH )

intraventricular hemorrhage (IVH )
The following table provides a thorough overview of the different types of
injuries that contribute to traumatic brain injury.44
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Primary brain
Cerebral Contusion
injury
mechanisms –
Contusions are hemorrhagic lesions resulting when
Focal
acceleration/deceleration forces cause differential movements
between the brain and the skull or at grey–white matter interfaces.
They may occur at the site of impact, referred to as a “coup” injury, if
local deformation has been sufficiently severe.
Contre-coup contusions may be found on the opposite side to that of
the impact, but are usually found on the crests of the gyri of the
cerebral hemispheres, especially in those areas most likely to have
contact with bony skull protuberances: the orbital plate of the frontal
bone, the sphenoidal ridge, the petrous portion of the temporal bone
and the sharp edges of the falces. As a result, the basal and polar
portions of the frontal and temporal lobes are most susceptible to
contusions. However, contusions may also be found on the medial
surfaces of the cerebral hemispheres and along the upper surface of
the corpus callosum (Graham, 1999). They contribute to local
neuronal destruction and ischemia, or reduced blood supply, depriving
neurons of oxygen and glucose.
Mechanisms of cell death occurring in contusional and pericontusional
areas are termed necrosis and apoptosis. Necrosis occurs more
quickly, as a result of membrane failure and ionic disruption, which
degrade the neuronal cytoskeleton and cytoplasm and cause swelling
and dilation of the mitochondria. Apoptosis occurs slowly over a longer
period, without disruption of the cell membrane. It may be caused by
neural excitation, radical-mediated injury or a disruption of calcium
homeostasis.
Intracranial Hematoma
Vascular injury may be seen as multiple tiny “petechial” hemorrhages
throughout the cerebral hemispheres.
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Tearing of larger blood vessels at the time of impact results in
bleeding inside the skull and the formation of a clot, which can
eventually cause compression of the brain and ischemia. This may
lead to the development of coma after a delay or to deterioration in
conscious state, necessitating prompt surgical intervention to stop the
bleeding and evacuate the hematoma.
Intracranial hematomas are classified according to their anatomical
location. An extradural hematoma results from bleeding between the
skull and outer covering of the brain, known as the dura mater. This is
most commonly a complication of a temporal skull fracture, where
meningeal vessels have been torn.
A subdural hematoma is a collection of blood between the dura mater
and the arachnoid mater. The elderly are at increased risk of chronic
subdural hematoma because of their increased risk of falls and the
greater intracranial space caused by cerebral atrophy.
A subdural hygroma is a collection of cerebrospinal fluid in the
subdural space through a tear in the arachnoid mater. It develops
days or weeks after injury, and may form after the evacuation of an
acute subdural hematoma.
A subarachnoid hemorrhage refers to bleeding between the arachnoid
and pia mater. This may cause arterial spasm, leading to ischaemic
brain damage. It can also lead to obstruction of the flow of
cerebrospinal fluid, resulting in communicating high-pressure
hydrocephalus.
An intracerebral hematoma is a hemorrhage within the brain caused
by a deep contusion or tear in the blood vessels. As with other
pathological consequences of TBI, intracerebral hematomata occur
most commonly in the frontal and temporal lobes.
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Primary brain
The mechanical force of injury may cause more diffuse neuronal
injury: Diffuse
membrane disruption. Some cells appear to be able to reorganize,
neuronal
restore their function and thereby survive this disruption, whereas
change and
others show persistent membrane dysfunction, with activation of
axonal injury
cysteine proteases (calpain and caspase), causing rapid necrotic cell
death. Similarly, mechanical forces can result in scattered and multifocal axonal change throughout the subcortical white matter, corpus
callosum and brain stem, termed diffuse axonal injury (DAI).
In the most severe injuries, axons may be torn and retract, expelling
axoplasm and forming “retraction balls”. More commonly, mechanical
strains cause focal alteration of the axolemma, or disruption of sodium
channels, resulting in an influx of ions such as calcium, that disrupt
the cytoskeleton. This results in progressive changes disrupting axonal
transport and causing local swelling of the axon, followed by
detachment from its downstream segment. Both myelinated and
unmyelinated fibers appear to be vulnerable. These processes may
take place over several hours or days after injury, creating a potential
opportunity for intervention. Various therapies aimed at protecting the
mitochondria, including the use of immunophilin ligands, cyclosporin A
and FK 506 and hypothermia, are under investigation.
Shearing strains are thought to decrease in magnitude from the
cortical surface to the center of the brain. They are enhanced along
interfaces between substances of different densities and therefore DAI
occurs most commonly in the grey–white matter junctions around the
basal ganglia, the periventricular zone of the hypothalamus, the
superior cerebellar peduncles, the fornices, fiber tracts of the corpus
callosum, and in the frontal and temporal poles.
A consequence of DAI is that of downstream deafferentation or
denervation. The downstream axon, disconnected from its sustaining
cell body, undergoes wallerian degeneration, which may take place
over several months after injury. Downstream nerve terminals
undergo neurodegenerative change.
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Although neoplastic responses are not well understood, there is some
evidence to suggest that, in the case of mild–moderate injury, diffuse
deafferentation may result in sprouting of adjacent intact nerve fibers,
leading to some recovery of synaptic input to the deafferented areas.
However, in the case of severe injury, there appear to be maladaptive
changes, with fiber ingrowth and changes in cytoarchitecture.
These processes, and potential means of influencing them, are the
focus of continuing experimentation.
Widespread metabolic changes also occur following TBI. Across the
spectrum of injury severity, TBI is followed by a short-lived increase in
glucose metabolism (a sign of metabolic stress), followed by a
decreased rate of glucose metabolism which may last for days or
weeks and shows some correspondence with the period of recovery
and with outcome. Elevated lactate and glutamate are also evident
and higher levels are associated with poorer outcome.
Petechial White Matter Hemorrhage
DAI is most commonly associated with injuries involving acceleration–
deceleration, such as motor vehicle accidents. Findings on computed
tomography or magnetic resonance imaging may include the presence
of petechial white matter hemorrhage as well as non-hemorrhagic
white matter lesions, diffuse edema, and small subarachnoid and
intraventricular hemorrhages.
Deeper lesions are indicative of more severe injury.
Adams et al. (1989) refer to three grades of DAI: Grade 1 where focal
hemorrhagic lesions are confined to the white matter of the cerebral
hemispheres; Grade 2 where there is involvement of the corpus
callosum; and Grade 3 where the dorsolateral upper brain stem is
involved. However, lesser degrees of DAI may also be seen in some
cases.
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Secondary
Both intracranial and extracranial complications may result in
brain injury
secondary brain injury, either as a consequence of cerebral ischemia
mechanisms
or distortion and/or compression of the brain/mass effect. Cerebral
ischemia, as a result of inadequate blood flow and consequent tissue
hypoxia, is usually the ultimate cause of secondary brain damage
associated with TBI.
Hypoxic damage is frequently found in the border zones of areas
supplied by the major cerebral arteries, particularly in the parasagittal
cortex, the hippocampus, the thalamus and basal ganglia. Intracranial
complications may include the following conditions outlined below.
Brain Swelling
There are two mechanisms, which lead to an increase in the volume of
the brain following TBI. The first is an increase in the cerebral blood
volume, termed hyperemia, caused by hypoxia, hypercapnia, or
obstruction of major cerebral veins as a result of cerebral edema. The
second is cerebral edema, resulting from an increased volume of intraor extracellular fluid in the brain tissue.
Cerebral edema may be caused by damage to the walls of cerebral
blood vessels, accumulation of fluid within the cell as a result of
ischemia, increased intravascular pressure, or an obstruction to the
flow of cerebrospinal fluid. These mechanisms may result in brain
swelling of either a localized or a diffuse nature. Damage to the brain
tends to be caused by a mass effect, with brain shift and/or raised
intracranial pressure, leading to hypoxia/ischaemia.
Infection
Infection, which may develop in the subacute phase after TBI, is a
complication associated with skull fracture. It can manifest itself in
two forms: meningitis and cerebral abscess, causing raised
intracranial pressure and/or brain shift.
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Raised Intracranial Pressure
Increases in intracranial pressure (ICP) are a common consequence of
the abovementioned intracranial complications, causing impairment of
brain function due to reduction in cerebral perfusion pressure and
consequently in cerebral blood flow, resulting in ischemia, and brain
shift. Uncontrolled intracranial pressure frequently causes diffuse
ischemic brain damage.
Cerebral autoregulation, or the ability of the brain to maintain a
constant blood flow to the brain, may be impaired or lost under
conditions such as increased intracranial pressure, ischemia, and
inflammation or low or high mean arterial pressure, rendering the
brain more vulnerable to ischaemia. Reductions in blood flow result in
metabolic changes, which ultimately result in neuronal disintegration.
Intracranial pressure and associated cerebral perfusion pressure are
therefore routinely monitored in severe TBI cases.
Another potential consequence of raised intracranial pressure,
hematoma and/or brain swelling is herniation. Subfalcine
herniation occurs when one cingulate gyrus herniates across the
midline. A more serious type is transtentorial herniation, where there
is downward displacement of the parahippocampal gyrus and uncus of
one or both temporal lobes through the tentorial hiatus into the
posterior fossa. Compression of the oculo-motor nerve, as well as
midbrain dysfunction, commonly results from tentorial herniation.
Unchecked tentorial herniation leads to a deterioration in brain stem
functioning, with consequent respiratory abnormality,
hyperventilation, decerebration and, eventually, death. Tonsillar
herniation occurs when the cerebellum is forced through the foramen
magnum, leading to symptoms of vagus nerve compression, hypoxia,
edema of the medulla and, eventually, respiratory arrest and death.
Decompressive craniectomy surgery involves temporarily removing a
portion of frontal skull bone to increase the volume of the cranial
cavity and to decrease intracranial pressure.
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The procedure carries risks, and the efficacy, optimal timing and
surgical methods, and neurological function in the survivors remain
uncertain. While some case series and case control studies have
shown decreased intracranial pressure and improved neurological
outcomes, the only randomized controlled trial in adults to date has
suggested that decompressive craniectomy results in poorer functional
outcomes.
Apart from damage due to pressure effects, secondary brain injury
following TBI is caused by hypoxia, cellular influx of calcium and other
ions, release of free radicals and excitotoxic neurotransmitters, and
apoptotic cell death, all of which are potentially preventable. Results of
clinical trials examining the efficacy of drugs that block various ion
channels, scavenge free radicals, inhibit excitatory neurotransmitters,
or block the internal signals for programmed cell death have,
however, been disappointing.
A number of reasons for this failure have been put forward, including
the differences in therapeutic time windows between animal and
human trials and the heterogeneity of neuropathology, which means
that treatments focused on one pathological process do not attenuate
other processes and thus have little overall impact in humans. There is
also debate over determination and matching of injury severity levels
across sites and studies and of sensitive outcome measures. Efforts
towards development of such treatments continue.
Extracranial Complications
Extracranial complications may occur where there are multiple
traumas. Injuries to other parts of the body may cause blood loss and
hypotension, pulmonary injury, aspiration of vomit, or cardiac or
respiratory arrest, with consequent hypoxia, causing further brain
damage. Thus, prevention of these complications in the acute
management stages is of paramount importance.
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Delayed
complications
of TBI
Post-Traumatic Epilepsy
TBI creates an increased risk of epilepsy. Jennett (1979) estimated
the overall incidence of post-traumatic epilepsy following non-missile
head injury at 5 per cent. He distinguished between early posttraumatic epilepsy, which occurs within the first week after injury
(most commonly in the first 24 hours), and late post-traumatic
epilepsy, which typically occurs more than three months post-injury.
Protracted seizures carry a risk of further brain injury, as a result of
increased metabolic requirements, disruption of spontaneous
respiration, and aspiration. Focal motor seizures and partial complex
“temporal lobe” seizures are seen most commonly. Children are more
susceptible to early epilepsy. Late epilepsy occurs in about 20 per cent
of those who experience early epilepsy.
Predisposing factors for epilepsy include the presence of brain
contusion with subdural hematoma, skull fracture, greater injury
severity and age over 65 years. In a study by Annegers and Coan
(2000), the relative risk of seizures was 1.5 following mild TBI (loss of
consciousness (LOC) less than 30 minutes), 2.9 following moderate
TBI (LOC 30 minutes–1 day) and 17.2 following severe injury (LOC
greater than one day).
The risk is greatest in the first two years after injury. Another study
found that patients with a Glasgow Coma Score (GCS) 3–8 had a
cumulative probability of late post-traumatic seizures by 24 months
post-injury of 16.8 per cent. The probability was 24.3 per cent for
those with GCS score of 9–12 and 8.0 per cent for those with GCS
score of 13–15, showing that GCS alone does not predict epilepsy risk.
In this study one-third of late posttraumatic seizures occurred within a
month of injury and 86 per cent within one year. There is also a high
risk of recurrence of late onset seizures. Although anticonvulsant
therapy during the first week after injury may reduce early-onset
epilepsy, there is no evidence to support prophylactic treatment with
anticonvulsants for prevention of late-onset post-traumatic seizures.
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While no anticonvulsants are without adverse effects, carbamazepine
and valproic acid have been found to be relatively free of adverse
cognitive effects relative to phenytoin. In view of the expense and
potential toxicity of anticonvulsants, most clinicians withdraw
medications after one to two seizure-free years.
Hydrocephalus
Communicating hydrocephalus, which occurs in 1–2 per cent of cases,
results from obstruction to the flow of cerebrospinal fluid by blood in
the subarachnoid space. This leads to ventricular enlargement and a
consequent decline in cognitive function, gait disturbance and
incontinence, although in the case of serious brain injury it may be
difficult to discern whether the hydrocephalus is clinically significant.
Shunting to treat hydrocephalus is most likely to be effective if there
has been evidence of clinical deterioration. It is important to note that
ventricular enlargement can also occur without signs of
communicating hydrocephalus, as a result of a general reduction in
the bulk of the cerebral white matter.
Levels Of Severity Of TBI
Severity of TBI is generally graded from mild to moderate or severe.
Severity can be classified in multiple ways, and each measure has different
predictive utility, including determining morbidity, mortality, or long-term
functional outcomes. Patients with more severe head injuries demonstrate
lower cognitive functioning and have more gradual cognitive improvements
following the initial injury. Degree of severity is often based on the acute
effects of the injury, such as an individual’s level of arousal or duration of
amnesia, and these are measured by the Glasgow coma scale, posttraumatic
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amnesia, duration of loss of consciousness, and degree of altered
consciousness.37
The majority of TBIs are mild, consisting of a brief change in mental status
or unconsciousness. Mild TBI is also referred to as a concussion. While most
people fully recover from mild TBI, individuals may experience both shortand long-term effects. Moderate-severe TBI is characterized by extended
periods of unconsciousness or amnesia, among other effects. The distinction
between moderate and severe injuries is not always clear; as such,
individuals with moderate and severe injuries are often grouped.45
These classification systems not only
determine the severity of TBI, but
also may be indicative of the degree
of long-term disability. The more
severe the injury, the more severe
and persistent the cognitive deficits
— though clinical measurements do
not always concur. Severity
measures graded during the acute
phase sometimes reflect variance
due to medications used during resuscitation, substance use, and
communication issues.35 Each category has specific criteria and
characteristics, which are outlined below.
Mild TBI

Loss of consciousness is very brief, usually a few seconds or minutes

Loss of consciousness does not have to occur - the person may be
dazed or confused
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
Testing and scans of the brain may appear normal

Most common: 75%-85% of all brain injuries are mild

90% of individuals recover within 6-8 weeks, often within hours or
days, but 10% experience deficits, which may not be evident
immediately

More than one mild brain injury over time (i.e., sports injuries or
domestic violence) increases the chance of deficits
Moderate TBI

Loss of consciousness lasts from a few minutes to a few hours

Confusion lasts from days to weeks

Physical, cognitive, and/or behavioral impairments last for months or
are permanent

EEG/CAT/MRI are positive for brain injury
Severe TBI

Prolonged unconscious state or coma lasts days, weeks, or months

Categories include:
o Coma
o Vegetative State
o Persistent Vegetative State
o Minimally Responsive State
o Locked-in Syndrome
Examples of common cognitive-communicative, physical, and psychosocial
or emotional consequences after mild, moderate, and severe TBI are
outlined below.4
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Mild TBI:

Cognitive-Communicative
o Decreased attention and concentration
o Decreased speed of processing
o Memory problems
o Getting lost or confused
o Decreased awareness and insight regarding difficulties

Psychosocial/Emotional
o Irritability
o Depression and anxiety
o Emotional mood swings

Physical
o Headache
o Fatigue
o Sleep disturbance
o Visual disturbance
o Dizziness
o Nausea
o Balance problems
Moderate and Severe TBI:

Cognitive-Communicative
o Decreased attention and concentration
o Distractibility
o Memory problems
o Decreased speed of processing
o Increased confusion
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o Perseveration
o Impulsiveness
o Decreased interaction skills
o Decreased executive function abilities (for example, planning,
organization, problem solving)
o Decreased awareness of, and insight regarding, difficulties

Psychosocial/Emotional
o Dependent behaviors
o Apathy
o Decreased lack of motivation
o Irritability
o Acting out
o Depression
o Denial of difficulties

