TRAUMATIC BRAIN INJURY

TBI
 Defined as an alteration in brain function, or other evidence of brain
pathology, caused by an external force or internal factors such as diseases
caused by bacteria and /pathogens.
 It is one of the major causes of disability worldwide
 Most TBIs are classified as closed head injuries, wherein the skull is not
actually penetrated.
 The nature of injury sustained in vehicular accidents and falls (e.g., blunt
impact, acceleration- deceleration)
 TBI affects all age groups
 But is most prevalent among the elderly
 The risk of TBI increases sharply after age 65
 TBI among the elderly are more frequently due to falls
 High impact sports such as football, rugby, hockey, and boxing all increase
the risk of TBI
BRAIN ANATOMY AND WHAT IT’S MADE
OF
 IT SERVES AS THE MAIN POINT OF THE CENTRAL NERVOUS SYSTEM IN MOST VERTABRATE AND
INVERTEBRATE ANIMALS.
 IN YOUR AVERAGE HUMAN, THE CEREBRAL CORTEX CONTAINS ABOUT 10-20 BILLION NEURONS, AND
THE ESTIMATED NUMBER OF NEURONS IN THE CEREBELLUM IS AROUND 55-70 BILLION
 YOUR BRAIN CONSIST OF 3 MEMBRANES OR MENINGES
 DURA MATER (OUTER LAYER)
 SUBARACHNOID SPACE (MIDDLE LAYER)
 PIA MATER (INNER LAYER)
 GRAY MATTER IS MADE UP OF ABOUT 100 BILLION NEURONS THAT GATHER AND TRANSMIT SIGNALS.
 WHITE MATTER IS MADE UP OF DENDRITES AND AXONS THAT THE NEURONS USE TO TRANSMIT SIGNALS.
 IT IS MOSTLY COMPOSED OF 75% WATER AND IS THE MOST FATTIEST ORGAN IN THE BODY, CONSISTING
OF A MINIMUM OF 60%
 THESE FATS ARE MOST COMMONLY KNOWN AS DHA(DOCOSAHEXAENOIC ACID) AND
EPA(EICOSAPENTAENOIC ACID)

 “MATABA ANG UTAK”

MECHANISMS OF INJURY

 Occurs at the moment of the impact and as a direct result of trauma A.

Contusions and lacerations of the brain surfaces B. Diffuse axonal injury C.
Diffuse vascular injury/multiple petechial hemorrhages D. Cranial nerve
injury E. Focal injuries
 SECONDARY CAUSES OF BRAIN INJURY
 Hypotension- Low blood pressure
 Hyperemia- Excess blood vessels
 Electrolyte imbalances
 Hyponatremia- low levels of sodium in the blood
 Anemia- blood lacks healthy red blood cells
 Infection
 Hyperthermia- high body temperature
 Carotid dissection
 Hyperglycemia- excess blood sugar
 Epilepsy/seizures- abnormal electrical activity in the brain
 Hypoglycemia- abnormal blood glucose
THE RANGE OF OUTCOMES

