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Definition
An alteration in brain function, or other evidence of brain pathology, caused by an external force.
Most TBIs are classified as closed head injuries, wherein the skull is not actually penetrated.
Traumatic brain injury is a heterogenous injury, with a wide variety of pathophysiological
mechanisms
This can be differentiated from head injury which is caused by a blow to the head or laceration
without causing injury to the brain
Definition of Terms
Skull The structure of bones that form the head and face of a person
Heterogeneous Made of parts that are different
Laceration A deep cut or tear of the flesh
Brain The organ of the body in the heat that controls functions, movements, sensations and
thoughts
Injury Harm or Damage to the physical body
II.
III.
Epidemiology
Traumatic brain injury is the leading cause of injury related death and disability in the United
States. Approximately 1.7 million people in the United States are admitted to emergency
departments with TBI each year. Of these, 50,000 people die as a result of the injury and
300,000 require hospitalization. In all likelihood these numbers underrepresent the true
incidence of TBI.
Falls are the leading cause of TBI (32%) followed by motor vehicle/traffic accidents
(19%), struck by/against events (18%), and assaults (10%). Children, older adolescents/
young adults (less than 25 years old), and older adults are most at risk for experiencing
TBI. Traumatic brain injuries are most common in young children (0 to 4 years old).
However, hospitalization and death as a result of TBI is most common in older adults (65
years old and over).
The long-term consequences of TBI on the health care system, society, and the individual are
high. There are approximately 5.3 million people living in the United States who are disabled
as a result of TBI. Four out of ten are not working 1 year after injury and one-third have
difficulty with social integration. One quarter of people with severe to moderate TBI require
assistance with activities of daily living (ADL), and approximately 40% report poor mental
and physical health.
Male to female ratio 2.5:1
Mortality in males is 34 times higher than in females
Anatomy
and an outer portion, the cerebral cortex which is composed of gray matter
the surface is marked by ridges called gyri separated by grooves called sulci
a. Cerebral Cortex
responsible for all conscious behavior by containing 3 kinds of functional
areas, which includes motor, sensory, and association areas:
Motor areas are located in the frontal cortex
Sensory areas are concerned with conscious awareness of
sensations and are located in the parietal, occipital, and temporal
cortex
Association areas include areas that are involved in many traits
like analyzing, interpreting sensory experiences, memory,
reasoning, verbalizing, judgment and emotions
Left Hemisphere
Right Hemisphere
Sequential analysis:
Holistic functioning:
information:
dancing
gymnastics
singing
arts
Visual spatial skills
language
mathematics
abstraction
reasoning
2. DIENCEPHALON
forms the central core of the forebrain
includes two important areas of gray matter:
a. Thalamus
central relay station for incoming sensory impulses (except smell) that directs
the impulse to the appropriate are of the cerebral cortex for interpretation
b. Hypothalamus
main visceral control center the body (i.e. regulates homeostasis)
i.
heart rate & blood pressure
ii.
body temperature
iii.
water & electrolyte balance
iv.
control of hunger & body weight
v.
control of digestive movements & secretions
vi.
regulation of sleep-wake cycles
vii.
control of endocrine system functioning
3. BRAIN STEM
located between the cerebrum and the spinal cord which provides pathway for
3 Major Parts:
a. Midbrain
located between diencephalon and pons
2 bulging cerebral peduncles on the ventral side
acts in reflex actions (visual and auditory)
also contains areas associated with reticular formation
b. Pons
literally means bridge or pathway of conduction tracts
center
relays nerve impulses to and from the medulla and cerebellum
c. Medulla oblongata
enlarged continuation of the spinal cord
contains an autonomic reflex center involved in maintaining homeostasis of
important visceral organs, and contains:
o cardiac center
o vasomotor center
o respiratory center
o reticular formation
THE BRAINSTEM PARTS
4. CEREBELLUM
large, cauliflower-like structure located dorsally to the pons and medulla and
BRAIN MENINGES
Meninges
The brain, as well as the spinal cord, is surrounded by three layers of membranes (the
meninges) a tough, outer layer (the dura mater), a delicate, middle layer (the arachnoid
mater), and an inner layer firmly attached to the surface of the brain (pia mater).