Physical
o Difficulty speaking and being understood
o Physical paralysis/weakness/spasticity
o Difficulties with sense of touch, temperature, movement,
position
o Chronic pain
o Decreased bowel and bladder control
o Sleep disorders
o Loss of stamina
o Appetite changes
o Partial or total loss of vision
o Weakness of eye muscles and/or double vision (diplopia)
o Blurred vision
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o Problems judging distance
o Involuntary eye movements (nystagmus)
o Intolerance of light (photophobia)
o Decreased or loss of hearing
o Ringing in the ears (tinnitus)
o Increased sensitivity to sounds
o Loss or diminished sense of smell (anosmia)
o Loss or reduced sense of taste
The following table provides a thorough overview of the neurobehavioral
consequences of the different severity levels of traumatic brain injury.18
Mild
Mild TBI is defined as those injuries where there is confusion or
disorientation, loss of consciousness for 30 minutes or less, PTA for less
than 24 hours and/or other transient neurological abnormalities such as
focal signs, seizure, and intracranial lesion not requiring surgery; and a
GCS score of 13–15 after 30 minutes post-injury or later upon
presentation for healthcare. These manifestations must not be due to
drugs, alcohol, or medications, or be caused by other injuries, treatment
for other injuries (i.e., systemic injuries, facial injuries or intubation),
other problems (i.e., psychological trauma, language barrier or
coexisting medical conditions) or penetrating craniocerebral injury.
Neurological deficits are rarely apparent following the acute stages of
mild TBI. However, the person may experience a range of symptoms,
including headache, dizziness, fatigue, blurred or double vision,
sensitivity to noise and/or bright lights, tinnitus, restlessness, insomnia,
reduced speed of thinking, concentration and memory problems,
irritability, anxiety and depression and poor balance. The most common
causes of these injuries are falls and motor vehicle accidents, but a
significant proportion of mild TBIs also result from sports-related
concussion, cycling accidents, assault and combat in the theatre of war.
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Typically, individuals who have sustained mild TBI and have no other
injuries return home within a few days, with the expectation of resuming
their normal activities. In many cases these so-called post-concussional
symptoms subside over a period of days or weeks. Neuro-psychological
studies have confirmed the presence of impaired speed of information
processing, attention and/or memory in the early days after injury.
Recovery from symptoms and cognitive impairments appears to take
place within two weeks following sports-related concussion. In other
etiological groups the timeframe of recovery is more variable, but in the
majority of cases symptoms have resolved within three months.
However, in 15–25 per cent of cases these difficulties persist and
sometimes result in significant ongoing disability and adjustment
problems. The cause of such ongoing problems, termed the persistent
post-concussive syndrome, remains a subject of much debate. Injury
severity measures, i.e., GCS and posttraumatic amnesia (PTA) do not
show a significant association with outcome following mild TBI.
Ponsford and colleagues (2000) found that the factors most strongly
associated with continuing symptoms following mild TBI were the
presence of pre-existing neurological or psychiatric problems, being a
student and the presence of other concurrent life stressors. A number of
other authors have drawn attention to the overlap of post-concussional
symptoms with symptoms associated with pain resulting from other
injuries, medication effects, post-traumatic stress, anxiety, depression,
pre-accident psychological adjustment issues, individual coping styles,
the presence of other stressors and/or litigation/compensation.
It would appear that these other issues interact with the effects of mild
TBI to exacerbate symptoms and distress and may, in some cases, be
the primary factors underpinning persistent post-concussive symptoms.
However, with the use of increasingly sophisticated imaging techniques,
such as DTI, MR spectroscopy, MRI-volumetry, gradient echo, diffusion
weighted and susceptibility weighted MR scanning sequences, it has become possible to identify cerebral changes which are not evident on CT
scans in at least a proportion of mild TBI cases.
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Moreover, recent studies have provided evidence of greater likelihood of
abnormal imaging findings and more significant ongoing
neuropsychological problems in individuals with “complicated” mild TBI,
suggesting that these injuries occur on a continuum of severity. In a
modeling study of concussion, Viano and colleagues (2005) showed 4–5
mm displacements of the hippocampus, caudate, amygdala, anterior
commissure and midbrain, which were associated with cognitive and
physical symptoms in football players.
Bigler (2008) suggests that these same regions are likely to be involved
in most concussive injuries to variable degrees, with long-coursing
axons such as those in the corpus callosum and anterior commissure
particularly vulnerable, and concomitant irritation to the vasculature and
the meninges, the extent of which depends on the direction and
magnitude of force associated with the injury. These forces disrupt the
cytoskeletal architecture, affecting cell function transiently or
permanently. According to Giza and Hovda (2004), within 25–50 msec
of such an impact there is evidence of transient biomechanically induced
ionic disturbance and upregulation of cellular glycolysis, followed by a
downregulation in glucose metabolism. The degree to which there are
lasting changes depends on the nature and extent of the force applied,
and also on factors associated with the person, which may include
genetic factors.
McAllister and colleagues (2006) have identified genetic polymorphisms
modulating central dopaminergic tone, that appear to affect cognitive
performance on tests of processing speed, attention and memory
following mild or moderate TBI. Findings regarding the effects of
multiple concussive head injuries, most of which have come from sports
concussion studies, have been mixed. Results of a recent meta-analysis
have suggested that multiple self-reported concussions were associated
with poorer performances on tests of delayed memory and executive
function. However, the clinical significance of these differences is
unclear. Outcomes are likely to depend on the severity of each injury.
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Overall, it appears that a number of factors interact to determine the
likelihood of continuing post-concussive symptoms. These relate to the
person who is injured (age, sex, physical, psychological, cultural,
genetic), injury factors (injury force, direction and site, its cause or
circumstances, other injuries), and post-injury factors such as pain,
post-traumatic stress, environmental demands and expectations, other
stressors, and litigation/compensation issues.
Moderate
and
Severe
In the case of moderate and severe TBI, where coma has persisted for
more than an hour, and PTA for more than 24 hours, cognitive and
behavioral changes are more extensive and persistent than in the case
of mild head injury. The nature and degree of these changes vary
widely, according to the site and extent of injury.
Disorders of language, perception or praxis may result from lesions
disrupting the systems responsible for these neuropsychological
functions. However, because of the high incidence of DAI, and damage
to the frontal and temporal lobes, problems with fatigue, attention,
memory, executive function and behavioral regulation are particularly
common. While some “executive” problems would be termed “cognitive”
and some “behavioral” problems, they will be considered together.
Fatigue
Numerous follow-up studies have reported fatigue to be one of the most
common symptoms experienced following mild, moderate and severe
TBI, with a reported frequency ranging from 32.4 per cent to 73 per
cent. Despite this, the nature and causes of fatigue remain relatively
poorly understood.
Results of recent studies suggest that fatigue may result from a number
of factors, including impairments of information processing speed,
attention and vigilance, sleep disturbance, pain and emotional factors.
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Attentional Deficits
Attentional problems also occur very frequently at all levels of severity
of injury following TBI. This is not surprising, given the neuropathology
of TBI, which frequently disrupts attentional neural networks via injury
to the fronto-striatal areas, the reticular formation, DAI and disruption
of catecholaminergic and serotonergic pathways. An attentional difficulty
most commonly reported is reduced speed of information processing,
leading to a reduced information processing capacity, with consequent
difficulties in focusing on more than one thing at once, or coping with
complexity. Poor selective attention (the capacity to focus on some
things and screen out others), which can manifest itself as distractibility
or poor attention to detail is also reported, along with problems in
sustaining attention over time, and difficulty in the allocation of
attentional resources in a goal-directed fashion.
Learning and Memory Problems
It has already been noted that people with TBI usually have a period of
confusion, disorientation and inability to remember ongoing events
immediately following their emergence from coma, lasting for days,
weeks, or, in the most severe cases, months, known as posttraumatic
amnesia (PTA). There is also frequently impairment of memory for
events, which immediately preceded the injury, termed retrograde
amnesia.
The period of retrograde amnesia is variable, being broadly related to
the period of unconsciousness. There may be “islands of memory” within
the period over which retrograde amnesia extends, and the period of
retrograde amnesia tends to “shrink” over time. The period of persistent
retrograde amnesia is usually too brief for it to give a reliable indication
of the severity of injury or probable outcome. After emergence from
PTA, many people who have sustained TBI report ongoing difficulties
with learning and memory. Follow-up studies conducted from six months
up to seven years after injury have found this to be one of the most
frequent subjective complaints of TBI individuals and/or their relatives.
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As with attentional difficulties, there is potential heterogeneity in the
nature and severity of memory difficulties experienced by TBI
individuals, depending on the site and extent of injury. Memory
problems may manifest as a severe amnesic syndrome, affecting the
ongoing storage and retrieval of all types of material, difficulty with
either verbal or non-verbal material, or most commonly an inefficient or
unreliable memory due to lack of use of organizational strategies and/or
attentional problems characteristic of frontal lobe injury.
Whatever the nature of the problem, there is usually a marked contrast
between the capacity to remember events and skills learned prior to the
injury, and the ability to learn and retain new material since the time of
injury, the former being relatively preserved. Implicit memory, such as
procedural learning, is also relatively spared in many individuals.
Impaired Planning and Problem-Solving
The high frequency of damage to the frontal lobes associated with TBI
means that many of those who have sustained TBI have difficulties in
analyzing, planning and executing the solutions to problems or complex
tasks. They may perform well in structured activities, which require little
initiative or direction. However, although there may be a willingness and
ability to perform each component of a task, people with planning and
problem-solving deficits are frequently unable to generate strategies for
efficient task performance, to follow through with the organization and
implementation of complex tasks, or to check for and correct errors.
TBI individuals often have difficulty in sustaining performance on tasks.
Complex behaviors may dissolve into inert stereotypes. There can be a
tendency to lose track of the task at hand, and to respond to
distractions or inappropriate cues in the environment. There also tends
to be a failure to look ahead, and to use past experience to prepare for
anticipated events. People with executive dysfunction have particular
difficulty in adapting to new situations.
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Concrete Thinking
Difficulties in forming or dealing with abstract concepts are common.
This can result in an inability to generalize from a single instance, or
distil the essence of a situation or a conversation, with a tendency to
focus on specific, concrete aspects, or be “stimulus-bound”. There may
also be difficulties in understanding humor or other forms of indirect
language. An inability to understand the implications of situations or
events is common. There may be problems in benefiting from
experience – in applying old solutions to new situations. Alternatively,
there may be an inability to think creatively and generate different
solutions to a given problem, with a tendency to repeatedly apply an
old, unworkable solution, resulting in failure and frustration.
Lack of Initiative
Some of those who have sustained TBI show a lack of initiative or drive
in some or all aspects of their behavior and thought processes. In
severe cases there may be a complete inability to initiate speech or any
activity without prompting. At a more subtle level, there may be a
tendency to lack spontaneity, to be somewhat passive in conversation,
to fail to move on to the next task once one is completed, or to move
from one step to another within tasks. Relatives may report that the TBI
person who was previously active achieves very little in a day and may
sit for hours in a chair watching television.
Inflexibility
Inflexibility in thought processes and behavior may be manifested as
difficulty in switching from one task to another, in changing train of
thought or shifting “mental set”. This may lead to frequent repetition or
“perseveration” of the same responses, comments, demands or
complaints.
There may be an inability to see other people’s points of view and a
tendency to rely on rigid adherence to routines. Sudden changes in
routine may cause the TBI individual to become upset.
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Dissociation Between Thought and Action
It is frequently reported that there is dissociation between what people
who have sustained TBI know or say, and how they actually behave.
This results in an inability to follow through with instructions, to correct
errors or modify behavior in the light of feedback. This, together with
the next few problems, appears to result from a reduced capacity to
control, regulate and monitor thought processes and behavior.
Impulsivity
A reduced capacity to control and monitor behavior commonly results in
impulsivity. There is a difficulty in inhibiting the tendency to respond to
problems or situations before taking account of all relevant information,
and before thinking of all the possible consequences of one’s actions.
Irritability/Temper Outbursts
One of the most commonly reported problems following TBI is a low
tolerance for frustration. Those who have sustained TBI are prone to
become irritable and to lose their temper easily. The anger may be
completely out of proportion to the situation, and there may be physical
aggression.
Communication Problems
While aphasia is uncommon following TBI, discourse problems are
frequently encountered. These can include excessive talking, with poor
turn-taking skills, a tendency to repeat oneself or have difficulty keeping
to the point. Word-finding difficulties and impaired auditory processing
are also common.
Socially Inappropriate Behavior
Lack of behavioral control can also lead to an inability to inhibit
inappropriate responses, such as swearing, sexual disinhibition,
tactlessness or other socially inappropriate behaviors.
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There may be a failure to respond to non-verbal cues given by others,
which normally let a person know when it is time to finish a conversation
or move on to another topic, or when someone else is feeling
uncomfortable with a certain behavior.
Self-centeredness
Those who have sustained severe TBI can be egocentric. This results in
a tendency towards demanding, attention-seeking and sometimes
manipulative behavior. It can also lead to jealousy, and insensitivity to
the feelings or emotional needs of others, as well as a failure to see
other people’s points of view. This is the source of many relationship
problems following TBI.
Changes in Affect
TBI can result in a flatness of affect, where there is reduced emotional
responsiveness, or an elevation of affect, with euphoria. Reduced
emotional control can also lead to a tendency to laugh or cry for no
apparent reason, or to show emotions which are quite out of proportion,
or inappropriate, to the situation.
Lack of Insight/Self-Awareness
Severe TBI frequently results in difficulty perceiving, or a lack of
awareness of, changes in cognitive function and behavior. This leads to
a tendency to attempt work or other tasks, which are beyond their
capabilities. There may also be a failure to recognize how impulsive,
irritable, childish or demanding they are in certain situations, with
disastrous consequences for interpersonal relationships. This results in a
degree of perplexity in the TBI person, who fails to understand the
reasons for failure at work or in social relationships.
Occasionally, one sees the emergence of frank delusions. Another
unfortunate consequence of lack of insight is the inability to understand
the need for rehabilitation or other forms of assistance in overcoming
limitations.
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The cognitive and behavioral changes described above frequently coexist in a complex fashion, being difficult to disentangle in an individual,
particularly as they are imposed upon varying premorbid personality
characteristics. Planning and problem-solving, abstract thinking,
initiative, mental flexibility, and control and regulation of thought
processes and behavior have been termed “executive functions” by
Lezak et al. (2004), Baddeley (1986) and Stuss and Benson (1986), and
this term is now commonly used. Lezak (1978), who has so ably
described the problems of those who have sustained TBI, referred to the
“characterologically-altered” brain-injured patient.
TBI Symptoms
An individual will experience a variety of symptoms as the result of a head
injury. Each patient will experience symptoms differently, and symptoms will
vary depending on the type and severity of the injury. The following are the
most common symptoms of a head injury.
Mild head injury:

Raised, swollen area from a bump or a bruise

Small, superficial (shallow) cut in the scalp

Headache

Sensitivity to noise and light

Irritability

Confusion

Lightheadedness and/or dizziness

Problems with balance

Nausea
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
Problems with memory and/or concentration

Change in sleep patterns

Blurred vision

"Tired” eyes

Ringing in the ears (tinnitus)

Alteration in taste

Fatigue/lethargy
Moderate to severe head injury (requires immediate medical attention)
symptoms may include any of the above plus:19

Loss of consciousness

Severe headache that does not go away

Repeated nausea and vomiting

Loss of short-term memory, such as difficulty remembering the events
that led right up to and through the traumatic event

Slurred speech

Difficulty with walking

Weakness in one side or area of the body

Sweating

Pale skin color

Seizures or convulsions

Behavior changes including irritability

Blood or clear fluid draining from the ears or nose

One pupil (dark area in the center of the eye) looks larger than the
other eye

Deep cut or laceration in the scalp

Open wound in the head

Foreign object penetrating the head
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
Coma (a state of unconsciousness from which a person cannot be
awakened; responds only minimally, if at all, to stimuli; and exhibits
no voluntary activities)

Vegetative state (a condition of brain damage in which a person has
lost his thinking abilities and awareness of his surroundings, but
retains some basic functions such as breathing and blood circulation)

Locked-in syndrome (a neurological condition in which a person is
conscious and can think and reason, but cannot speak or move)
The above is a list of the general symptoms of mild to severe head injuries.
The following section will provide more detailed information on each of the
most common symptoms.
Bleeding
Bleeding is common with head injuries. With penetrating head injuries,
bleeding can occur externally or internally.46 Internal bleeding is most
common in the brain tissue or between the cranial layers.47 In blunt trauma
injuries, bleeding typically occurs internally, although there may be minimal
bleeding at the site of impact.36 Bleeding is not always apparent when it is
internal. Therefore, it is important to utilize radiologic imaging to identify
any internal areas of bleeding.2
Bruising
Bruising is common in instances of blunt head trauma.48 Most patients will
experience external bruising at the site of impact.23 External bruises can
range in severity and appearance, depending on the amount of force used
and the area of the head that is bruised. Some patients will experience
internal bruising, otherwise known as contusions.49
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A contusion is defined as bruising of the brain, and it is caused by bleeding
and edema within the brain tissue.50 It is a secondary injury, as it is caused
by a primary injury that swells, bleeds and results in increased intracranial
pressure.23 Contusions can occur in instances of blunt and penetrating
trauma.36 In some patients, the contusion will appear at the site of impact as
a coup injury. In other patients, the contusion will appear on the opposite
side of the injury as a contrecoup injury.51 It is most common for patients to
experience a contusion in the frontal or temporal lobes.5
Neurological Deficits
Many patients will experience cognitive deficits as a result of head trauma.
The specific deficits will vary depending on the location and severity of the
injury. The following is a list of the most common cognitive deficits
experienced by head trauma patients:52