 Injury type and severity vary widely. In some injuries, commonly referred to
as concussions or mild traumatic brain injuries, the individual may suffer only
a period of confusion or a brief episode of unconsciousness.
 What is a concussion?
 a concussion is a type of mild traumatic brain injury or TBI caused by a
bump, blow, or jolt to the head or by a hit to the body that causes the
head and brain to move rapidly back and forth.
 BRODMANN’S AREAS
 312=SOMATOSENSORY CORTEX- FOR TACTILE TOUCH LESIONS AFFECTING THIS
ARE RESULT IN LOSS OF VIBRATION, AGRAPHESTHESIA, ASTEREOGNOSIA,
HEMIHYPESTHESIA
 4=PRIMARY MOTOR CORTEX- WORKS IN ASSOCIATION WITH OTHER MOTOR
AREAS INCLUDING PREMOTOR CORTEX TO PLAN AND EXECUTE MOVEMENTS
 5,7=SOMATOSENSORY ASSOCIATION AREA- INVOLVED IN SOMATOSENSORY
PROCESSING AND ASSOCIATION
 6=PREMOTOR CORTEX- THIS LARGE AREA OF THE FRONTAL CORTEX IS BELIEVED
TO PLAY A ROLE IN PLANNING OF COMPLEX, COORDINATED MOVEMENTS.
 8=FRONTAL EYEFIELD- RESPONSIBLE FOR SACCADIC EYE MOVEMENTS FOR THE
PURPOSE OF VISUAL FIELD PERCEPTION AND AWARENESS, AS WELL AS
VOLUNTARY EYE MOVEMENT
 9,10=DORSOLATERAL PREFRONTAL CORTEX- is the executive functions, such
as working memory, cognitive flexibility, planning, inhibition, and abstract
reasoning.[
 11=ORBITOFRONTALIS AREA- is a prefrontal cortex region in the frontal lobes in
the brain which is involved in the cognitive processing of decision-making
 17=PRIMARY VISUAL CORTEX-It is highly specialized for processing information
about static and moving objects and is excellent in pattern recognition
 18=SECONDARY VISUAL CORTEX- this area receives strong feedforward
connections from the primary visual cortex
BRODMANN’S AREAS CONTINUATION
 19=ASSOCIATIVE VISUAL CORTEX- works in harmony with 17 and 18
 20=INFERIOR TEMPORAL GYRUS-associated with the representation of complex object
features, such as global shape. It may also be involved in face perception and in the
recognition of numbers
 21=MIDDLE TEMPORAL GYRUS- recognition of known faces, and accessing word meaning
while reading.
 22=WERNICKES AREA- for language and speech comprehension
 36=FUSIFORM GYRUS- it has been linked with various neural pathways related to
recognition. Additionally, it has been linked to various neurological phenomena such
as synesthesia, dyslexia, and prosopagnosia.
 38=TEMPOROPOLAR AREA- bind complex, highly processed perceptual inputs to visceral
emotional responses. It is the first area to be affected by alzheimers
 39=ANGULAR GYRUS- is a region of the brain in the parietal lobe, that lies near the superior
edge of the temporal lobe, and immediately posterior to the supramarginal gyrus; it is
involved in a number of processes related to language, number processing and spatial
cognition, memory retrieval, attention, and theory of mind.
 40=SUPRAMARGINAL GYRUS- language perception and processing lesions to this area
cause receptive aphasia

 41,42=HESCHLS GYRUS- contains the primary auditory cortex

BRODMANNS AREA CONTINUATION

 44,45=BROCAS AREA- language processing and speech production

EPIDEMIOLOGY

 Traumatic brain injury is the leading cause of injury related death and
disability
 Falls are the leading cause of TBI (32%) followed by motor vehicle/traffic
accidents (19%), and assaults (10%)
 Overall incidence of traumatic brain injury 200 per 100,000 vs. 70-116 per
100,000)
 There is some evidence that TBI incidence is decreasing in the USA
comparing numbers from the 1970’s and 1980’s
 Motor vehicular accidents is the most common cause (overall)of head
injury
 Violence/assault is the second most common cause of TBI in young adults
 alchol use clearly related to TBI – Alcohol detected in blood in up to 86% of
TBI patients – blood levels 0.10% or higher in 51% to 72% of patients at the
time of the injury
TYPES OF BRAIN INJURY

 FOCAL
 Results from direct mechanical forces
 Usually associated with brain tissue damage visible to the naked eye
 Most common cause is usually penetrating head injury in which the skull is
perforated
 As frequently occurs in auto accidents, blows and gunshot wounds
 Typically have symptoms that are related to the damage area of the brain
 Strokes usually produce focal damage that is associated with signs and
symptoms that correspond to the part of the brain that has been damaged
SUB-TYPES OF FOCAL BRAIN INJURIES

 CEREBRAL CONTUSION -IS A BRUISE TO THE BRAIN TISSUE THAT COMMONLY

RESULTS FROM CONTACT OF THE BRAIN WITH THE INSIDE OF THE SKULL
 CEREBRAL LACERATION- IN WHICH THE PIA ARACHNOID IS DAMAGED OR
TORN
 EPIDURAL HEMORRHAGE – IS BLEEDING BETWEEN THE DURA MATER AND THE
SKULL, IT IS COMMONLY ASSOCIATED WITH DAMAGE TO THE MIDDLE
MENINGEAL ARTERY, OFTEN RESULTING FROM A SKULL FRACTURE
 SUBDURAL HEMORRHAGE – IS BLEEDING BETWEEN THE DURA MATER AND THE
ARACHNOID
 INTRAVENTRICULAR HEMORRHAGE- IS BLEEDING WITHIN THE VENTRICLES OF
THE BRAIN
TYPES OF BRAIN INJURY