1. Dura mater
2. Arachnoid mater
a. Subarachnoid space
3. Pia mater
THE KORBINIAN BRODMANN
The cerebral cortex has been divided by KORBINIAN BRODMANN into 47 distinct regions,
each having a Brodmanns number
Functional Areas:
BRODMANNS
NAME
FUNCTION
AFFECTATION
AREA
FRONTAL LOBE (Motor Function)
Area 4
Primary motor area
Voluntary movement of
Immediate paresis if
Area 6
Premotor cortex/
skeletal muscles
Appropriate response of
damaged
Complex defects of
Motor association
movement
movements in the
absence of weakness
Defective scanning of
Area 8
area
Frontal eye field
movement area
opposite side, no
Area 9,10,11,12
Prefrontal
Insight, emotion
Area 44
cortex/area
Brocas area
Speech production
Impaired 2 point-
area/ Somatosensory
discrimination, touch,
area
Area 5, 7
Sensory association
Interprets tactile
stereognosis
--
Area 43
area
Primary gustatory
sensations
Taste sensation
Loss of taste
Area 39, 40
area
Gnostic/Common
integration areas
desires
syndrome (aka
Area 39:
Gerstmanns syndrome);
Angular gyrus
combined acalculia,
agraphia, finger agnosis
Area 40:
R-L disorientation
Temporal gyrus
Hearing
Complete cortical
Heschls gyrus
Area 21, 22
Speech integration/
deafness
Wernickes/fluent/expres
cortex
Wernickes area
language interpretation
sive/posterior aphasia
Sight
area
Visual association
Interpretation of visual
--
areas
stimulus
The brain receives it arterial supply from two pairs of vessels, the vertebral and internal carotid
arteries, which are interconnected in the cranial cavity to produce an arterial circle (of Willis).
The two vertebral arteries enter the cranial cavity through the foramen magnum and just inferior
Vertebral Arteries
Each vertebral artery arises from the first part of each subclavian artery in the lower part of the neck,
and passes superiorly through the transverse foramina of the upper six cervical vertebrae. On entering the
cranial cavity through the foramen magnum each vertebral artery gives off a small meningeal branch.
Continuing forward, the vertebral artery gives rise to three additional branches before joining with its
companion vessel to form the basilar artery:
one branch joins with its companion from the other side to form the single anterior spinal
artery, which then descends in the anterior median fissure of the spinal cord;
a second branch is the posterior spinal artery, which passes posteriorly around the medulla then
descends on the posterior surface of the spinal cord in the area of the attachment of the posterior
The basilar artery travels in a rostral direction along the anterior aspect of the pons. Its branches in a
caudal to rostral direction include the anterior inferior cerebellar arteries, several small pontine arteries,
and the superior cerebellar arteries. The basilar artery ends as a bifurcation, giving rise to two posterior
cerebral arteries.
Internal Carotid Arteries
The two internal carotid arteries arise as one of the two terminal branches of the common carotid arteries.
They proceed superiorly to the base of the skull where they enter the carotid canal.
Entering the cranial cavity each internal carotid artery gives off the ophthalmic artery, the posterior
communicating artery, the middle cerebral artery, and the anterior cerebral artery.
Arterial Circle
The cerebral arterial circle (of Willis) is formed at the base of the brain by the interconnecting
vertebrobasilar and internal carotid systems of vessels. This anastomotic interconnection is accomplished
by:
an anterior communicating artery connecting the left and right anterior cerebral arteries to each
other;
two posterior communicating arteries, one on each side, connecting the internal carotid artery
with the posterior cerebral artery.