Arousal or over-stimulation

Attention and filtering issues

Information coding and retrieval (memory) issues

Learning, both using old information and acquiring new information

Problem solving

Higher-level thinking skills also known as “executive skills”
Some of the cognitive deficits listed above will be short-term problems and
will be eliminated over time with the aid of therapy and rehabilitation
services.53 However, other cognitive deficits will persist long term and may
not ever resolve themselves.46 In some instances, persistent cognitive
deficits can be minimized or eliminated through the use of more intensive
rehabilitation services.44
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Cognitive deficits have a direct correlation with neurobehavioral problems.54
Therefore, it is important to discuss the two together. Neurobehavioral
problems are directly related to specific components of head trauma.
Depending on the injury, the patient may experience neurobehavioral
problems that cause changes in behavior and attitudes.
The following is a list of the common neurobehavioral problems experienced
by brain injury patients:55

Reduced inhibitions and judgment

Difficulty with self-regulation or self-control

Impulse control

Over-arousal

Frustration tolerance

Problems in perception

Overreaction to situations

Anger without provocation

Socially inappropriate behaviors
Treatment for neurobehavioral problems includes therapy, medication, and
behavior modification.56
Some patients will experience neuromotor problems. These are also a direct
result of specific head injuries and will vary depending on the type and
location of injury. Neuromotor problems affect the patient’s physical
movement and ability to control the body.57
The following is a list of the most common neuromotor problems:8

Initiating or starting a movement

Maintaining muscle control
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
Sustaining a movement

Executing a complex movement, such as walking
If a patient experiences neuromotor problems, he or she will be treated
using specific therapies and strategies that will help improve motor functions
and regain skills.58
Amnesia
Patients who sustain head injuries may experience some degree of amnesia.
Amnesia is defined as a loss of memory for any period of time.59 Amnesia is
broken into two categories, depending on the way that it presents itself.
Retrograde Amnesia
The patient loses memories of
events that occurred prior to the
injury. Some patients may only lose
a few seconds or a minute of
memory.60 In these instances, the
patient may remember part of the
accident, but not the entire accident.
Other patients may experience the
loss of a longer duration of time, up
to days or years.61
In some instances, patients may not remember the accident at all, or even
the year prior to the accident.46 Most patients will recover their memories as
the damage heals. However, there is no standard time period or pattern that
the return of memories follow.59
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Anterior Amnesia
Patients who experience anterior grade amnesia will lose memories of the
events that occurred following the injury. In these instances, they will
continue to lose new memories, while still retaining memories of events that
occurred prior to the injury.61
Changes in Pupil Shape and Size
Different complications of head trauma can cause changes in the shape and
size of the pupil. Therefore, a standard examination should include an
assessment of the patient’s pupils. Any changes should be noted and used to
determine the extent of injury. The following table provides information on
the areas of the pupil that may experience changes.62
Area of Change
Pupil Size and
Equality
Description
Pupil size is reported as the width or diameter of each pupil in
millimeters. A standardized pupil gauge should be used to report the
pupil size in millimeters. The use of this gauge aids in decreasing
subjectivity, particularly when serial assessments are performed.
The normal diameter of the pupil is between 2 and 5 mm, with the
average pupil measuring 3.5 mm. Although both pupils should be
equal in size, a 1-mm discrepancy is considered a normal deviation.
This condition is known as anisocoria and is present in 15% to 17%
of the population without any known clinical significance. Pupil size
should be assessed both before and after the pupil responds to
direct light.
Pupil Shape
Pupil shape is reported as round, irregular, or oval. The normal
shape of the pupil is round. An irregular-shaped pupil may be the
result of ophthalmological procedures such as cataract surgery or
lens implants, and this should be noted on the initial assessment and
confirmed with the patient or family.
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A pupil that is oval in shape may indicate the early compression of
cranial nerve III due to increased intracranial pressure (ICP), and
thus should be addressed immediately. If an oval pupil is detected,
measures should be taken to decrease ICP.
As ICP is reduced, the oval-shaped pupil should resolve. However, if
ICP continues to rise or is not treated, the oval-shaped pupil will
become further dilated and will eventually become nonreactive to
light.
Pupil Reactivity
Pupil reactivity is reported as the response or reflex of each pupil to
direct light. Reactivity is assessed through shining a low-beam
flashlight inward from the outer canthus of each eye. Each eye
should be checked separately. The light should not shine directly
into the pupil because the glare or reflection may obscure
visualization.
The reaction that each pupil has to the light stimulus should be
recorded. The speed of pupillary reactivity is recorded as brisk,
sluggish, or nonreactive. Normally, pupils should constrict briskly in
response to light. A sluggish or slow pupillary response may indicate
increased ICP, and nonreactive pupils are often associated with
severe increases in ICP and/or severe brain damage.
A complete pupillary reactivity examination also includes assessment
of the consensual pupillary response and accommodation. The
consensual pupillary response is the constriction that normally
occurs in a pupil when light is shown into the opposite eye.6
Because of this response, the trauma nurse should wait for several
seconds before assessing pupillary light reflex in the second eye, as
that pupil may be temporarily constricted. Accommodation is the
constriction of pupils that occurs when a conscious patient is
focusing on a close object. Pupils should normally constrict
bilaterally when an object is held within 4 to 6 inches of a patient's
nose.
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General Pupil
When performing pupillary examinations in patients with TBI,
Abnormalities
trauma nurses may detect abnormalities, such as an irregular pupil
size, shape, or a sluggish or nonreactive pupil. When an abnormality
is detected, the trauma nurse should first identify whether the
abnormality was present on the previous pupillary examination. If an
abnormal pupil is present on the initial pupillary examination, it
should be clearly documented, and a physician should be
immediately notified.
Immediate notification of a physician should occur with changes in
pupillary response. Comparing the current examination with the
previous to provide time-oriented data for the physician is wise but
should never delay immediate physician notification.
General
Indications
A complete neurologic examination should be performed and any
changes in the patient's condition should be noted and reported to a
physician. An abnormal pupil in a patient with TBI is often indicative
of increasing ICP due to progression of the hematoma/hemorrhage
or cerebral edema. However, the trauma nurse should be aware of
other clinical factors that may cause an abnormal pupil response.
Abnormal pupils may be seen in TBI patients and due to both
physiologic and clinical factors contributing to the abnormalities.
Regardless of the cause of an abnormal pupil, the trauma nurse
should always notify a physician immediately when an abnormal
pupil is detected. A CT scan and continuous ICP monitoring will aid
in definitively identifying the cause of the abnormal pupil.
Stiff Neck
Within the twenty-four hours following a head injury, a patient may
experience a stiff neck. This is often indicative of a more serious
complication and should be monitored closely.43
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Headache
It is common for a patient to
experience a headache immediately
after experiencing a blow to the head.
Most patients will experience headaches
within the first few weeks following a
head injury.63 However, most
headaches should stop within four
weeks of the injury.64 Headaches are
not cause for concern as long as they
do not get worse over time.43
Headaches are classified using three
distinct categories:64

Mild: A mild headache improves or goes away completely with home
treatment, medication, or rest. It may return when the medication
wears off.

Moderate: A moderate headache improves with home treatment,
medication, or rest, but it never completely goes away. The patient is
always aware that the headache is present.

Severe: A severe headache is incapacitating. Home treatment,
medication, and rest do not relieve this headache.
If a patient experiences a continuous headache that gets worse over time, it
should be taken into consideration. These headaches are often indicative of
swelling and/or bleeding on the brain, or within the areas surrounding the
brain.65 In some instances, the blood and swelling will occur between the
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brain and the covering of the brain. The bleeding may occur rapidly, or it
may slowly develop.64 Some patients will display symptoms within minutes
of hours of the injury, while other patients will not experience symptoms
until weeks after the injury.66
If a patient reports a new and persistent headache that does not develop
immediately following the injury, he or she may have a blood clot. Along
with the headache, the patient may experience confusion and sleepiness.46
While most headaches are not cause for alarm, any headache that is
persistent and accompanied by other symptoms (i.e., drowsiness and
personality changes) is concerning and must be assessed immediately. This
type of headache is often indicative of an increase in pressure around the
brain, which can be life threatening if left untreated.67
Physical Deficits
Many patients will experience physical deficits as a result of a brain injury.
The most common physical problems experienced after injury include:30

Hearing loss

Tinnitus (ringing or buzzing in the ears)

Headaches

Seizures

Dizziness

Nausea

Vomiting

Blurred vision

Decreased smell or taste

Reduced strength and coordination in the body, arms, and legs
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Vomiting/Nausea
Vomiting and nausea are common symptoms in instances of head trauma
and can occur with mild to severe trauma. When a patient experiences
vomiting or nausea, it is important to make sure he or she is comfortable
and that there is no chance of asphyxiation.68
Loss of Consciousness
It is common for TBI patients to experience loss of consciousness
immediately following a head injury. Some patients will only lose
consciousness for a few seconds, while others may remain unconscious for
hours or days.69 Loss of consciousness can affect the patient even after he or
she awakens. The following is a list of the most common side effects a
patient will experience after a loss of consciousness:70

Drowsiness

Confusion

Restlessness

Agitation upon waking

Vomiting

Seizures

Impaired balance

Lack of coordination

Impaired ability to think

Inability to control emotions

Difficulty moving

Inability to feel things

Difficulty with speech

Loss of vision

Hearing impairment

Memory impairment or loss
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Altered Consciousness
A coma is defined as a deep state of unconsciousness.71 A patient who
experiences a coma is alive, but loses the ability to move or respond to the
environment and external stimulation.47 Most comas last an average of two
to four weeks, but some patients can remain in a coma for an extended
period of time. The duration of a coma and the extent of recovery will vary
depending on the cause, severity and location of the damage.72 Some
patients will recover completely from a coma, while others will experience
long-term physical, mental, intellectual and emotional problems.71 A patient
who remains in a coma for an extended period of time (months or years) is
at an increased risk of developing an infection such as pneumonia, which can
be life threatening.73
During a coma, a patient is completely unconscious and cannot be aroused.
The patient is also unresponsive and unaware of his or her surroundings.71
Patients will not respond to external stimuli and do not experience sleepwake cycles.74 A coma is typically the result of severe trauma to the brain,
and is most common with injuries to the cerebral hemispheres of the upper
brain and the lower brain or brainstem.72 In most instances, a coma will only
last for a few days or a few weeks. However, in some extreme situations, a
patient may progress to a vegetative state.75
When a patient appears to be in a coma, the trauma team will first stabilize
the patient and assess the vital signs and basic neurological signs. After the
vital signs and basic neurologic functions are assessed, the emergency
medical provider will assess the patient’s level of consciousness and
neurologic functioning.74 This assessment is done using the Glasgow Coma
Scale, which is a standardized, 15-point test that measures neurologic
functioning using three assessments: eye opening, best verbal response,
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and best motor response. A patient will be determined to be in a coma if he
of she meets the criteria on the coma scale.4
The Center for Disease Control provides guidelines for the Glasgow Coma
Scale. This will be discussed later on in more detail within the section on
Diagnosis Of TBI; however, in brief, when assessing patients’ level of
consciousness the provider or nurse caring for the TBI patient may use the
Glasgow Coma Scale to measure the following:
Eye Opening Response

Spontaneous - open with blinking at baseline 4 points

To verbal stimuli, command, speech 3 points

To pain only (not applied to face) 2 points

No response 1 point
Verbal Response

Oriented 5 points

Confused conversation, but able to answer questions 4 points

Inappropriate words 3 points

Incomprehensible speech 2 points

No response 1 point
Motor Response

Obeys commands for movement 6 points

Purposeful movement to painful stimulus 5 points

Withdraws in response to pain 4 points

Flexion in response to pain (decorticate posturing) 3 points
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
Extension response in response to pain (decerebrate posturing) 2
points

No response 1 point
Categorization includes:
Coma: No eye opening, no ability to follow commands, no word
verbalization (3-8)
Head Injury Classification:

Severe Head Injury ---- GCS score of 8 or less

Moderate Head Injury ---- GCS score of 9 to 12

Mild Head Injury ---- GCS score of 13 to 15
The following is a standard disclaimer that accompanies the Glasgow Coma
Scale:
Based on motor responsiveness, verbal performance, and eye opening
to appropriate stimuli, the Glasgow Coma Scale was designed and
should be used to assess the depth and duration coma and impaired
consciousness. This scale helps to gauge the impact of a wide variety
of conditions such as acute brain damage due to traumatic and/or
vascular injuries or infections, metabolic disorders (i.e., hepatic or
renal failure, hypoglycemia, diabetic ketosis), etc.75
The coma is one form of altered consciousness that occurs during brain
injury. If the trauma is severe enough, patients may experience one of the
other types of altered consciousness. These altered states of consciousness
are often considered different types of comas, even though they have
different symptoms. The symptoms are briefly described as follows:
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
Stupor
When a patient experiences a stupor, he or she is often unresponsive
but is able to be aroused, if only briefly, by a strong stimulus.11

Vegetative State
When a patient is in a vegetative state, he or she is completely
unaware of the surroundings. However, unlike with a coma, patients in
a vegetative state continue to have a sleep-wake cycle. In addition,
patients may experience periods of alertness.6 Patients in a vegetative
state will often open their eyes and show other signs of movement and
function, which may include groaning and some reflex responses.11 In
many instances, a vegetative state is the result of trauma to the
cerebral hemispheres with the absence of injury to the lower brain and
brainstem.76
Most patients will only remain in a vegetative state for a few weeks,
but some may progress to a persistent vegetative state, which is
defined as longer than thirty days.11 Once a patient has been in a
vegetative state for a year, the chances of recovery are extremely
low.7

Minimally Conscious State
This term (coined by the Aspen Neurobehavioral Workgroup)
accommodates the need to differentiate between patients who meet
criteria for the diagnosis of vegetative state and those who display
some, albeit limited and inconsistent, meaningful responses. As such,
the minimally conscious state shares with the vegetative state a
severe alteration of consciousness, but is differentiated by evidence of
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“… minimal but definite behavioral evidence of self or environmental
awareness”. In this respect it is clinically differentiated from the
vegetative state by virtue of a small but demonstrable and
reproducible repertoire of behaviors, such as following simple
commands, gestural or verbal yes/no responses (even if inaccurate),
intelligible verbalization, and some form of purposeful behavior, such
as contingent vocalization, smiling or crying in response to input that
has some emotional salience, and reaching for objects in a way that
signals awareness of the object’s size and shape.
As noted by participants at the Aspen Neurobehavioral Workgroup
(ANW) in 1994, however, clear differentiation of the border-zones of
the vegetative and minimally conscious state may not be
straightforward at all. The ANW participants suggested that clinicians
need to consider the relative weight of consistency and complexity in
the patient’s responses, where there is less need to demonstrate
consistency of a complex response such as verbalization than of a
simple response such as a finger movement to command. When
patients are able to demonstrate consistent and reliable functional
communication, they are deemed to have emerged from the minimally
conscious state.
In spite of the concerted efforts of multidisciplinary working parties in
recent years, there are some persisting tensions around the use of
terminology. Older terms such as apallic syndrome, coma vigile, and
akinetic mutism are no longer in use. However, the locked-in
syndrome must be clearly distinguished from vegetative/minimally
responsive states. This rare syndrome has been discussed in some
detail in the literature and usually results from a lesion (infarction,
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hemorrhage or demyelination) in the ventral pons or medulla. The
person is typically quadriparetic and mute, but can demonstrate
significantly preserved cognitive abilities via vertical eye movements
and/or blinking.
Unlike the person in a vegetative or minimally responsive state, the
person in a locked-in state is able to give clear signs of awareness of
self and the environment. Furthermore, measures of cerebral glucose
metabolism in these patients are near normal. It is also important (but
less difficult) to differentiate vegetative/minimally responsive states
from brain death, which results in the absence of both brainstem and
supratentorial function.
Brain death is confirmed by the presence of various combinations of
coma, apnea, dilated pupils, absent cephalic reflexes and
electrocerebral silence on EEG recording, and is not compatible with
survival once artificial respiration is removed.