 DIFFUSE
 ALSO CALLED MULTIFOCAL INJURY
 DUE TO HYPOXIA, MENINGITIS AND DAMAGE TO BLOOD VESSELS
 ARE USUALLY HARD TO DETECT USING IMAGING
 RESULTS FROM ACCLERATION/DECELERATION INJURIES
 CAN ALSO BE CAUSED BY ROTATIONAL FORCES
 THESE FORCES ARE COMMON IN DIFFUSE INJURIES SUCH AS CONCUSSIONS
AND DIFFUSED AXONAL INJURIES
SUB-TYPES OF DIFFUSED INJURIES

 DIFFUSE AXONAL INJURY- IS WIDESPREAD DAMAGE TO THE WHITE MATTER OF

THE BRAIN THAT USUALLY RESULTS FROM ACCELERATION AND DECELERATION
TYPES OF INJURY
 ISCHEMIC BRAIN INJURY-RESULTING FROM INSUFFICIENT BLOOD SUPPLY TO
THE BRAIN, IS ONE OF THE LEADING CAUSES OF SECONDARY BRAIN
DAMAGE AFTER TRAUMA
 VASCULAR INJURY- USUALLY CAUSES DEATH SHORTLY AFTER AN INJURY
ITSELF, DIFFUSE VASCULAR INJURY IS GENERALLY MORE LIKELY TO BE CAUSED
BY FOCAL THAN DIFFUSE INJURY
 SWELLING- COMMONLY SEEN AFTER TBI, CAN LEAD TO DANGEROUS
INCREASES IN INTRACRANIAL PRESSURE.
GERIATRICS

 The risk of TBI increases sharply after age 65

 TBI among the elderly are more frequently due to falls
 Severity of TBI among the elderly tends to be higher than that observed in
other age groups; mortality is also higher in the elderly compared to other
groups
PEDIATRICS

 TBI is the leading cause of death in children > 1 year of age

 10 in every 100,000 children die each year secondary to head injuries
 Annual incidence of TBI in children—185 per 100,000
 Causes:
 Transportation related (39%)
 Falls (28%)
 Sports and recreational (17%)
 Assault (7%)
Anatomy
 The brain is composed of three parts: the brainstem, cerebellum, and
cerebrum. The cerebrum is divided into four lobes: frontal, parietal,
temporal, and occipital
FRONTAL LOBE

 Personality, behavior, emotions

 Judgement, planning, problem solving
 Speech: speaking and writing (Broca’s area)
 Body movement (motor strip)
 Intelligence, concentration, self awareness
PARIETAL LOBE

 Parietal Lobe
 Interprets language, words
 Sense of touch, pain, temperature, (sensory strip)
 Interprets signals from vision, hearing, motor, sensory, and memory
 Spatial and visual peprception
OCCIPITAL LOBE

 Interprets vision (color, light, movement)

TEMPORAL LOBE

 Understanding language (Wenicke’s area)

 Memory
 Hearing
 Sequencing and organization
Deeper structures

 Hypothalamus
 Pituitary gland
 Pineal gland
 Thalamus
 Basal ganglia
 Limbic system
Mechanism of injury

 The brain damage results from external forces that cause brain tissue to
make direct contact with an object (bony skull or penetrating object),
rapid acceleration or deceleration forces, or blast waves from an explosion
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.
 Contusion—bruising of cerebral (cortical) tissue
 Occurs on the undersurface of the frontal lobe (inferior frontal or
orbitofrontal area) and anterior temporal lobe
 May occur from relatively low velocity impact, such as blows and falls
 Acceleration and deceleration cause shear, tensile, and compression
forces within the brain, which causes diffuse axonal injury (DAI)
 DAI most often occurs in discrete areas: the parasagittal white matter of
the cerebral cortex, the corpus callosum, and the pontine-mesencephalic
junction adjacent to the superior cerebellar peduncles
 The acceleration/deceleration forces cause disruption of neurofilaments
within the axon leading to Wallerian-type axonal degeneration.
Blast Injury