The middle layer, tunica media, makes up the bulk of the arterial wall. It includes
smooth muscle fibers, which encircle the vessel, and a thick layer of elastic connective
tissue.
The outer layer, tunica adventitia, is relatively thin and consists chiefly of connective
tissue with irregularly arranged elastic and collagen fibers. This layer attaches the artery
diameter of the vessels increases. In this case, the vessels are said to undergo vasodilatation.
Changes in the diameters of arteries and arterioles greatly influence the flow and pressure of
blood.
IV.
Etiology
Physical force
Vehicular Accident
V.
Pathophysiology
External
Force
Hypoxia
Brain Tissue
Damage
Primary
Injury or
Secondary
Injury
Edema
Elevated
Intracranial
pressure
The pathophysiologic processes associated with TBI are complex and consists of:
Primary Injury
Blast Injury
Secondary Injury
Primary Injury
Primary TBI results from either brain tissue coming into contact with an object (e.g., bony skull
or external object such as a bullet or sharp instrument creating a penetrating injury) or rapid
acceleration/deceleration of the brain. Contact injuries often result in contusions, lacerations, and
intracerebral hematomas.
This damage is generally focal in nature as the brain comes into contact with bony protuberances
on the inside surface of the skull or damage from the penetrating object. Common areas of focal
injury are the anterior temporal poles, frontal poles, lateral and inferior temporal cortices, and
orbital frontal cortices.
Acceleration and deceleration cause shear, tensile, and compression forces within the brain,
which causes diffuse axonal injury (DAI), tissue tearing, and intracerebral hemorrhages. Diffuse
axonal injury is the predominant mechanism of injury in most individuals with severe to
moderate TBI. It is common in high-speed motor vehicle accidents (MVAs) and can be seen in
some sports related TBIs.
The mechanism of DAI is microscopic, so often there are minimal initial findings on computed
tomography (CT) and magnetic resonance imaging (MRI). The acceleration/deceleration forces
cause disruption of neurofilaments within the axon leading to Wallerian-type axonal
degeneration.
Blast Injury
Blast injury is considered a signature injury of the U.S. military conflicts in the Middle East.
When an explosive device detonates a transient shock wave is produced, which can cause brain
damage. Primary blast injury results from the direct effect of blast overpressure on organs (in this
case the brain), secondary injury results from shrapnel and other objects being hurled at the
individual, and tertiary injury occurs when the victim is flung backward and strikes an object.
The exact mechanisms are not fully understood, there appear to be three mechanisms by which
primary blast brain injury may occur:
o Direct transcranial blast wave propagation
o The transfer of kinetic energy from the blast wave through the vasculature, which
triggers pressure oscillations in the blood vessels leading to the brain;
o Elevations in cerebrospinal fluid (CSF) or venous pressure caused by
compression of the thorax and abdomen and by propagation of a shock wave
through the blood vessels or CSF.
Blast-related brain injury can result in edema, contusion, DAI, hematomas, and hemorrhage. A
wide spectrum of injury severities ranging from mild (blast concussion) to severe and fatal can
result from blast TBI.
Secondary Injury
Secondary cell death occurs as a result of a chain of cellular events that follow tissue damage in
addition to the secondary effects of hypoxemia, hypotension, ischemia, edema, and elevated ICP.
Secondary processes develop over hours and days, and include glutamate neurotoxicity, influx of
calcium and other ions, free radical release, cytokines, and inflammatory responses that can lead
to cell death.
Normal ICP is 5 to 20 cm H2O. Severely increased ICP typically results in herniation of the
brain, requiring prompt emergency treatment.
Common types of herniations are uncal, central, and tonsillar.
It is important to keep in mind that both primary and secondary mechanisms of injury are not
mutually exclusive and often do not occur in isolation.
The release of glutamate and other excitatory neurotransmitters exacerbates ion-channel leakage
and contributes to brain swelling and raised ICP.
VI.