Locked-In Syndrome
With Locked-In Syndrome, the patient is unable to move or
communicate normally as the result of paralysis of the body.
However, the patient is fully aware and awake.4 Locked-In Syndrome
is caused by damage to areas in the lower brain and brainstem, but
not by damage to the upper brain.47 Typically, patients use
movements and eye blinking to communicate. Ultimately, most
patients do not gain their motor control back once they are in a
locked-in state.11
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
Brain Death
Brain death is a newer diagnosis that has occurred due to the
development of assistive devices that artificially maintain blood flow
and breathing.11 Brain death is defined as a lack of measurable brain
function. This is typically caused by injuries to the cerebral
hemispheres and brainstem.7 There is also a loss of integrated activity
within specific areas of the brain.11 This condition is irreversible. If a
patient does not remain on assistive devices, he or she will experience
immediate cardiac arrest and will stop breathing.28
The various unconscious states listed above are easy to diagnose as the
result of advancements in imaging and other technologies. Using these new
technologies, practitioners can identify the area of the brain affected and
diagnose the patient based on the level of activity present in different
regions of the brain.6 Most commonly, doctors use CT and MRI to identify
the affected areas of the brain. However, other diagnostic imaging tools such
as cerebral angiography, electroencephalography (EEG), transcranial
Doppler, ultrasound, and single photon emission computed tomography
(SPECT) may be used.77
Complications of TBI
Traumatic brain injuries can cause a number of complications that may occur
during the onset of the injury, as well as after the injury has been treated
and resolved. In some instances, these complications may be mild and easily
treatable and manageable; whereas, in other instances, these complications
can pose a significant threat to the individual. Some complications can be
life threatening, while others may cause long-term disability.10
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A traumatic brain injury can cause some significant initial complications
within the following categories:7

Arousal

Consciousness

Awareness

Alertness

Responsiveness
The above conditions are complications that are specific to traumatic brain
injury. However, there are also conditions that can occur immediately after a
traumatic brain injury that are not specific to TBI, but that occur as a direct
result of the injury. These complications increase in prevalence in direct
correlation to the severity of the injury.
Complications of TBI include:47

Immediate seizures

Hydrocephalus or posttraumatic ventricular enlargement

CSF leaks

Infections

Vascular injuries

Cranial nerve injuries

Pain

Bed sores

Multiple organ system failure in unconscious patients
Seizures
It is common for patients with TBI to experience seizures. In fact, 25% of
patients with brain contusions or hematomas will experience seizures, while
approximately 50% of patients with penetrating head injuries will experience
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seizures.78 In these patients, seizures typically occur within the first 24
hours of the injury.79 While some patients who experience immediate
seizures will have an increased risk of developing seizures that occur within
hours or days of the injury, there is no risk of the patient developing
posttraumatic epilepsy. Typically, patients who experience immediate or
early seizures are treated with anticonvulsants if the seizures are persistent
and recurring.78
Hydrocephalus and Posttraumatic Ventricular Enlargement
Hydrocephalus or posttraumatic ventricular enlargement is a condition that
is caused by the accumulation of cerebrospinal fluid in the brain. This excess
fluid causes dilation of the cerebral ventricles and an increase in intracranial
pressure (ICP).80 This condition is common during the acute stage of
traumatic brain injury, but it can also occur during later stages.5 It is most
common within the first year of the injury.81 It is characterized by worsening
neurologic outcome, behavioral changes, incontinence, axtaxia, and
impaired consciousness.52 This condition typically develops as a result of
meningitis, subarachnoid hemorrhage, intracranial hematoma, or various
other injuries that have the potential to produce pressure.11 Typical
treatment involves shunting and draining the fluid.6
Infections
Individuals with traumatic brain injury are prone to a number of infections
that can occur within the intracranial cavity. Depending on the type of
injury, infections can occur in a variety of locations in the brain, including
the dura, below the dura, below the arachnoid, and within the space of the
brain.5 The majority of infections will develop within a few weeks of the
trauma. They can result from penetrating injuries or from skull fractures.
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Patients are typically treated with antibiotics. However, surgery may
occasionally be used to remove sections of the infected tissue.11
Vascular Injuries
Traumatic brain injury patients are especially prone to vascular injuries due
to the damage caused to the head and/or brain. While damage to small
blood vessels rarely has a significant impact on the patient, damage to the
large blood vessels can result in severe complications. For instance, damage
to a major artery may result in a stroke due to bleeding from the artery or
as a result of the formation of a clot.81
Common types of vascular injuries include:82

Hemorrhagic stroke – bleeding directly from the artery

Ischemic stroke – blocked blood flow to the brain

Thrombus or thrombosis – the formation of a clot at the site of the
injury

Vasospasm – an exaggerated, persistent contraction of the walls of the
blood vessel

Aneurysms – blood filled sacs caused by stretching of an artery of
blood vessel
Patients with the above conditions may experience headaches, vomiting,
partial paralysis (often on one side of the body) and semi-consciousness.
These symptoms often appear several days after the injury.5 Depending on
the specific complication, different treatments will be used. For example,
anticoagulants are often used to treat ischemic strokes. However, surgery is
typically used to treat hemorrhagic strokes.11
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The conditions included above occur immediately following the onset of a
traumatic brain injury. Therefore, they are often identified and treated
during the initial stage of injury.6 In addition to injuries that occur during the
initial stage of injury, there are other complications that will develop over
time and that will typically last throughout the individual’s lifetime, or at
least for a significant period of time.7 These complications are considered
TBI related disabilities.
Traumatic brain injury related disabilities vary depending on the location of
the injury, the severity of the injury and the age and general health of the
patient. The most common types of TBI related disabilities affect the
following areas:80

cognition (thinking, memory, and reasoning)

sensory processing (sight, hearing, touch, taste, and smell)

communication (expression and understanding)

behavior or mental health (depression, anxiety, personality changes,
aggression, acting out, and social inappropriateness)
It is quite common for TBI patients to develop a range of symptoms and
complications as a result of the injury. In fact, approximately 40% of all TBI
patients develop post concussion syndrome (PCS), which is defined simply
as a collection of symptoms, within days or weeks of suffering an injury.83
PCS is common in all TBI patients, not just those who have experienced a
concussion or loss of consciousness. In fact, a number of patients who are
being treated for mild TBI are diagnosed with PCS.84 The following
symptoms are common in patients with PCS:41

Headache

Dizziness
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
Vertigo (a sensation of spinning around or of objects spinning around
the patient)

Memory problems

Trouble concentrating

Sleeping problems

Restlessness

Irritability

Apathy

Depression

Anxiety
These symptoms may last for a few weeks after the head injury. Typical
treatment involves the use of medicines and therapy to reduce the impact of
the symptoms and help the patient cope.85
Cognitive Impairments
It is common for patients with traumatic brain injury to experience cognitive
disabilities, especially if they have lost consciousness. In many patients, the
impairments include a loss of higher level mental skills.54 Of the different
cognitive impairments, memory loss is the most common, with patients
experiencing the loss of specific memories and the inability to form or store
new memories. In some instances, patients may develop posttraumatic
amnesia. There are two types of posttraumatic amnesia:86

Anterograde – impaired memory of events that happened after the TBI

Retrograde – impaired memory of events that happened before the
TBI
It is common for patients with cognitive impairments to become confused
easily or to have problems with distraction. These patients will typically
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experience difficulty concentrating and focusing their attention. Some
patients may also experience problems with higher level functions, which
includes planning, organizing, abstract reasoning, problem solving, and
making judgments.54 Patients experience the greatest recovery during the
first six months, after which the recovery becomes more gradual. Cognitive
impairments are more common in patients with moderate or severe TBI.11
Sensory Problems
Sensory impairments are common in TBI patients. The most common form
of sensory impairment is with vision. It is common for TBI patients to
experience difficulty registering what they are seeing or recognizing various
objects.52 TBI patients are also prone to problems with hand eye
coordination. Due to these impairments, TBI patients often experience
difficulty maneuvering through spaces and often bump into objects or drop
them.90 Sensory impairments produce a general instability in TBI patients.
As a result, many TBI patients are unable to operate a motor vehicle or
complex machinery.52 Many of these sensory issues cannot be treated and
remain with the patient indefinitely. However, in some instances, optometric
vision therapy has produced good results in patients with oculomotor
dysfunctions.87
While vision impairments are the most common form of sensory impairment
in TBI patients, some patients will also develop problems with hearing,
smell, taste, or touch. These impairments are the result of damage to the
areas of the brain that controls these senses. These conditions are difficult to
treat.52
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Language and Communication Problems
Many TBI patients experience language and communication problems. Some
patients only experience difficulties with subtle aspects of communication,
such as body language and emotional, nonverbal signals.88 However, others
will actually experience difficulty understanding and producing spoken and
written language. This type of impairment is called aphasia.89 The following
is a list of the different forms of aphasia:88

Broca’s Aphasia (nonfluent/motor):
Broca’s aphasia involves difficulty recalling words and/or speaking in
complete sentences. Characterized by broken phrases and frequent
pauses. Patients often experience extreme frustration.

Wernicke’s Aphasia (fluent/sensory):
Patients display little meaning in their speech, but typically they speak
in complete sentences and use correct grammar. Wernicke’s aphasia is
characterized by the use of flowing gibberish and sentences that
include nonessential and invented words. Patients are often unaware
that they are not making sense and express frustration when others
do not understand them.

Global Aphasia:
In global aphasia there is extensive damage to the portions of the
brain responsible for language. It is characterized by severe
communication disabilities.
In some instances, TBI patients may experience difficulties with spoken
language as a result of damage to the section of the brain that controls the
speech muscles. This disorder is called dysarthria, and it affects patients
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differently than other impairments. With dysarthria, the patient is able to
understand and think of appropriate words/language. However, the patient
is unable to speak the words because of damage to the speech muscles.93
Therefore, speech may be slurred and garbled. Some patients experience
difficulty with intonation or inflection. This is called prosodic dysfunction.90
Emotional and Behavioral Problems
Many TBI patients experience emotional and behavioral difficulties, which
are often classified as general psychiatric issues.91 It is common for a TBI
patient to exhibit personality changes and behavioral issues. The following is
a list of the common psychiatric problems experienced by TBI patients.56

Depression

Apathy

Anxiety

Irritability

Anger

Paranoia

Confusion

Frustration

Agitation

Insomnia or other sleep problems

Mood swings
Typically, behavioral problems include the following:92

Aggression and violence

Impulsivity

Disinhibition and acting out

Noncompliance

Social inappropriateness
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
Emotional outbursts

Childish behavior

Impaired self-control

Impaired self-awareness

Inability to take responsibility or accept criticism

Egocentrism

Inappropriate sexual activity

Alcohol or drug abuse/addiction
In some instances, the personality issues may be severe enough to warrant
a diagnosis of borderline personality disorder.93 Other TBI patients may
experience developmental stagnation. When this occurs, the patient fails to
mature emotionally, socially, or psychologically after the trauma.92 This is
especially problematic for children and young adults who suffer from a TBI.
Typical treatment for the various emotional and behavioral problems
includes medication and therapy.6
Coup and Contrecoup Effect
In some instances, the patient will experience a coup or contrecoup injury to
the head. These terms are used to identify a range of head injuries, but they
are most commonly used in instances of cerebral contusions.51 The two
terms are used to identify the specific injury pattern and the location of the
damage. The following is a description of the different types of injury.
Coup Injury
Damage to the brain at the point of initial impact or blow.
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Contra Coup Injury
Damage to the brain on the side opposite the side that received the initial
impact or blow.
Coup- Contrecoup Injury
Damage to the brain on both sides- the side that received the initial impact
or blow and the side opposite the initial impact. This occurs when the force
of the initial blow is great enough to cause brain damage at the site of initial
impact between the skull and brain and is also great enough to cause the
brain to move in the opposite direction and hit the opposite side of the skull,
causing damage at that site.94
Diagnosis Of TBI
Assessment and treatment of traumatic brain injury should begin as soon as
possible. Therefore, emergency personnel are often the first individuals who
assess and treat the injury.11 Typically, treatment begins as soon as
emergency responders arrive on the scene or as soon as an individual
arrives at the emergency room. Initial brain damage that is caused by
trauma cannot be reversed. So, initial treatment involves stabilizing the
patient and administering treatment that will prevent further damage.6
The key components of the trauma assessment are as follows:
1. ABC’s:
Assess the airway with stabilization of the cervical spine, breathing,
circulation, heart rate and blood pressure before the neurological
exam.
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2. Examination of the Skull:
Assess for periorbital and postauricular ecchymosis, cerebrospinal fluid
otorrhea and rhinorrhea, hemotympanum, penetrating injury or
depressed fracture, and lacerations.
3. History:
Gather information related to the mechanism of injury and care prior
to hospitalization.
4. Neurological Exam:37
Cerebral function
Assess the level of consciousness,
mental status, awareness, arousal,
cognitive function, and behavior.
Cranial Nerve and pupillary
This reflects brainstem function.
examination
Assess the pupils, eye movements,
cough reflex, corneal reflex and gag
reflex.
Motor and cerebellar function
Assess strength, movement, gait,
and posture. Each extremity must be
assessed separately. It is important
to document the degree and type of
stimulus applied to elicit the motor
activity. Central stimuli include
sternal rub, trapezius pinch and/or
supraorbital pressure. Abnormal
findings include abnormal posturing,
flaccidity, and focal motor
movements.
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Sensory examination
Assess tactile and pain sensations.
Reflex examination
Assess superficial and deep tendon
reflexes.
Glasgow Coma
This is a valuable component of the
Scale
neurological exam because it is
nationally and internationally
recognized. It is only one part of the
neurological exam.
Severe Head Injury: GCS # 8 or a
decrease in 2 points or more after
admission.
Moderate Head Injury: GCS 9-12
Mild Head Injury: GCS 13-15
Due to the diverse causes of head injury and the differing needs of patients,
initial contact with the patient involves an assessment of the cause of the
injury and a screening to determine the extent of the injuries.6 This is
important, as the mechanism of injury will determine the type of treatment
needed. For example, blast trauma related head trauma is more complex
than other forms of head trauma.95 Due to the complexity of the blast
related head injury, the assessment and treatment can be difficult to
administer and determine. Therefore, in combat, it is more common to
evaluate all service members who have been exposed to a blast and identify
those that present symptoms of head injury.95 However, in civilian instances
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of head trauma, it is more common to assess each patient individually based
on the symptoms present as non blast related causes of head trauma tend
to be less complicated.6
Prior to conducting a full assessment of an individual who is suspected of
having a traumatic brain injury, the primary concern is ensuring that the
patient is stabilized and that any further injury is prevented. During the
initial stage of contact, medical personnel are primarily concerned with
ensuring that the patient has a proper supply of oxygen to the brain and the
rest of the body.96 Another priority is to maintain an adequate blood flow
while controlling blood pressure. This will help stabilize the patient while
minimizing further damage to the brain.6
Once a patient is stabilized, medical personnel will assess the patient and
determine the extent of the injury. Primary assessment includes measuring
vital signs and reflexes, as well as administering a thorough neurological
exam. The initial exam includes checking the patient’s temperature, blood
pressure, pulse, breathing rate, pupil size and response to light.35
After the vital signs and basic neurologic functions are assessed, the
emergency medical provider will assess the patient’s level of consciousness
and neurologic functioning. This assessment is done using the Glasgow
Coma Scale, as previously stated, which is a standardized, 15-point test that
measures neurologic functioning using three assessments: eye opening, best
verbal response, and best motor response. These measures are used to
determine the severity of the brain injury. A test score of 13 to 15 is
classified as mild, 9 to 12 as moderate, and 3 to 8 as severe. Though well
known and widely used, this classification scheme is most useful in
predicting acute survival and gross outcome, and performs more poorly in
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predicting later and more detailed functional outcomes, particularly in
cognitive and emotional realms.97
The Center for Disease Control provides the following guidelines for the
Glasgow Coma Scale. Medical responders should use this scale to assess the
level of severity of brain injury when performing a diagnostic work-up, as
mentioned in the prior section and also highlighted in the table below. The
Glasgow Coma Scale is frequently available as a quick access guide within
many flow-charts or documentation templates and electronic health records
so that health teams can easily trend patient care outcomes.
After the Glasgow Coma Scale is administered, further testing is conducted
to determine the level of damage and the severity of the injury. Imaging
tests are used to assist with the diagnosis of the patient as well as to make a
determination about the prognosis of the patient.6 Skull and neck x rays are
used to check for bone fractures and spinal instability in patients with mild to
moderate injuries.98
In patients with mild head injuries, a diffusion tensor imaging is sometimes
used. This device can reliably detect and track brain abnormalities and is
sensitive enough to be used on patients with mild injury.8 In some cases, a
magnetoencephalography may be used to obtain further information
regarding a mild case of head trauma.99 Additional diagnostic imaging is
used in cases of moderate to severe head injury. In these instances, patients
will be assessed using a computed tomography (CT) scan. This scan creates
cross sectional X-ray images of the head and brain and is used to identify
any bone fractures that might be present in the skull. The CT scan also
indicates if there is the presence of hemorrhage, hematomas, contusions,
brain tissue swelling, and tumors.100
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Glasgow Coma Scale
Eye Opening Response

Spontaneous--open with blinking at baseline 4 points

To verbal stimuli, command, speech 3 points

To pain only (not applied to face) 2 points

No response 1 point
Verbal Response

Oriented 5 points

Confused conversation, but able to answer questions 4 points

Inappropriate words 3 points

Incomprehensible speech 2 points

No response 1 point
Motor Response

Obeys commands for movement 6 points

Purposeful movement to painful stimulus 5 points

Withdraws in response to pain 4 points

Flexion in response to pain (decorticate posturing) 3 points

Extension response in response to pain (decerebrate posturing) 2 points

No response 1 point
Categorization
Coma:

No eye opening, no ability to follow commands, no word verbalizations (3-8)
Head Injury Classification:

Severe Head Injury ---- GCS score of 8 or less

Moderate Head Injury ---- GCS score of 9 to 12

Mild Head Injury ---- GCS score of 13 to 15)
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Once the initial assessment is
complete, in addition to the diagnostic
testing already mentioned, other
imaging may be conducted. In these
instances a magnetic resonance
imaging (MRI) is often used to
determine if there is additional damage
beyond the scope of the initial
assessment. The MRI is used to
determine if there have been any subtle
changes in the brain tissue and are
used when more detail is needed than
standard X-rays can provide.29 MRI’s are not used during the initial
emergency assessment as they require a significant amount of time and are
not always available during the initial assessment.17 However, an MRI is an
important diagnostic tool and should be used when appropriate and
available.
Examination
When a patient presents with a
head injury, he or she will undergo
a complete examination with the
purpose of assessing the trauma
and identifying specific injuries.
While the examination will vary
depending on the patient’s needs,
there are standard examination methods that are typically used during the
initial examination.
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Regardless of the type of injury (blunt or penetrating, open or closed) the
initial examination will be conducted as soon as possible and will often occur
in conjunction with resuscitation.101 It is important to conduct the initial
assessment as soon as possible to identify any life-threatening injuries and
to minimize any additional damage. Early identification of any complications
will reduce the likelihood of the patient developing secondary injuries.85
While it is important to manage any damage caused by an open head
wound, it should not interfere with the initial stabilization of the patient.
Therefore, the initial stage of the patient examination will include assessing
and managing the airway, breathing, circulation, and related components.43
Once that is complete, the emergency provider will begin the primary
survey. The primary survey or examination will focus on identifying any
complications or secondary injuries.102 The following table includes the
guidelines provided for the primary and secondary examination of the
patient.101
Primary Examination
As part of the primary survey, the pupillary size and reactions are noted and the
conscious state is assessed. Disturbances of consciousness may follow focal damage to
the reticular formation, which extends from the rostral midbrain to the caudal medulla.
It receives input from all sensory pathways and projects widely to the cerebral cortex
and limbic system. Focal cortical lesions do not affect consciousness, but coma may
result from general depression of the cerebral cortex.
Using purely descriptive methods to assess conscious state is problematic. One
observer’s “somnolent” is another’s “drowsy”. When is a person stuporous and when
are they obtunded? What is semi-conscious and when does a clouded conscious state
become coma? Consciousness is a continuum and the Glasgow Coma Scale (GCS) is
used as a measure (albeit crude) of level of consciousness.
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Secondary Examination
Once the primary survey is complete, the secondary survey should include a more
thorough neurological examination, starting with a reassessment of the Glasgow Coma
Scale, and an examination of the head, face and neck. The head and face should be
examined for lacerations and fractures. Scalp lacerations can be palpated with a gloved
finger. If there is an underlying depressed fracture, surgery will be required. Profuse
bleeding may occur from a scalp laceration and this can be controlled with a pressure
dressing or by a few temporary full-thickness sutures.
The nose and ears are inspected for leaks of cerebrospinal fluid (CSF). This is usually
mixed with blood and results in a thinner discharge that will separate on blotting paper.
If this is not available, the separation can also be observed on a sheet or pillowcase. If
there is CSF rhinorrhea or otorrhoea, a basal skull fracture is present (regardless of
whether it can be seen on radiographs).
Bilateral periorbital hematomas (raccoon eyes) and subconjunctival hemorrhages
where the posterior margin cannot be seen are both indicators of anterior fossa
fracture. Hemotympanum or bruising over the mastoid (Battle’s sign) suggests a
middle fossa fracture. Battle’s sign usually takes several hours to develop. The nose,
mid face and orbits should also be palpated for fractures that may require treatment
later.
When the patient is logrolled, the back of the head and cervical spine should also be
examined. The neurological examination will be limited because of the lack of
cooperation of the patient, but it should still be possible at least to determine if there
are lateralizing signs such as a hemiparesis or a third cranial nerve palsy.
Higher functions are assessed first. Most often this will be limited to level of
consciousness and, in particular, the “voice” component of the GCS. In a relatively
cooperative patient with a focal injury it may be possible to assess language further,
but in the early period after a head injury it will be difficult to differentiate dysphasia
from confusion. Memory becomes important later and the period of post-traumatic
amnesia is used as an indicator of injury severity.
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Cranial Nerves
Many of the cranial nerves can be assessed even in the unconscious patient. These are
outlined below.
I (olfactory):
Assessment obviously requires cooperation, but this nerve should be examined when
possible, as it is the most commonly affected cranial nerve after head injury and is
often ignored. Anosmia may seem trivial but it has significant effects beyond
enjoyment of food and wine. Anosmic patients will not be able to smell smoke from a
fire or leaking gas, both of which may potentially put them at risk.
II (optic):
The pupillary reactions to light depend on the integrity of the optic and oculomotor
nerves, as well as their connections. Normally both pupils should constrict when light is
shone in either eye or when the patient looks at a near object (accommodation reflex).
A pupil that responds to direct light implies that the ipsilateral optic and oculomotor
nerves are intact. If it responds to direct light, but not consensually, this implies
damage to the contralateral optic nerve. A pupil reacting only consensually suggests
ipsilateral optic nerve damage. An oculomotor nerve injury will produce an ipsilateral
dilated pupil, which does not respond directly or consensually, but the contralateral
pupil will constrict when light is shone in either eye. One must remain aware that the
most common cause of a dilated pupil after head injury is traumatic mydriasis due to
local ocular trauma. This should be suspected if the dilated pupil was present right from
the time of injury and there is local trauma to the globe or orbit.
During examination of the eyes the fundi are assessed. One would not expect to see
papilledema in the early hours after a head injury, and funduscopy is done more for the
purpose of assessing the integrity of the eye itself (checking for retinal detachment or
hemorrhage, vitreous hemorrhage, corneal laceration, etc.). Contact lenses should be
looked for and removed. Visual fields can be checked by confrontation in a cooperative
patient or by menace in an uncooperative patient. They are not clinically assessable in
the unconscious patient.
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III, IV and VI (oculomotor, trochlear and abducens):
The pupils are assessed as above. Ptosis (III) is difficult to assess in patients who are
unconscious. Ocular movements can be observed and any dysconjugate movements
noted. If the patient is cooperative this is easy. An alert but uncooperative patient can
be made to look at objects quite readily by placing them in their field of vision. This
also applies to children. Oculocephalic reflexes test the third, fourth and sixth cranial
nerves and their connections. Movement of the head from side to side or up and down
will be accompanied by movement of the eyes in the opposite direction, resulting in a
constant point of fixation.
The term “doll’s eyes” is often used to describe oculocephalic reflexes but this
frequently leads to confusion. Whether doll’s eyes are normal or abnormal depends on
the sophistication of the doll. One with eyes painted on would describe the abnormal
and one with eyes free to rotate would better approximate the normal situation. It is
preferable to avoid the term altogether and describe oculocephalic reflexes as being
normal or abnormal.
It is not usually recommended to test oculocephalic reflexes in a head-injured patient
owing to the high risk of associated cervical spinal injury. If it is important to know if
these reflexes are intact (i.e., in assessing brain death).
V (trigeminal):
The motor component of the trigeminal nerve can be tested in a cooperative patient,
but the sensory part can be assessed even in the unconscious. Painful stimuli applied to
the supraorbital nerve should usually produce a response and the corneal reflex tests
trigeminal function as well as facial nerve function.
VII (facial):
Facial movements are readily assessed in the cooperative patient, but can also be
observed when painful stimuli are applied and as part of the corneal reflex. Facial nerve
palsies are often seen with middle fossa fractures and this nerve should be assessed
early in any patient with CSF otorrhoea or Battle’s sign. Taste is not usually tested.
Patients often complain of loss of taste after a head injury (usually due to anosmia).
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VIII (acoustic):
This is hard to test clinically in the unconscious patient. An alert but uncooperative
patient can be observed for reaction to sudden noises. Assessment in the unconscious
usually requires brainstem auditory evoked potential monitoring. This nerve is also
often injured in middle fossa fractures.
IX (glossopharyngeal), X (vagus):
There is usually little more to do than observe swallowing and test the gag reflex,
either directly or by moving an endotracheal tube.
XI (accessory):
Sternomastoid and trapezius function can be tested, but it is unusual for the accessory
nerve to be injured intracranially.
XII (hypoglossal):
A hypoglossal nerve injury will force the protruded tongue to the ipsilateral side. Over
time the ipsilateral side of the tongue becomes wasted.
Motor Function
The sophistication of motor testing depends on the level of cooperation of the patient.
At the least, it is possible to detect asymmetry in movement or responses to pain as
described above in assessing the GCS. Reflexes are often brisk but may be absent with
associated spinal cord injury (spinal shock). Plantar reflexes will usually be extensor
after a significant head injury. Priapism and loss of anal tone are other indicators of
spinal cord injury that should be sought.
Sensory Function
The same applies as for motor function. If there is a response to pain, this can be
compared in different areas. This is important when a spinal cord injury is suspected
and one is attempting to determine at what level. Sometimes there can be movement
of limbs through local spinal cord reflexes; hence, when assessing a patient for brain
death, it is mandatory that the painful stimulus be applied to a cranial nerve
distribution.
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Traumatic Brain Injury Assessment
If traumatic brain injury is suspected, the patient will undergo a more
thorough examination, which will include the following physical and mental
evaluation.103
Cognitive

Orientation

Command following (single, multistep)

Attention

Concentration

Memory (short- and long-term)

Naming/repetition

Abstract thinking

Judgment
Behavioral

Depression

Anxiety

Irritability

Agitation

Restlessness

Disinhibition
Musculoskeletal

Manual muscle (strength) testing

Joint range of motion (including temporomandibular joint)

Muscle tone

Mobility
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
Balance — sitting, standing, dynamic

Transfers

Gait — indoor, outdoor, stair
Neurologic

Cranial nerve testing

Sensory function

Special sensory
o Vision
o Hearing
o Smell/taste

Deep tendon reflexes

Primitive reflexes (frontal release signs)
o Palmomental reflex
o Snout reflex
o Glabellar (tap) reflex
o Palmar grasp reflex

Brainstem reflexes
o Oculocardiac reflex
o Horizontal oculocephalic/oculovestibular reflex
o Pupillary light reflex
o Vertical oculocephalic/oculovestibular reflex
o Fronto-orbicular reflex

Bowel/bladder reflexes
o Cremasteric reflex
o Bulbocavernosus reflex
o Anal wink reflex
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
Cerebellar testing
o Finger to nose (upper extremity dysmetria)
o Heel to shin (lower extremity dysmetria)

Fine and gross motor coordination (tremor)

Autonomic nervous system
General Medical Exam

Skin

Heart/circulation

Lung

Abdomen
o Digestive
o Bowel

Genitourinary

Endocrine
Radiologic Imaging
In many instances, the examination will include radiologic imaging. The
following tables,104 provided by the American College of Radiology (ACR),
give specific recommendations for the different radiologic procedures that
are used in head trauma situations. The rating scale for each procedure is
shown and explained at the end of each table; for example, the numerical
rating relative to the level of appropriateness to perform a specific procedure
for a particular condition. Additionally, the relative radiation level (RRL) is
shown using the symbol [ ] or [O] (zero) to indicate the amount of
exposure during the procedure. Each table title identifies the specific
condition and corresponding GCS score. Major recommendations to evaluate
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the appropriateness of a radiologic procedure, as shown in the tables below,
include: ACR Appropriateness Criteria® and Clinical Condition/ Head
Trauma. Abbreviations used in the tables are not reviewed in depth here,
but may be referenced at the ACR website: http://www.acr.org/QualitySafety/Standards-Guidelines.
Variant 1: Minor or mild acute closed head injury (GCS ≥13), without risk factors
or neurologic deficit.
Radiologic Procedure
Rating
Comments
RRL*
CT head without contrast
7
MRI head without contrast
4
MRA head and neck without
3
contrast
MRA head and neck without
Known to have low yield.
O
Rarely indicated with mild
O
trauma.
3
O
and with contrast
CT head without and with
3
contrast
CTA head and neck with
3
contrast
MRI head without and with
Rarely indicated with mild
trauma.
2
O
contrast
CT head with contrast
1
X-ray head
1
FDG-PET/CT head
1
US transcranial with Doppler
1
Arteriography cervicocerebral
1
Tc-99m HMPAO SPECT head
1
O
Rating Scale: 1,2,3 Usually not appropriate; 4,5,6 May be
*Relative
appropriate; 7,8,9 Usually appropriate
Radiation
Level
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Variant 2: Minor or mild acute closed head injury, focal neurologic deficit and/or
risk factors.
Radiologic Procedure
Rating
Comments
RRL*
CT head without contrast
9
MRI head without contrast
6
For problem solving.
O
MRA head and neck without contrast
5
If vascular injury is
O
suspected. For
problem solving.
MRA head and neck without and with
5
contrast
If vascular injury is
O
suspected. For
problem solving.
CTA head and neck with contrast
5
If vascular injury is
suspected. For
problem solving.
MRI head without and with contrast
3
CT head without and with contrast
2
CT head with contrast
1
Tc-99m HMPAO SPECT head
1
FDG-PET/CT head
1
US transcranial with Doppler
1
X-ray head
1
Arteriography cervicocerebral
1
O
O
Rating Scale: 1,2,3 Usually not appropriate; 4,5,6 May be
*Relative
appropriate; 7,8,9 Usually appropriate
Radiation
Level
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Variant 3: Moderate or severe acute closed head injury.
Radiologic Procedure
Rating
Comments
RRL*
CT head without contrast
9
MRI head without contrast
6
O
MRA head and neck without contrast
5
O
MRA head and neck without and with
5
O
contrast
CTA head and neck with contrast
5
CT head without and with contrast
2
MRI head without and with contrast
2
X-ray head
2
CT head with contrast
1
US transcranial with Doppler
1
FDG-PET/CT head
1
Arteriography cervicocerebral
1
Tc-99m HMPAO SPECT head
1
O
O
Rating Scale: 1,2,3 Usually not appropriate; 4,5,6 May be
*Relative
appropriate; 7,8,9 Usually appropriate
Radiation
Level
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Variant 4: Mild or moderate acute closed head injury, child <2 years old.
Radiologic Procedure
Rating
CT head without contrast
9
MRI head without contrast
7
Comments
RRL*
Diffusion weighted imaging
O
especially helpful for nonaccidental
trauma.
MRI head without and with
4
contrast
MRA head and neck without
Potentially useful in suspected
O
nonaccidental trauma.
4
If vascular abnormality suspected.
O
4
If vascular abnormality is
O
contrast
MRA head and neck without
and with contrast
CTA head and neck with
suspected.
4
contrast
X-ray head
If vascular abnormality is
suspected.
2
Appropriate as part of skeletal
survey in suspected nonaccidental
trauma. May be appropriate when
screening for patients suspected of
having penetrating head trauma or
foreign bodies.
CT head without and with
2
contrast
CT head with contrast
1
FDG-PET/CT head
1
Tc-99m HMPAO SPECT head
1
US transcranial with Doppler
1
Arteriography cervicocerebral
1
O
Rating Scale: 1,2,3 Usually not appropriate; 4,5,6 May be
*Relative
appropriate; 7,8,9 Usually appropriate
Radiation
Level
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Variant 5: Subacute or chronic closed head injury with cognitive and/or neurologic
deficit(s).
Radiologic Procedure
Rating
Comments
RRL*
MRI head without contrast
8
O
CT head without contrast
6
Tc-99m HMPAO SPECT head
4
For selected cases.
FDG-PET/CT head
4
For selected cases.
MRA head and neck without
4
For selected cases.
O
4
For selected cases.
O
4
For selected cases.
contrast
MRA head and neck without
and with contrast
CTA head and neck with
contrast
MRI head without and with
3
O
contrast
CT head without and with
2
contrast
CT head with contrast
2
X-ray head
2
MRI functional (fMRI) head
2
O
US transcranial with Doppler
1
O
Arteriography cervicocerebral
1
without contrast
Rating Scale: 1,2,3 Usually not appropriate; 4,5,6 May be
*Relative
appropriate; 7,8,9 Usually appropriate
Radiation
Level
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Variant 6: Closed head injury, rule out carotid or vertebral artery dissection.
Radiologic Procedure
CTA head and neck with
Rating
Comments
RRL*
8
contrast
MRA head and neck without
8
Add T1 neck images.
O
8
Add T1 neck images.
O
MRI head without contrast
8
Include diffusion-weighted images.
O
CT head without contrast
8
CT head without and with
6
Consider perfusion.
Arteriography cervicocerebral
6
For problem solving.
MRI head without and with
6
contrast
MRA head and neck without
and with contrast
contrast
O
contrast
CT head with contrast
4
X-ray head
2
Tc-99m HMPAO SPECT head
1
US transcranial with Doppler
1
FDG-PET/CT head
1
Consider perfusion.
O
Rating Scale: 1,2,3 Usually not appropriate; 4,5,6 May be
*Relative
appropriate; 7,8,9 Usually appropriate
Radiation
Level
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Variant 7: Penetrating injury, stable, neurologically intact.
Radiologic Procedure
Rating
CT head without contrast
9
CTA head and neck with
7
Comments
RRL*
contrast
MRA head and neck
6
If there is no MRI contraindication.
O
6
If there is no MRI contraindication.
O
5
If vascular injury is suspected.
5
If there is no MRI contraindication.
4
Consider perfusion.
4
If there is no MRI contraindication.
without contrast
MRA head and neck
without and with contrast
Arteriography
cervicocerebral
MRI head without
O
contrast
CT head without and with
contrast
MRI head without and
O
with contrast
X-ray head
4
CT head with contrast
2
US transcranial with
1
O
Doppler
Tc-99m HMPAO SPECT
1
head
FDG-PET/CT head
1
Rating Scale: 1,2,3 Usually not appropriate; 4,5,6 May be
*Relative
appropriate; 7,8,9 Usually appropriate
Radiation
Level
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Variant 8: Skull fracture.
Radiologic Procedure
Rating
CT head without contrast
9
CTA head and neck with
7
Comments
RRL*
If vascular injury is suspected.
contrast
MRI head without
6
O
contrast
X-ray head
5
For selected cases.
MRI head without and
4
Useful if infection suspected.
O
with contrast
CT head without and with
4
contrast
MRA head and neck
4
O
4
O
without contrast
MRA head and neck
without and with contrast
CT head with contrast
2
US transcranial with
1
O
Doppler
Tc-99m HMPAO SPECT
1
head
Arteriography
1
cervicocerebral
FDG-PET/CT head
1
Rating Scale: 1,2,3 Usually not appropriate; 4,5,6 May be
*Relative
appropriate; 7,8,9 Usually appropriate
Radiation
Level
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The tables above list the guidelines and recommendations for all forms of
radiologic imaging used in head trauma situations. However, the two most
commonly used diagnostic assessments are the Non-contrast CT and the
MRI.77
Computed Tomography
Computed tomography (CT scan) is a diagnostic imaging procedure that
produces horizontal, or axial, images of the body. These images are often
called “slices.”105 The CT scan uses a combination of X-Ray imaging and
computer technology to obtain the images in a noninvasive format.106 A CT
scan is an important diagnostic tool as it is able to provide detailed images
of different parts of the body. It is especially useful in obtaining images of
the bones, muscles, fat and organs.107
Computed tomography scans are used more frequently than standard
X-Rays because the images are more detailed.100 Standard X-Rays use a
single beam of energy that is aimed at the specific body part being analyzed.
The image is captured on a plate that is placed behind the body, once the
beam of light passes through the various body parts (skin, bone, muscle,
and tissue).2 X-Rays are limited in their ability to provide detailed imaging,
as they cannot capture images of internal organs and other structures of the
body. Therefore, a CT scan is often the primary assessment used.
A CT scan uses a moving X Ray beam to capture the images. The beam
circles around the body, thereby capturing a number of different views of the
same body part.106 The information is transmitted to a computer, which then
interprets the data and creates a two dimensional form. The form is
displayed on a monitor, which is then reviewed by the radiologist.108
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CT scans are conducted in two ways, as contract and non-contract.
Contrast
Patients ingest a substance orally or receive an injection intravenously. The
contrast solution enables the radiologist to view the specific body part or
region more clearly.105
Non-Contrast
The CT scan is conducted without the use of any solution. In instances of
head trauma, the patient will undergo a non-contrast CT scan.109
A CT scan is especially useful in instances of head trauma as it can provide
detailed images of the brain structure and brain tissue. CT scans can help
the treating physician identify any underlying injuries or infections of the
brain, especially when other examinations of images are inconclusive.107 The
scan is often used to identify the following complications of head trauma:110

Intracranial bleeding

Structural anomalies

Infections

Clots
The following are the CDC Guidelines for using a CT scan with patients that
have mild traumatic brain injury. The guidelines provide recommendations
for determining which patients with a known or suspected mild brain injury
require a head CT and may be safely discharged.111
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CDC Brain Injury Guidelines for Adults: Fact Sheet

A noncontrast head CT is indicated in head trauma patients with loss of consciousness or
posttraumatic amnesia in presence of specific symptoms.