 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
 Tertiary injury occurs when the victims flung backward and strikes an object
Sequelae of TBI

 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.
 Cognitive impairments
 Cognition is the mental process of knowing and applying information
 People with TBI are particularly susceptible to cognitive impairments. Such
as complex neural processes, including arousal, attention, concentration,
memory, learning, and executive functions
 Coma, vegetative state, and minimally conscious state are disordered
arousal states seen after severe brain injury
 Coma- a state of deep unconsciousness that lasts for a prolonged or
indefinite period, caused especially by severe injury or illness
 Arousal system is not functioning
 Patient’s eyes are closed
 No sleep/wake cycles
 Ventilator dependent
 No auditory/visual/cognitive/communicative function
 Abnormal motor and postural reflexes
 Vegetative state- there is disassociation between wakefulness and
awareness
 The brainstem is able to manage basic cardiac, respiratory, and other
vegetative functions
 Patient can be weaned off the ventilator
 Sleep/wake cycles are present
 Eyes may be open though awareness of surroundings is absent
 Patients may startle to visual or auditory stimuli and briefly orient to sound or
visual stimuli
 Meaningful cognitive and communication function is absent
 Reflexive smiling/crying may be present
 Although patients in a vegetative state may appear to have purposeful
movement, these movements are non-purposeful and reflexive in response
to external stimuli
 Minimally conscious state-there is minimal evidence of self or
environmental awareness
 Cognitively mediated behaviors occur inconsistently and are reproducible
or sustained such that they can be differentiated from reflexive behaviors
 Sleep/wake cycles are present
 Patients may localize to sound location and demonstrate sustained visual
fixation and visual pursuit
 Neurobehavioral Impairments
 Patients can exhibit profound behavioral changes as they progress through
recovery
 Common behavioral sequelae include low frustration tolerance, agitation,
apathy, emotional lability, aggression, impulsivity, and irritability
 Communication Impairment
 Common language and communication deficits include disorganized oral
or written communication, imprecise language, word retrieval difficulties,
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
 Dysautonomia
 Elevated sympathetic nervous system activity occurs as a normal response
to trauma; following TBI this response may become overactive
 Increased sympathetic activity results in increased heart rate, respiratory
rate, and blood pressure, diaphoresis and hyperthermia
Posturing secondary to head injury

 Decerebrate posturing
 Seen with midbrain lesions/compression; also with cerebellar and posteria
fossa lesions
 In its fully developed form it consists of opisthotonus, clenched jaws, and
stiff, extended limbs with internal rotation of arms and ankle plantar flexion
 Decoritcate posturing
 Posturing due to lesions at a higher level (than in decerebrate posture)
seen in cerebral hemisphere/white matter, internal capsule and thalamic
lesions
 Flexion and adduction of the upper limbs and extension of the lower limbs
Recovery mechanisms