Impairments
Neuromuscular Impairments
Individuals with TBI commonly exhibit
impaired motor function. Upper extremity
(UE) and lower extremity (LE) paresis,
impaired coordination, impaired postural
control, abnormal tone, and abnormal gait
may be present as life-long impairments.
Abnormal, involuntary movements such as
tremor and chorea form and dystonic
movements are less common. Patients may
also present with impaired somatosensory
function, depending on the location of the
lesion.
Cognitive Impairments
Cognition is the mental process of knowing
and applying information.
Cognition includes many complex neural
processes, including arousal, attention,
concentration, memory, learning, and
executive functions. Executive functions can
be categorized into the following main areas:
planning, cognitive flexibility, initiation and
self-generation, response inhibition, and serial
ordering and sequencing.
Neurobehavioral Impairments
Patients can exhibit profound behavioral
changes as they progress through recovery.
These impairments can be closely linked to cognitive impairments and are often more debilitating
in the long run than physical disability.
Common behavioral sequelae include low frustration tolerance, agitation, disinhibition, apathy,
emotional lability, mental inflexibility, aggression, impulsivity, and irritability.
Communication
Language and communication deficits after brain injury are generally nonaphasic in nature and
are related to cognitive impairment.
Common language and communication deficits include disorganized and tangential oral or
written communication, imprecise language, word retrieval difficulties, and disinhibited and
socially inappropriate language.
Patients may also exhibit difficulties communicating in distracting environments, reading social
cues, and adjusting communication to meet the demands of the situation.
Secondary Impairments and Medical Complications
Due to the high potential of prolonged immobility and concomitant injury, patients with TBI are
at risk of developing a number of secondary impairments and other medical issues.
VII.
Differential Diagnosis
Brain tumor
Encephalitis
Bacterial meningitis
Stroke
Cerebral aneurysm
Arteriovenous malformations
VIII.
Diagnostic Tools
1. CT Scan
In the acute postinjury period, CT scanning can detect intracranial hemorrhage,
brain swelling, hydrocephalus, and infarction. The raw data can be adjusted to
better evaluate structures of different radiodensities.
However, CT is not sensitive in identifying small contusions, white matter injury,
or in the evaluation of the posterior fossa.
In the postacute phase, CT scanning can be useful, especially when a patients
neurological status is deteriorating or failing to progress as anticipated. In such
situations, CT may identify progression of hydrocephalus or hygromas, evidence
of increased ICP, or new bleeds.
2. Brain MRI
MRI has some advantages over CT, including lack of x-ray exposure, greater
resolution in the brainstem, better identification of isodense collections of blood,
and detection of small white matter lesions.
However, MRI takes longer to perform, and requires that the patient not have any
MRI incompatible implants or equipment. In the broadest sense, CT is of greatest
use in the acute setting, while MRI may be more appropriate in the sub-acute and
chronic setting.
3. PET, SPECT, fMRI
Single photon emission CT (SPECT), positron emission tomography (PET), and
functional MRI (fMRI) can all measure regional cerebral perfusion, although
only PET and perfusion fMRI can quantify blood flow in absolute terms.
Since perfusion may be compromised in structurally intact brain tissue, either as
a result of reduced vascular delivery, or reduced perfusion demand by inactive
neural tissue, reductions in flow may identify areas of functional compromise.
Pharmacological Treatment
Benzodiazepines
Are GABAnergic agents often used in controlling agitation and anxiety. They have minimal
hemodynamic effects, and lorazepam does not diminish the respiratory drive.
They have no direct effect in decreasing ICP, but long-term use can delay neurologic recovery.
Barbiturates
Can be used to induce a coma and decrease the metabolic requirements of the brain. Pentobarbital
can also control ICP.
Profopol infusion
Can provide the same CNS depression as the barbiturates, and its short half-life can allow for
frequent neurologic examinations.
It can produce dose-dependent hemodynamic and respiratory depression, and should be used only
in hemodynamically stable patients.