A noncontrast head CT should be considered for head trauma patients with no loss of
consciousness or posttraumatic amnesia in presence of specific symptoms. Even without
a loss of consciousness or amnesia, a patient could still have an intracranial injury.
Identifying those patients at risk is key.


A patient with an isolated mild TBI and a negative CT is at minimal risk for developing an
intracranial lesion and may be safely discharged.


Discuss discharge instructions with patients and give them a discharge instruction sheet
to take home and share with their family and/or caregiver. Be sure to:

Alert patients to look for post concussive symptoms (physical, cognitive,
emotional, and sleep) since onset of symptoms may not occur until days after the
initial injury.

Instruct patients on what to expect, what to watch for, and when it is important
to return immediately to the emergency department.

Emphasize that getting plenty of rest and sleep is very important after a
concussion, as it helps the brain to heal. Patients should gradually return to their
usual routine only after they start to feel better.
The CDC also provides leveled recommendations for determining which
patients in the emergency department should undergo a non-contrast CT
scan. They are outlined below.111
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CDC Brain Injury Guidelines for Adults: Fact Sheet
Level A recommendations:
A noncontrast head CT is indicated in head trauma patients with loss of consciousness or
posttraumatic amnesia only if one or more of the following is present: headache,
vomiting, age > 60 years old, drug or alcohol intoxication, deficits in short-term memory,
physical evidence of trauma above the clavicle, posttraumatic seizure, GCS score < 15,
focal neurologic deficit, or coagulopathy.
Level B recommendations:
A noncontrast head CT should be considered in head trauma patients with no loss of
consciousness or posttraumatic amnesia if there is a focal neurologic deficit, vomiting,
severe headache, ≥ 65 years old, physical signs of a basilar skull fracture, GCS score <
15, coagulopathy, or a dangerous mechanism of injury. Dangerous mechanism of injury
includes ejection from a motor vehicle, a pedestrian struck, and a fall from a height of > 3
feet or 5 steps.
Level C recommendations: None specified.
Magnetic Resonance Imaging
Magnetic Resonance Imaging (MRI) is a radiologic scan that produces
images of various body structures using a combination of magnetism, radio
waves and computer technology. The MRI is conducted using a large circular
magnet that surrounds a scanner tube.112 Images are obtained by placing
the patient on a movable surface and inserting him or her into the magnetic
tube. Once the patient is in the tube, a strong magnetic field is created. This
magnetic field aligns the protons of the hydrogen atoms. Once the hydrogen
atoms are aligned, they are exposed to a beam of radio waves. The radio
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waves impact the protons within the body, causing them to spin, thereby
producing a faint signal, which is easily detected by the MRI receiver. The
information obtained by the scanner is sent to a computer, where it is
processed to produce an image.106
An MRI utilizes high-resolution technology, which allows it to produce highly
detailed images that will show changes in many of the structures in the
body.113 In some instances, additional agents will be used to enhance the
accuracy of the images. It is most common to use contrast agents such as
gadolinium.29 Due to the MRI’s high level of sensitivity, it is able to detect
many brain injuries that are undetectable using other methods.17 In fact, an
MRI is often used to identify asymptomatic brain damage in patients who
appear to be normal.113
While an MRI and CT scan both use the slicing technique for obtaining
images, the process is different for each. The MRI uses a magnetic field
while the CT scan uses X Rays.110 As a result, the MRI provides more
detailed images than a CT scan and is able to detect damage that is as small
as 1 – 2 mm. A CT scan cannot detect damage this small.106 The CT scan is
more appropriate for identifying fresh blood in and around the cranial
region.114 However, an MRI better detects old blood that has been
hemorrhaged into the cranial cavities.17 Whether or not to use an MRI will
depend on the type, cause and location of the head injury.
Other Diagnostic Imaging Procedures
While the CT scan and the MRI are the most widely used forms of diagnostic
imaging for a head injury, there are a number of other procedures that are
being used more frequently as the technology is developing and as the
diagnostic needs of the patient and the provider are changing. The following
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table provides a list of the more commonly used alternate forms of
diagnostic imaging.106
Diagnostic
Description
Procedure
SUSCEPTIBILITY
This is a software program that enables an MRI to more accurately
WEIGHTED
show tiny hemorrhages known as micro hemorrhages. These small
IMAGING (SWI)
white dots actually show up on the MRI because of the iron content
MRI
left behind after blood has been in an area through injury. These tiny
capillaries in the brain are torn and the small amounts of blood can be
seen on SWI-MR. In persons fifty or older, there are white dots, which
can often be from aging. In the younger person, or in an older person,
where these abnormalities are clustered at the grey-white junction
(where the grey matter meets the white matter) these are generally
traumatically caused.
For those undergoing a MRI after a trauma, especially a trauma
involving a high-speed collision or a fall from a height, make sure to
ask your doctor to prescribe an SWI MRI so that these abnormalities
can be detected. There can be as many as several hundred of these
small injuries throughout the brain, but they are an objective
unarguable type of evidence for brain injury and are exceedingly
helpful in any brain injury litigation. They can also identify the areas of
the brain that have been shaken, and aid in rehabilitative strategies.
DIFFUSION
Diffusion Tensor Imaging is a type of MRI that uses special software to
TENSOR
view parts of the brain a normal MRI cannot. The interesting premise
IMAGING (DTI)
of this new technology is that it measures the movement of water
molecules in relation to the white track fibers of the white matter of
the brain. If the fibers are healthy and untorn, then the water
molecules will show parallel movement along those tracks as they
slide along them. Torn or missing white matter fiber will allow
perpendicular movement of the water molecules.
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This new technology allows for visualization of natural damage to the
white matter. It is a very impressive technology and will be impressive
to jurors and others involved in TBI litigation.
Most radiology groups do not have this software, so if you would like
to have this test run, try University centers first. DTI will be especially
helpful in cases involving high velocity change injury, such as high
speed car accidents, falls from a height, and other accidents in which
the injury is suspected to be Diffused Axonal Injury (DAI).
MRA (MAGNETIC
MRA, or magnetic resonance angiography, is a means of visualizing
RESONANCE
the carotid and vertebral arterial systems in the neck and brain
ANGIOGRAPHY)
without having to inject contrast into the bloodstream. The resolution
is not as good as with conventional arteriography, but the patient is
spared the risks of catheterization and allergic reactions to the dye.
(In conventional arteriography, a catheter is threaded from the
femoral artery in the groin backward up the aorta into a carotid or
vertebral artery in the neck, and then dye is injected up the catheter.
As the dye flows into the brain, x-rays are taken of the cerebral
vasculature).
EEG
Monitors the brain's electrical activity by means of wires attached to
(ELECTROENCEP
the patient's scalp. These wires act like an antenna to record the
HALOGRAM)
brain's electrical activity. Normally, the resting brain emits signals at a
frequency of 8 to 13 cycles per second (cps), called alpha activity,
which is best seen in the occipital regions.
Anything faster than 8-13cps is called beta activity. Slower rhythms
include theta activity (6-7 cps) and delta activity (3-5 cps). Theta and
delta activity occur in the normal brain as the patient descends into
sleep. If the patient is awake, any slowing of electrical activity in a
focal area of the brain may indicate a lesion there. Similarly,
widespread slowing indicates a widespread disturbance of brain
function, often due to a blood borne insult like low blood sugar, drug
intoxication, liver failure, etc.
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"Spiking" (sharp waves of electrical activity) discharges indicate an
irritable area of cerebral cortex. If allowed to spread, the spikes can
produce a seizure.
It is not uncommon for an EEG to be normal between seizures in
patients with bonafide seizures. During a seizure, however, the EEG is
almost invariably abnormal. Conversely, 15% of the population shows
mild abnormalities on EEG, representing old head trauma, old strokes,
migraine, viral infections, and most of the time for unknown reasons.
QUANTITATIVE
This test is performed in a way similar to EEG. Brain wave activity
EEG (QEEG,
varies throughout the day depending on the state of alertness. Each
BEAM, BRAIN
area of the brain normally spends a characteristic amount of time in
MAPPING)
alpha, beta, theta, and delta activity.
Brain mapping computers are now capable of creating a map of the
brain's electrical activity depicting how long each area of the brain
spends in each of the basic rhythms. By comparing the patient's map
with that of a control population, it is possible to localize areas of focal
slowing of electrical activity. Alone, a QEEG is insufficient to diagnose
brain damage but in conjunction with other neurologic tests, QEEG can
be confirmatory.
PET SCAN
PET scanning (positron emission tomography) is based on the fact that
(POSITRON
the brain uses glucose for energy. By labeling a glucose molecule with
EMISSION
a radioactive "tag," and then inhaling radioactive glucose and placing
TOMOGRAPHY)
the patient's head under a large geiger counter, one can identify
abnormal areas of the brain that are underutilizing glucose. Because
cyclotrons are needed to generate the radioactive gas, PET scanning is
not widely available.
SPECT SCAN
SPECT scanning (single photon emission computed tomography) is
(SINGLE
similar to PET scanning in that a radioactive chemical is administered
PHOTON
intravenously to the patient, but the radioactive chemical remains in
EMISSION
the bloodstream and does not enter the brain.
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COMPUTED
As a result, the SPECT scan maps the brain's vascular supply. Because
TOMOGRAPHY)
damaged brain tissue normally shuts down its own blood supply, focal
vascular defects on a SPECT scan are circumstantial evidence of brain
damage.
The advantage of a SPECT scan over a PET scan is its ready
availability and relatively cheap cost. Recent studies have
demonstrated abnormal SPECT scans after head trauma when the CAT
and MRI were normal, suggesting that the SPECT scan is more
sensitive to brain injury then either CT or MRI scans. Because the
radioactive chemicals used in SPECT and PET scans are carried to all
parts of the body by vascular tree, SPECT scans and PET scans are
used judiciously in patients of reproductive age.
EVOKED
Evoked studies take advantage of the fact that each time a sensory
POTENTIALS
system of the body -- vision, hearing, touch -- is stimulated, an
electrical signal is generated in the brain. These electrical signals can
be detected with electrical wires on the scalp. Thus, visual evoked
recordings (VER) are recorded over the occipital lobes; brainstem
auditory evoked recordings (BAER) over the temporal lobes; and
somatosensory potentials (SSEP) over the parietal lobes.
LUMBAR
A lumbar puncture (spinal tap - not the band) is used to analyze
PUNCTURE
cerebrospinal fluid. An analysis of the fluid can help tell doctors, for
example, if there is any bleeding in the brain and spinal cord areas.
MAGNETIC
This is an exciting new tool, used in conjunction with MRI that detects
RESONANCE
the intra-cellular relationship of brain metabolites. Studies show that
SPECTROSCOPY
in an injured brain, the relationship between the amount of certain
(MRS)
compounds in the brain changes in predictable ways, which can be
picked up, non-invasively, by MRS. While MRS is in its early stages, it
holds great promise in the "objectification" of brain injury. THIS DATA
CAN AND SHOULD BE CAPTURED ON MRI WITHIN SIX WEEKS OF
INJURY.
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Treatment
Many individuals experience long-term complications and disabilities as the
result of a traumatic brain injury.115 Therefore, long-term treatment is often
needed beyond the emergency treatment that is provided initially. Initial
treatment for patients with moderate to severe traumatic brain injury is
focused on stabilizing the patient and is often done within the emergency
department or intensive care unit. Once the patient is stabilized, further
treatment may be required depending on the type and severity of the injury.
Most long-term treatment involves rehabilitation, as the goal is to have the
patient regain the appropriate neurologic functions. This component of
treatment is often conducted in a subacute unit of the hospital or in an
independent rehabilitation center.11 In addition, some long-term treatment
will be conducted through outpatient services.6 Treatment at this stage is
diverse and is tailored to the specific recovery needs of the patient.
Most long term treatment includes physical therapy, occupational therapy,
speech and language therapy, psychiatric care, psychological services, social
support and life skill development, and physiatry.116 The specific
rehabilitative program will utilize the services of experts in the above areas
to develop a comprehensive program that addresses the specific treatment
needs of the program. Initial treatment will most likely be extensive, with
longer-term treatment being less frequent.53 As the patient regains the
appropriate skills, treatment will be reevaluated and modified to continue to
meet the needs of the patient.93
The goal of long-term treatment is to bring the patient to a level of
functioning that enables him or her to live independently and integrate with
society. When patients experience a long-term or permanent disability as
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the result of a head injury, the rehabilitation team will provide treatment
and therapy that focuses on adapting to the disability and developing new
skills that will enable the patient to function within the constraints of the
disability.115 Long-term rehabilitation will typically be conducted in a variety
of settings, including hospital outpatient programs, inpatient rehabilitation
centers, day treatment programs, hospital outpatient programs and
independent living centers. The specific setting will be determined based on
the rehabilitation needs of the patient and the specific services available in
the geographic area.54
Pressure Monitoring
In many instances, a patient will experience swelling in the brain. When this
occurs, fluids accumulate within the brain and pressure begins to build. This
causes additional swelling and disruptions to the fluid balance.4 With other
injuries, swelling and fluid accumulation is normal and poses little risk.
However, when this occurs within the brain, it can be extremely dangerous.
The skull limits the space for expansion, so the brain is unable to expand.
Therefore, the accumulation of fluid causes unnecessary pressure on the
brain, referred to as intracranial pressure (ICP).22
When a patient presents with swelling in the brain, it is necessary to monitor
the swelling to ensure that it does not cause additional damage. This is
accomplished using a probe or catheter.11 The instrument is inserted into the
skull and is placed at the subarachnoid level to ensure accurate
measurements. Once the instrument is properly placed, it is connected to a
monitor that displays information regarding the patient’s ICP. This
information is closely monitored so that action can be taken if the ICP
reaches an alarming level.6 If this occurs, the patient may have to undergo a
ventriculostomy. This procedure is used to drain cerebrospinal fluid as a way
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to reduce pressure on the brain.39 In some instances, pharmacological
agents may be used to decrease ICP. These drugs include mannitol and
barbituates.11
Rehabilitation
To enhance recovery of brain injury survivors, clinicians and researchers
utilize cognitive as well as physical rehabilitation. They employ a range of
therapies for patients with nontraumatic brain injuries, such as stroke, that
causes language (aphasia) or visuospatial skill impairments. Likewise, for
traumatic brain injury (TBI), clinicians and researchers include a range of
therapies for attention, memory, and executive function impairments; and
for treatments for social and behavioral problems and programs for
adjusting to disability.115
Rehabilitation is often considered in regard to improving physical disabilities.
For a person with paralysis, rehabilitation might examine whether the
individual’s strength could be improved through exercise, whether the
tendons of nonparalyzed muscles could be surgically transferred to a
mechanically useful site, whether braces or a wheelchair might allow the
person to navigate the community despite the paralysis, and even whether
architectural modifications, urban planning, or transportation services could
help overcome barriers to mobility. The treatment interventions used in
physical rehabilitation include traditional drug and surgical treatments, as
well as physical exercise, technology (i.e., braces, wheelchairs), skill training
(i.e., learning how to use a wheelchair), and social policies and services (i.e.,
accessible transportation).52
However, rehabilitation is not limited to improving physical disability.
Cognitive rehabilitation attempts to enhance functioning and independence
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in patients with cognitive impairments as a result of brain damage or
disease, most commonly following TBI or stroke. As with physical
rehabilitation, cognitive rehabilitation may include interventions that aim
to lessen impairments, or interventions that aim to lessen the disabling
impact of those impairments. Interventions are applied through technology
and other compensatory strategies that may allow the individual with
cognitive impairment to accomplish important life activities and more fully
participate in society.55
Cognitive rehabilitation therapy (CRT) is used to rehabilitate thinking skills
(i.e., attention, memory) impaired by a brain injury. Cognitive behavioral
therapy is commonly used for a variety of emotional and psychiatric
disorders, including mood, anxiety, and psychotic disorders, as well as sleep
disturbance and chronic pain. Cognitive behavioral therapy typically centers
on modifying maladaptive thoughts and emotional behaviors and using
psychoeducation regarding symptoms and expectations for recovery.89
Patients with TBI often have multiple identifiable cognitive impairments,
coupled with mood or other behavioral disturbances, a reduced awareness of
their own cognitive and behavioral limitations, and reductions in social
competence. Although some patients with isolated impairments may achieve
substantial treatment benefits in terms of activities and participation from
treatment of a single deficit, others may require a combination of treatments
aimed at multiple problems to achieve comparable outcomes.52
Rehabilitation is a long term process for individuals and occurs in the
following stages, depending on the specific needs of the patient, as outlined
below.35,67,71,88,115,117,118
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
Acute Rehabilitation
As early as possible in the recovery
process, individuals who sustain
brain injuries will begin acute
rehabilitation. The treatment is
provided in a special unit of the
trauma hospital, a rehabilitation
hospital or another inpatient setting.
During acute rehabilitation, a team
of health professionals with
experience and training in brain
injury work with the patient to regain as many activities of daily living
as possible. Activities of daily living include dressing, eating, toileting,
walking, speaking and more.