 Plasticity
 Brain plasticity is when the damaged brain has the capabilities to repair
itself by means of morphologic and physiologic responses
 It occurs via 2 mechanisms:
 1) Neuronal regeneration/neuronal sprouting
 2) Unmasking neural reorganization
 Neuronal Regeneration
 Intact axons establish synaptic connections through dendritic and axonal
sprouting in areas where damage has occurred
 May enhance recovery of function, may contribute to unwanted
symptoms, or may be neutral (with no increase or decrease of function)
 Thought to occur weeks to months post-injury
 Functional Reorganization/Unmasking
 Healthy neural structures not formerly used for a given purpose are
developed (or reassigned) to do functions formerly subserved by the
lesioned area.
Other related phenomena associated
with head injury recovery
 Redundancy-Recovery of function based on activity of uninjured brain
areas (latent areas) that normally would contribute to that function (and
are capable of subserving that function)
 Vicariation- Functions taken over by brain areas not originally managing
that function. These areas alter their properties in order to subserve that
function
 Functional Substitution/Behavioral Substitution
 Techniques/new strategies learned to compensate for deficits and achieve a
particular task
Diagnosis
Predictors of outcome after TBI
 Traumatic brain injury is generally categorized as severe, moderate, or mild
using the Glasgow Coma Scale (GCS), the most widely used clinical scale
that measures level of consciousness and helps define and classify the
severity of injury
 GCS is comprised of three response scores: motor response, verbal
response, and eye opening. The scores from the separate responses are
summed to provide a score between 3 and 15
 Scores of 8 or less are classified as severe
 scores between 9 and 12 are defined as moderate
 scores of 13 to 15 are classified as mild brain injury
 Glasgow-Liege scale: Born (1985) proposed the addition of the brain stem reflex
scale to the Glasgow Coma Scale—Glasgow-Liege Scale
 The Glasgow-Liege Scale has been tested for reliability and prognostic power
and has been shown to amplify the information provided by the standard GCS
in comatose patients
 Brain stem reflexes included in this scale:
 Fronto-orbicular reflex (orbicularis oculi): Orbicularis oculi contraction on percussion of
the glabella
 Vertical oculocephalic and horizontal oculocephalic or oculovestibular reflex: “Doll’s
eye” maneuver (horizontal—moving head forward from side to side; vertical—moving
head up and down)
 The pupillary light reflex
 The oculocardiac reflex: Bradycardia induced by increasing pressure on the eyeball
 Posttraumatic Amnesia (PTA)
 PTA is one of the most commonly used predictors of outcome
 PTA is the interval of permanently lost memory that occurs following the injury
 Galveston Orientation and Amnesia Test (GOAT)—developed by Harvey Levin
and colleagues, is a standard technique for assessing PTA. It is a brief, structured
interview that quantifies the patient’s orientation and recall of recent events
 The GOAT includes assessment of orientation to person, place, and time, recall of the
circumstances of the hospitalization, and the last preinjury and first postinjury memories
 The GOAT score can range from 0 to 100, with a score of 75 or better defined as
normal
 Disability Rating Scale (DRS)
 This is a 30-point scale covering the following eight dimensions:
 1. Eye opening
 2. Verbalization/communication
 3. Motor responsiveness
 4. Feeding*
 5. Toileting*
 6. Grooming*
 7. Overall level of functioning/dependence
 8. Employability
 Rancho Los Amigos Levels of Cognitive Function Scale (LCFS)
 Eight-level global scale that focuses on cognitive recovery and behavior
after TBI
Mild TBI

 Mild TBI constitutes 80% to 90% of TBI cases in the United States
 The American Congress of Rehabilitation (1995) has defined mild TBI as a
traumatically induced physiologic disruption of brain function with at least
one of four manifestations:
 Any loss of consciousness (LOC)
 Any loss of memory for events immediately before or after the injury
 Any alteration in mental status at the time of the accident
 Focal neurological deficits that may or may not be transient
 Usually, mild TBI has negative radiological findings (CT/MRI)
 Most mild TBI patients have a good recovery with symptoms clearing within
the first few weeks or months postinjury (usually within 1 to 3 months)
 The injury cannot exceed the following severity criteria:
 LOC greater than 30 minutes
 Posttraumatic amnesia (PTA) > 24 hours
 Initial GCS ≤ 12 (13 to 15)
 Signs and symptoms after mild TBI include:
 Headache (most common)
 Dizziness
 Tinnitus
 Hearing loss
 Blurred vision
 Altered taste and smell
 Sleep disturbances/insomnia
 Fatigue
 Sensory impairments
 Attention and concentration deficits
 Slowed mental processing (slowed reaction and information processing time)
 Memory impairment (mostly recent memory)
 Lability
 Irritability
 Depression
 Anxiety
Treatment

 Preventive therapeutic interventions may be implemented:

 – Manage bowel and bladder (B/B) function
 – Maintain nutrition
 – Maintain skin integrity
 – Control spasticity
 – Prevent contractures
 Pharmacologic treatment/intervention
 A. Elimination of unnecessary medicines (e.g., histamine-2 blockers,
metoclopramide, pain meds, etc.) and selection of agents with fewest adverse
effects on cognitive and neurologic recovery
 B. Addition of agents to enhance specific cognitive and physical functions
 – In patients emerging out of coma or VS, the recovery process may be
(theoretically) hastened through the use of pharmacotherapy
 Agents frequently used include:
 Methylphenidate
 Dextroamphetamine
 Dopamine agonists (levocarbidopa and carbidopa)
 Amantadine
 Bromocriptine
 Antidepressants
 Patient/family- Sociologist
 Physical Therapist
 Neurologist
 Speech