Believed to manifest its effect through the GABAA system; can be used for sedation in patients
who are intubated in the ICU. It has a relatively favorable side-effect profile, with a rapid return
to consciousness after the infusion is discontinued
Clinical Rating Scale
Glasgow Coma Scale
The GCS is a simple scale for assessing
the depth of coma.
Lower GCS scores are associated with
worse outcomes based on the best GCS
within the first 24 hours.
Using the highest GCS score within the
first few hours after the injury is
preferred, as this reduces the likelihood
of using excessively low, very early
scores (often before CPR) and
confounding factors such as decreased
arousal due to use of sedatives or
paralytic agents.
Severity of TBI:
GCS score 3 to 8 = severe
TBI (coma)
GCS score 9 to 12 =
moderate TBI
GCS score 13 to 15 = mild
TBI
Galveston Orientation and Amnesia Test (GOAT)
Measure of PTA
Series of standardized questions related to
orientation and the ability to recall events
prior to and after the injury high interrater
reliability.
o Scores between 100 and 76 are
considered normal
o Score >700 indicates emergence from
coma
Descriptive scale used to examine cognitive ad behavioural recovery in individuals with TBI as
they emerge from coma and progress after a brain injury together with the GCS, is among the
most widely used in clinical facilities.
RLA LOCF
Level
I
II
III
Description
No response: Total Assistance
IV
VI
VII
Able to attend to highly familiar tasks in nondistracting environment for 30 minutes with
moderate redirection.
Able to attend to highly familiar tasks in a nondistraction environment for at least 30 minutes with
minimal assist to complete tasks.
VIII
Overestimates abilities
IX
Depressed; irritable
Score
1
2
4
`5
PT Management
Physical Therapy Mx of Moderate to Severe Traumatic Brain Injury in the Acute Stage
Preventing Secondary Impairments
Because of the patients inability to move at these levels, he or she is susceptible to indirect
impairments such as contractures, decubiti, pneumonia, and DVT.
Early Mobility
Upright sitting is extremely important because it addresses elements of treatment goals for the
early levels of recovery. As soon as medically stable, the patient should be transferred to a sitting
position and out of bed to a wheelchair.
Sensory Stimulation
Sensory stimulation is an intervention used to increase the level of arousal and elicit movement in
individuals in a coma or persistent vegetative state.
Fatigue and cardiopulmonary pathology are common after TBI. The severity of deconditioning
found in persons with TBI is significantly greater than that found in sedentary persons without
disabilities.
Aerobic training is effective for persons with TBI.
Appropriately dosed aerobic exercise has the potential to not only reduce long-term
cardiovascular risks, but also may improve sleep hygiene and reduce both depression and reports
of fatigue.
Resistance Training
Interventions aimed at improving force-production capacity may be beneficial supplements to the
physical therapists POC.
There is currently a dearth of literature investigating the role of strength training in TBI
rehabilitation.
There is, however, evidence of a positive effect in other progressive and nonprogressive
neurological disorders.
Electrical Stimulation
The application of functional electrical stimulation (FES) to motor rehabilitation has increased
significantly in the last decade.
Patient/Family/Caregiver Education
Patient/family/caregiver education and training are important goals across each level of
rehabilitation.
The goals of this education and training will vary based on the cognitive and behavioral abilities
of the patient.
Behavioral Factors
Therapists may encounter a variety of behavioral barriers to examining and treating patients with
moderate to severe TBI.
As the patient begins to emerge from coma, he or she often experiences a period of acute posttraumatic agitation.
Reference:
DeLisa, Joel. DeLisas Physical Medicine & Rehabilitation: Principles and Practice. 5th ed.
OSullivan, Susan & Schmitz, Thomas. Physical Rehabilitation. 5th ed.
Snell's Clinical Anatomy by Regions 9th Edition
Physical Medicine and Rehabilitation, Braddom