Postacute Rehabilitation
When patients are well enough to participate in more intensive
therapy, they may be transferred to a postacute rehabilitation setting,
such as a residential rehabilitation facility. The goal of postacute
rehabilitation is to help the patient regain the most independent level
of functioning possible. Rehabilitation channels the body's natural
healing abilities and the brain's relearning processes so an individual
may recover as quickly and efficiently as possible.
Rehabilitation also involves learning new ways to compensate for
abilities that have permanently changed due to brain injury. There is
much that is still unknown about the brain and about brain injury
rehabilitation. Treatment methods and technologies are rapidly
advancing as knowledge of the brain and its function increases.
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
Subacute Rehabilitation
Patients who cannot tolerate intensive therapy may be transferred to a
subacute rehabilitation facility. Subacute rehabilitation programs are
designed for persons with brain injury who need a less intensive level
of rehabilitation services over a longer period of time. Subacute
programs may also be designed for persons who have made progress
in the acute rehabilitation setting and are still progressing but are not
making rapid functional gains. Subacute rehabilitation may be
provided in a variety of settings, often a skilled nursing facility or
nursing home.

Day Treatment (Day Rehab or Day Hospital)
Day treatment provides rehabilitation in a structured group setting
during the day and allows the person with a brain injury to return
home at night.

Outpatient Therapy
Following acute, postacute or subacute rehabilitation, a person with a
brain injury may continue to receive outpatient therapies to maintain
and/or enhance their recovery. Individuals whose injuries were not
severe enough to require hospitalization or who were not diagnosed as
having a brain injury when the incident occurred may attend
outpatient therapies to address functional impairments.

Home Health Services
Some hospitals and rehabilitation companies provide rehabilitation
therapies within the home for persons with brain injury.
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
Community Re-entry
Community re-entry programs generally focus on developing higherlevel motor, social, and cognitive skills in order to prepare the person
with a brain injury to return to independent living and potentially to
work. Treatment may focus on safety in the community, interacting
with others, initiation and goal setting and money management skills.
Vocational evaluation and training may also be a component of this
type of program. Persons who participate in the program typically live
at home.

Independent Living Programs
Independent living programs provide housing for persons with brain
injury with the goal of regaining the ability to live as independently as
possible. Usually, independent living programs will have several
different levels to meet the needs of people requiring more assistance
and therapies as well as those who are living independently and being
monitored.
Pharmacological Treatment
Many patients will require
pharmacological treatment as part
of the rehabilitation process. Some
medications may be given short
term to assist with acute recovery,
while others may become part of
the patient’s long-term treatment
plan. The following is a list of the
most common pharmacological
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treatments used with TBI patients.53

Analgesics may be used for pain relief and pain management.

Anti-anxiety agents may lesson feelings of uncertainty, nervousness,
and fear.

Anti-coagulants may be used to prevent blood clots.

Anti-convulsants may be used to prevent seizures.

Anti-depressants may be used to treat symptoms of depression.

Anti-psychotics may be used to target psychotic symptoms of
combativeness, hostility, hallucinations, and sleep disorders.

Muscle relaxants may be used to reduce muscle spasms or spasticity.

Sedative-hypnotic agents may be used to induce sleep or depress the
central nervous system in areas of mental and physical response,
awareness, sleep, and pain.

Stimulants may be used to increase levels of alertness and attention.
Surgery
In some instances, surgery may be required as part of the treatment
process. Surgery is most common in the acute stage of treatment, as it is
often used to minimize additional damage to brain tissue or to address other
complications associated with head injury. The following types of surgery are
most common in instances of traumatic brain injury.27

Removing clotted blood (hematomas)
Bleeding outside or within the brain can result in a collection of clotted
blood (hematoma) that puts pressure on the brain and damages brain
tissue.
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
Repairing skull fractures
Surgery may be needed to repair severe skull fractures or to remove
pieces of skull in the brain.

Opening a window in the skull
Surgery may be used to relieve pressure inside the skull by draining
accumulated cerebral spinal fluid or creating a window in the skull that
provides more room for swollen tissues.
Prognosis
The natural process of recovery following TBI depends upon the initial injury
severity, as described with the GCS, though there can be considerable
variability even within categories. With most injuries there is a gradual
resolution of symptoms. For most mild, single concussive injuries, the
majority of patients are symptom-free within several weeks. Several metaanalyses indicate the path to preinjury symptom levels following a mild TBI
is approximately 2 weeks, and no more than 3 months. Development of new
symptoms following resolution of the initial symptoms in individuals with
mild TBI occurs infrequently. However, with multiple mild TBIs, both the
number and duration of symptoms are likely to increase.44
The course of recovery from severe TBI is more prolonged, with greatest
function recovery occurring within 1 to 2 years of injury. One study reported
that an increasing number of people were independent at 6 to 12 months,
and up to 5 years, post injury and following rehabilitation. In another study
assessing recovery in people with severe TBI, approximately 22 percent of
individuals were found to have improved from year 1 to year 5; however, 14
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to 15 percent declined, and approximately 62 percent remained
unchanged.80
Impact On The Patient’s Family
Traumatic brain injury can create a
significant burden for the families
of those who are injured, as it is
they who most frequently must
provide long-term support,
socialization and assistance to the
TBI individual. Indeed the impact
of TBI for relatives can be as
devastating as for the person who
is injured. It is therefore essential
to extend rehabilitation efforts to the family, as well as to the person with
TBI.37
The occurrence of TBI creates an immediate crisis for relatives, potentially
disrupting established relationships, roles, expectations and goals within the
family unit. Emotional reactions are likely to be heightened by the fact that
the injury occurred suddenly and may have been avoidable. Family
responses include (1) the initial shock response; (2) emotional relief, denial
and unrealistic expectations; (3) bargaining, mourning or working through;
and, (4) acceptance and restructuring. There are likely to be differences in
the sequence and rate at which families pass through such phases, and not
all families will experience any or all of these emotional responses. Factors
such as the pre-existing family structure, cohesion, coping skills and
available resources significantly influence family responses.47
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Initially, families tend to experience a state of shock. Once the immediately
life-threatening phase is passed there is frequently a sense of relief. As the
TBI family member emerges from coma, and initially recovers relatively
rapidly, there are likely to be feelings of expectancy, optimism, and hope for
full recovery. In many instances, there is a tendency to deny or ignore
obvious changes in cognition and behavior. It is much easier to focus on
physical disability, which may show relatively rapid improvement, than on
cognitive and behavioral changes, which tend to be more persistent but are
less readily apparent.88,119
Denial can be a source of considerable conflict in the relationship between
family members and rehabilitation staff. However, denial may serve a
beneficial purpose in the early stages of recovery, as families are trying to
cope emotionally with the idea that life may never be the same again.
Professionals working with families need to understand and respect this.
Attempts to confront denial frequently undermine the relationship between
rehabilitation staff and family. Awareness of the reality of the impact of the
injury tends not to come until after the TBI individual has been discharged
from hospital, at which point families experience more directly the injured
family member’s coping difficulties and cognitive-behavioral changes.120
There is likely to be significant disruption of relationships and roles, which
existed in the family prior to injury. Middle-aged or elderly parents, who
were making plans for retirement, or enjoying new-found freedom since
adult children have left the family home, may be faced with caring for a
newly dependent son or daughter at the expense of their own health and
needs. They will be concerned as to what will happen to the injured child or
adult when they can no longer provide the care that is needed. However,
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where both parents are still alive they are able to support each other and
share the burden to some extent.121
Spouses carry a somewhat different burden from that of parents. Where
there are children, the spouse of an injured individual must take on the role
of both parents, supporting the children as well as the newly injured
husband or wife. Additionally, there are responsibilities for running the
household, dealing with financial matters and earning an income for the
family. The spouse who is injured may be childish, self-centered and
irritable, and therefore unable to offer the emotional support that formed an
integral part of the relationship prior to injury.122
Children of an individual with TBI may also have to take on new
responsibilities. The uninjured parent is frequently absent, visiting at the
hospital. When at home, he or she is likely to be tired, irritable and
emotionally drained, having limited energy to devote to dealing with issues
of importance to the children. The children may experience, therefore, not
only a loss of affection and support from the injured parent, but also from
the one who is not injured. The mother or father who has sustained an
injury may be irritable or aggressive towards the children, unpredictable in
his or her responses and no longer willing or able to share activities with
them.123
Faced with such changes, children may find it difficult or embarrassing to
invite their friends into the home. As a consequence, children might drift
away from home and withdraw from their parents, particularly if they are
adolescents. They may be reluctant to share their feelings with others and
tend to deny what is happening and avoid dealing with it. Younger children
can develop behavior problems in such circumstances. Siblings of those
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injured may also feel neglected and forced to take on additional
responsibilities.
Given their crucial long-term role as caregivers, decision-makers and
providers of support to those who sustain TBI, families will need to be
involved, supported and assisted throughout the phases of acute care,
rehabilitation and beyond. Involvement with and assistance to families may
take a number of forms. These include provision of information regarding
TBI and its impact on the injured family member, active involvement in goalsetting and the therapy process itself, supportive counseling and, if deemed
necessary, family therapy. The amount of intervention required may depend
on the nature and extent of disability in the TBI individual, how the family
was functioning prior to the injury, and how the “family system” is affected
by the injury.116,120
The following table provides an overview of the different approaches and
considerations:116,120-122,124
Early
Provision of information and support should begin in the intensive care
Intervention
unit. High rates of anxiety, depressive and post-traumatic stress
symptoms have been identified in the relatives of patients treated in
intensive care. Families frequently report traumatic memories of how
they were treated by medical or other hospital staff in this acute stage, in
“being prepared for the worst”, which can have a lasting impact on their
attitudes to health professionals. Whether such memories are well
founded or reflect their confused state of mind at the time is unclear.
However, in view of their fragile state, families are likely to be assisted
by the presence of a support worker who understands their situation and
has time to explain and interpret the sometimes overwhelming
information provided by doctors.
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Neurosurgical staff face the difficult and stressful task of minimizing the
likelihood of mortality and morbidity in the injured patient. It is difficult
for them to look after families as well. This is acknowledged by Marks and
Daggett (2006), who evaluated the implementation of a critical care plan
for families of patients with severe TBI. This comprised the provision of
health information, emotional support, involvement in patient care tasks,
encouragement to families to look after themselves, working as a team to
train families to take over long-term care of the patient, and linking them
with community-based resources for support and assistance. Nursing
staff involved in this evaluation suggested that a designated person not
involved in caring for the patient should undertake the role of
communicating with families.
When the TBI individual emerges from coma of significant duration,
referral will, hopefully, be made for rehabilitation, either in another unit
of the same hospital or at another center. Having just got to know and
trust the staff in the neurosurgical unit, families are faced with a new
environment, many new faces, and a change in routine. It is important
that families are welcomed into the rehabilitation setting by a team
member who is identified as someone to whom the family can turn for
information, assistance and support throughout the rehabilitation period.
Continuity of involvement is important. The designated staff person
should provide the family with orientation to the ward and therapy areas,
the treatment program and staff who will work with the injured person.
These staff should also take time to introduce themselves and explain
their role. A written booklet containing information about TBI and its
consequences, and how the rehabilitation program works is helpful. It is
likely that by this stage close family members are feeling exhausted,
having spent day and night at the bedside. There may also be pressure
for them to return to work. It will be important to families to see their
injured relative settled into the new environment, but once this has been
achieved, they should be given permission to spend less time at the
hospital, provided they feel comfortable with this.
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Family
A comprehensive assessment should be made of the family’s
Assessment
constellation; the roles played by different members, including the one
who has been injured, the nature of relationships and communication
within the family. It is also important to consider other stresses on the
family. The Head Injury Family Interview (Hi-Fi) was developed by Kay
and colleagues (1995) as a structured interview to guide the collection of
background information from individuals with TBI and their families and
document the impact of the injury on family members.
Where staff with the appropriate family assessment skills is available, the
clinical interview may be supplemented by the use of a standardized
assessment tool to examine objectively the family system and the
responses of individuals to the injury. Such methods include self-report
measures and observational techniques. No such tools have been
specifically designed for use with the TBI population.
The Family Assessment Device (FAD) is a self-report questionnaire
designed to assess the six dimensions of the McMaster Model of Family
Functioning and overall level of family functioning. The dimensions
assessed include Problem Solving, Communication, Roles Dimension,
Affective Responsiveness, Affective Involvement, Behavior Control and
General Functioning. It has been the measure most frequently used to
study responses of family members across different disability groups,
including those with TBI. It has been shown to have good psychometric
properties. Numerous recent studies have documented high rates of
unhealthy functioning on FAD subscales in families of those with TBI,
although there has been some variation in the subscales most affected.
In the course of the initial assessment period, families may want to
discuss the circumstances of the accident and their feelings about this.
The emotional reactions and needs of children and siblings should also be
explored. It is important to establish what resources are available to the
family, financially, in terms of support and assistance from extended
family or friends, and whether they are able to have time off from
employment.
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Arrangements may need to be made for home help, financial or legal
assistance. The family’s cultural background and beliefs and their value
system should also be assessed in detail and taken into consideration in
planning the rehabilitation process and optimal modes of communicating
with the family. Where English is not spoken, it is important to ensure
clear communication, using an interpreter, and involving a social worker
who understands their cultural background.
This person can convey to the rehabilitation team an understanding of
family reactions to the injury and attitudes to the rehabilitation process,
as well as act as an advocate for the family. Wherever possible, written
information should be translated into the family’s native language. Family
members usually provide invaluable information regarding the TBI
individual’s previous lifestyle, abilities, behavior and personality.
Such information is a vital aspect of the REAL approach, to enable the
team to set realistic and appropriate goals.
It is important to gain an understanding of the family’s perception of the
impact of the injury on the injured individual, physically, cognitively and
behaviorally. Their expectations regarding the rehabilitation process, its
goals and outcome, and their role in that process should also be
explored. In many instances families may have quite different priorities
and expectations from those of rehabilitation staff. Although these may
seem inappropriate or unrealistic, they are likely to be maintained and
conveyed to the TBI family member, even in the face of logical argument
to the contrary by team members.
The views of the family deserve respect and consideration from the
rehabilitation team. Wherever possible an attempt should be made to
negotiate goals, which incorporate the aims and priorities of the family,
as well as the TBI person. In some cases, the family’s wishes and needs
may not be congruent with, or in the best interests of the injured person.
In others the views of different family members may conflict with one
another. Where this is seen to be the case, active family participation in
goal setting and therapy is less helpful.
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Family
It is likely to be helpful to enable families to talk with one another during
Education
and after the rehabilitation phase, sharing information and emotional
and Support
support. The general community tends to have little knowledge of TBI
Groups
and its consequences, so that friends and other family members may not
understand what the injured person and family are going through.
The issues addressed by family support groups will vary according to the
setting, time since injury, and nature of the relationship with the TBI
family member. In the acute stages of recovery, families may be less
ready to discuss their emotional reactions to the trauma, still focusing
intensely on the needs of the injured family member. They may,
however, benefit from educational input, both in structured form from
members of the rehabilitation team or community agencies, and from
other families who have already had the experience. Topics of interest
may include mechanisms of TBI, management of coma and PTA, medical
complications, such as epilepsy, the nature and management of disorders
of mobility, communication, swallowing, cognition, behavior and emotion,
vocational issues, accessing community resources, and financial and legal
issues.
It is wise to tailor the content of educational sessions to the needs of the
group. Supplementary notes are also helpful, as many issues may not be
fully understood until much later. Such educational sessions may form a
basis for broader discussion of issues relevant to individual group
members, leading to a sharing of information and support. Depending on
the time since injury and their stage of adjustment, families may benefit
from the opportunity of sharing their emotional reactions to the situation
and discussing the impact of the injury on the family. Suitably trained
rehabilitation professionals should take a facilitative role in this process,
to ensure that all families are encouraged to participate actively and that
all relevant issues are covered. Some issues raised may need to be taken
up individually. Such groups may help families to realize that others
share their experiences and reactions. This relieves their sense of
isolation and provides family members with a feeling that they are
accepted and understood.
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The issues of importance to spouses of TBI individuals may be somewhat
different from those of parents of injured adolescents or adults. Spouses
may feel uncomfortable about discussing relationship issues or their
feelings about changes in behavior and personality.
It is therefore useful to enable spouses to talk with one another,
providing relief from the guilt, which many experience regarding their
negative feelings about the injured partner. Many families form strong
bonds through participation in family groups. Such relationships provide a
useful resource for the future, when there is no longer active
rehabilitation support. In this respect it is useful for support groups to be
ongoing, so that families may return in times of need. If this is not
possible within the rehabilitation setting, referral should be made to an
accessible community-based group.
Indeed it is after return to the community that family support groups
may be most helpful, as there is likely to be less support from other
sources, and family members may be more ready to benefit from them.
Supportive
Even those families who show relatively healthy functioning are greatly
Counseling
stressed by the occurrence of TBI. Provision of supportive counseling is a
and Family
useful means of assisting them to adjust to the impact of the injury, both
Therapy
in terms of the emotional reactions of individual family members and of
the family system itself. Where there are pre-existing problems in the
family, or where family reactions to the injury are considered to be
maladaptive, formal family therapy may be appropriate. Supportive
counseling should provide an opportunity for family members to express
and work through their emotional responses at different stages, including
feelings of anxiety, helplessness, hope, denial, depression, guilt, anger,
loss and grief.
The counselor will need to be flexible in this respect, as individuals within
the family are likely to be experiencing differing responses at a given
point in time. Many will not be ready to talk about their feelings until long
after the injured relative has been discharged.
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Counseling also provides a forum in which to raise practical problems,
particularly those occurring after discharge, and to discuss issues
regarding management of the newly acquired disabilities of the TBI
individual within the family. Assistance may be required in restructuring
the family system. As the family initially mobilizes itself to deal with the
crisis, this involves changes, which are seen as temporary.
Family members tend to put aside their own interests and needs in order
to give maximum support to the injured relative. Such sacrifices cannot
usually be sustained without a significant physical or emotional toll. At
some point, longer-term adaptations need to be made. However, it is
usually not possible to consider long-term changes until the family has
realized the permanency of the situation. A great deal of work may first
be required to assist the family in becoming realistic and grieving
effectively. As Perlesz et al. (1989) have pointed out, grieving the losses
resulting from TBI is complicated by the prolonged period of uncertainty
regarding outcome. This tends to encourage unrealistic hope for
recovery.
It is also very difficult to “mourn in the presence of the one being
mourned for”. This is particularly so when the changes being mourned
are relatively intangible alterations in personality, behavior and cognition,
rather than physical disability or disfigurement. The restructuring process
may not begin, therefore, until many years after injury and may never be
fully accomplished.
Many dimensions of the family system may be affected by TBI. In
particular, there is likely to be a need for significant reorganization of
roles and relationships, as well as modes of communication, decisionmaking and problem solving. The extent to which such changes can be
made successfully will depend on the quality of functioning in these areas
prior to the injury, and the family’s level of cohesion and adaptability.
Coping with role changes has been identified as a significant source of
stress, particularly by spouses of those who have sustained TBI.
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The extent to which family members can successfully adopt new roles will
depend on the flexibility of family beliefs, which may be influenced by
cultural background, individuals’ experience in adopting different roles
and the extent to which resources can be utilized to provide information
and support. For example, a wife who has never worked, has been reliant
on her husband for management of the family finances, and has difficulty
asserting herself is going to find it much more difficult to take
responsibility in these areas than one who has well-developed
professional skills and previously played an active role in decision-making
and financial management.
Family therapy is one means of assisting families who have not been able
to grieve effectively and to resolve maladaptive patterns of
communication and interaction, which impede the adjustment of the
injured individual and/or the family. A forum is provided in which family
conflicts can be re-enacted and more adaptive strategies developed for
resolving issues. Cultural influences and family belief systems can be
explored. Families are encouraged to understand that the problems they
are experiencing are often more related to the resources, coping styles
and family system, than to the limitations of the injured family member.
Advocacy
The heterogeneity and complexity of problems which result from TBI
and Support
places considerable demands on families, not only in terms of their
Agencies
interactions with the injured individual, but also in terms of the necessity
to deal with many different professionals and agencies. Both they and the
person who is injured are likely to be faced with choices regarding
appropriate forms of treatment - who will deliver it and how long it
should continue.
In many instances there is a need for ongoing negotiation with insurance
agencies in order to obtain funding. Later, decisions may be required
regarding long-term care, guardianship and legal issues. By virtue of
limitations in their background knowledge and capacity to comprehend
information provided, the majority of families and TBI individuals are ill
equipped to make such decisions.
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Emotional distress adds further to their difficulties. In order to ensure
that the TBI individual receives the best possible services it is important
that assistance is offered to both the injured person and the family
through explanation, interpretation, and advocacy. Where no family
support exists, advocacy for the person who has sustained the injury
becomes even more important.
This form of support is frequently offered during the rehabilitation phase,
but after discharge the TBI individual and the family has few resources on
which to draw. In this respect, agencies such as Headway in Britain, the
National Head Injuries Foundation (NHIF) in the USA and Brain Injury
Australia offer invaluable service, in assisting brain-injured individuals
and their families to negotiate their way through rehabilitation services
and options for long-term accommodation and support, to become better
informed, and to deal with financial, guardianship and legal issues.
Some of these organizations also provide a support network in the form
of regional support groups. However, the most important function of
these organizations is that of drawing the attention of the public and the
government to the unique and devastating consequences of TBI, and the
policies and services which are required to meet the needs of TBI
individuals and their families. Rehabilitation professionals working with
TBI have an obligation to contribute to such efforts.
Summary
Traumatic brain injury has many causes, including sports injuries, violence,
vehicular accidents, and falls. Each instance is unique and outcomes can be
difficult to predict, which is why every patient with a potential TBI needs to
be appropriately assessed and provided with immediate, intensive care to
address his or her needs. Traumatic brain injuries can present with a wide
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array of symptoms and every symptom needs to be treated seriously. Even
cases that present as mild can become serious in a matter of seconds. Over
5 million people in the United States are survivors of traumatic brain
injuries. Many of them have long-term disabilities as a result of their injury.
Medical professionals who understand the unique needs of TBI patients are
the key to minimizing the potential impact of these disabilities.
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1.
Head trauma may include an alteration in consciousness that
involves any trauma to the
a. Scalp
b. skull
c. brain
d. *All of the above.
2.
A majority of traumatic brain injury cases occur as the result of
a. gunshot wounds
b. *transportation accidents
c. sports injuries
d. domestic violence
3.
Mild injuries typically cause all EXCEPT:
a. brief, change in mental status.
b. *seizure disorder.
c. no long-term adverse affects.
d. temporary loss of consciousness.
4.
The nervous system is comprised of two regions:
a. *Central Nervous System and Peripheral Nervous System
b. Central Nervous System and Autonomic Nervous System
c. Autonomic Nervous System and Peripheral Nervous System
d. Autonomic and Parasympathetic Nervous Systems.
5.
The cranial bones include the
a. frontal, temporal, occipital, parietal, lacrimal
b. *foramen magnum, frontal, temporal, occipital, parietal
c. maxilla, malar, temporal, occipital, parietal
d. foramen magnum, volar, frontal, temporal, occipital
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6.
The three layers of the meninges are:
a. *dura mater, arachnoid, pia mater
b. grey matter, white matter, arachnoid
c. arachnoid, pia mater, grey matter
d. None of the above.
7.
The __________________ is the layer of the meninges that is
located closest to the surface of the brain.
a. arachnoid
b. dura mater
c. *pia mater
d. None of the above.
8.
__________ cranial nerves originate in the brainstem.
a. Five
b. Eight
c. *Ten
d. Twelve
9.
According to the CDC, approximately ____________ Americans
are living with a TBI-related disability.
a. *5.3 million
b. 7.5 million
c. 10 million
d. 12.5 million
10. Approximately _______ of TBIs are due to violence, such as
firearm assaults and child abuse.
a. 15%
b. *20%
c. 25%
d. 30%
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11. About _______ of TBIs are due to sports injuries.
a. *3%
b. 5%
c. 10%
d. 22%
12. Leading causes of TBI in combat zones include
a. bullets
b. blasts
c. assaults
d. *All of the above.
13. __________________ are a leading cause of TBI for active-duty
military personnel in war zones.
a. *Blasts
b. Motor vehicle-traffic crashes
c. Fragments
d. Falls
14. The left hemisphere controls the following functions:
a. *Speech, comprehension, arithmetic, writing
b. Creativity, comprehension, spatial ability, artistic ability
c. Creativity, musical skills, artistic skills, writing
d. Speech, writing, spatial ability, arithmetic
15. The right hemisphere controls the following functions:
a. Speech, writing, spatial ability, arithmetic
b. Speech, comprehension, spatial ability, writing
c. *Creativity, spatial ability, artistic skills, musical skills
d. Creativity, comprehension, spatial ability, artistic ability
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16. The _____________ arteries supply the brain with
approximately 80% of the blood flow.
a. *carotid
b. subclavian
c. vertebral
d. aortic
17. Broca's area, important in language production, is found in
a. *the frontal lobe, usually on the left side.
b. the frontal lobe, usually on the right side.
c. the occipital lobe, usually on the left side.
d. the occipital lobe, usually on the right side.
18. True or False. The carotid arteries are responsible for providing
circulation to the anterior region of the brain.
a. *True
b. False
19. The limbic system includes the
a. *hypothalamus, thalamus, amygdala, hippocampus.
b. thalamus, thyroid, parathyroid, amygdala
c. thalamus, hypothalamus, gonadal, thyroid
d. None of the above.
20. True or False. Components of the limbic system are involved in
hormone and emotional regulation.
a. *True
b. False
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21. Blunt trauma produces a ____________
a. *closed head injury
b. open injury
c. penetrating injuries
d. both b and c above.
22. With blunt trauma, one of the following types of force will occur:
a. *Deceleration, Acceleration, Acceleration-deceleration, Rotational,
Deformation
b. Acceleration not deceleration
c. Deceleration not acceleration
d. Rotational and deformation only
23. True or False. Contracoup injury occur at the site of impact and
the coup injury occurs at the opposite side or at the rebound site
of impact.
a. True
b. *False
24. Battle’s Sign is a sign that involves
a. *closed Injury
b. open injury
c. raccoon eyes
d. leakage of cerebrospinal fluid
25. True or False. Focal brain injuries are confined to one specific
region of the brain. They cause localized damage and are easily
identifiable.
a. *True
b. False
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26. Types of Diffuse Injuries include:
a. Extradural, intracranial, brain edema
b. *Concussion, brain edema, diffuse axonal injury
c. Concussion, contusion, intracranial hematoma
d. Brain edema, Intracranial, diffuse axonal injury
27. Intracerebral hematoma (ICH ), subarachnoid hemorrhage
(SAH) and intraventricular hemorrhage (IVH ) examples of the
types of:
a. parietal injuries
b. diffuse injuries
c. *focal injuries
d. Both b and c above.
28. Metabolic changes occur following TBI, such as rate of
__________ glucose metabolism lasting for days or weeks.
a. *glucose
b. protein
c. fat
d. Both b and c above.
29. Cerebral edema may be caused by
a. damage to the walls of cerebral blood vessels.
b. accumulation of fluid within the cell as a result of ischemia.
c. increased intravascular pressure or obstruction to the flow of
cerebrospinal fluid.
d. *All of the above.
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30. Infection, in the subacute phase after TBI, is a complication
associated with skull fracture that manifests as:
a. Meningitis
b. Cerebral abscess
c. Intracranial pressure without brain shift
d. Both *a and b above.
31. Decompressive craniectomy surgery involves temporarily
removing a portion of _____________ skull bone to increase
the volume of the cranial cavity and to decrease intracranial
pressure.
a. posterior
b. parietal
c. *frontal
d. occipital
32. Early post-traumatic epilepsy usually occurs within the first
a. 12 hours
b. *24 hours
c. 1-3 months
d. 3-6 months
33. The following anticonvulsants have been found to be relatively
free of adverse cognitive effects
a. Phenytoin and Keppra
b. Keppra and Lamortrigine
c. *Carbamazepine and Valproic acid
d. Oxcarbamazepine and Keppra
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34. Severity measures graded during the acute phase sometimes
reflect variance due to
a. medications used during resuscitation
b. substance use
c. communication issues
d. *All of the above.
35. Mild brain injury involves ______________ of all brain injuries.
a. *75%-85%
b. 50%-65%
c. 45-50%
d. <50%
36. In mild brain injury cases, 90% of individuals recover within
a. *6-8 weeks
b. 3 months
c. 4-6 months
d. 6 months but sometimes lasting more than a year.
37. True or False: Locked-in Syndrome is a condition indicative of
moderate TBI.
a. True
b. *False
38. In a case of mild TBI there may be symptoms of
a. headache
b. insomnia
c. irritability and anxiety/depression
d. *All of the above.
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39. The most common causes of mild TBI identified include all
EXCEPT:
a. *Shaken baby syndrome
b. Falls
c. Motor vehicle accidents
d. Sports-related injuries
40. Attentional difficulty most commonly reported is
a. reduced speed of information processing
b. difficulties in focusing on more than one thing at once
c. coping with complexity
d. *All of the above.
41. Impairment of memory for events immediately preceded a TBI is
termed
a. posttraumatic amnesia
b. *retrograde amnesia
c. antegrade amnesia
d. prodromal amnesia
42. Difficulties to form or deal with abstract concepts for TBI
individuals also include:
a. inability to generalize from a single instance
b. a tendency to focus on specific, concrete aspects - “stimulus-bound”.
c. inability to think creatively
d. *All of the above.
43. True or False. The TBI individual often encounters inflexibility in
thought processes and difficulty to switch from one task to
another, leading to frequent repetition or “perseveration” of the
same responses, comments, demands or complaints.
a. True
b. *False
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44. TBI can result in a flatness of affect, where there is reduced
emotional responsiveness but NOT an elevation of affect, with
euphoria.
a. True
b. *False
45. Some of the most common cognitive deficits experienced by TBI
patients include:
a. Attention and filtering issues
b. Information coding and retrieval (memory) issues
c. Problem solving
d. *All of the above.
46. Depending on the injury, the patient may experience
neurobehavioral problems, such as
a. seizures
b. *changes in behavior and attitudes
c. Both a and b above.
d. None of the above.
47. Treatment for neurobehavioral problems includes
a. medication
b. electroconvulsive therapy
c. behavior modification
d. *Answers a and c above.
48. A pupil that is oval in shape may indicate the early compression
of _____________ due to increased intracranial pressure.
a. cranial nerve II
b. *cranial nerve III
c. cranial nerve IV
d. cranial nerve VII
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49. A headache that is persistent and accompanied by other
symptoms, such as drowsiness and personality changes,
a. must be assessed immediately.
b. is often indicative of an increase in pressure around the brain.
c. can be life threatening if left untreated.
d. *All of the above.
50. A patient in a coma will need to be assessed using the Glasgow
Coma Scale, which is a standardized, 15-point test that
measures neurologic functioning using three assessments
EXCEPT:
a. eye opening.
b. best verbal response.
c. *best auditory response.
d. best motor response.
51. Using the GCS, a score of 8 or less is indicative of a
a. Mild head injury
b. Moderate head injury
c. *Severe head injury
d. Catatonic patient
52. The person in a locked-in state
a. is vegetative.
b. *able to give clear signs of awareness of self and the environment.
c. has cerebral glucose metabolism that are severely below normal.
d. Both a and c above.
53. Rehabilitation involves a range of therapy services for
a. nontraumatic brain injuries
b. traumatic brain injuries
c. *Both a and b above.
d. None of the above.
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54. Children with a TBI parent might
a. feel embarrassed and avoid inviting friends home.
b. drift away from home and withdraw from their parents
c. be reluctant to share their feelings and deny what is happening
d. *All of the above.
55. The family system is generally affected when a family member
has had a TBI with challenges being:
a. significant reorganization of roles and relationships.
b. modes of communication.
c. decision-making and problem solving.
d. *All of the above.
56. Most commonly, diagnostic imaging used for a TBI patient may
be
a. X-Ray and CT
b. *CT and MRI
c. EEG and SPECT
d. EEG and XRay
57. To target psychotic symptoms of combativeness, hostility,
hallucinations, and sleep disorders,
_________________medication may be used.
a. *antipsychotic
b. muscle relaxants
c. sedative-hypnotic agents
d. sleep and pain
58. Medication used to increase levels of alertness and attention is
a. antidepressant
b. *stimulant
c. memory aid
d. antipsychotic
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59. Long-term rehabilitation will typically be conducted in a variety
of settings, including all EXCEPT
a. hospital outpatient programs
b. inpatient rehabilitation centers
c. *county prisons
d. day treatment programs
60. A subacute rehabilitation program involves
a. less intensive level of rehabilitation services over a longer period of
time.
b. persons who are still progressing but not making rapid functional
gains.
c. a variety of settings, often a skilled nursing facility or nursing
home.
d. *All of the above.
Correct Answers:
1.
d
2.
b
3.
b
4.
a
5.
b
6.
a
7.
c
8.
c
11. a
21. a
31. c
41. b
51. c
12. d
22. a
32. b
42. d
52. b
13. a
23. b
33. c
43. b
53. c
14. a
24. a
34. d
44. b
54. d
15. c
25. a
35. a
45. d
55. d
16. a
26. b
36. a
46. b
56. b
17. a
27. c
37. b
47. d
57. a
18. a
28. a
38. d
48. b
58. b
19. a
29. d
39. a
49. d
59. c
20. a
30. d
40. d
50. c
60. d
nursece4less.com nursece4less.com nursece4less.com nursece4less.com nursece4less.com nursece4less.com
9.
a
10. b
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