Traumatic Brain Injury

Definition:
an injury or damage to the brain caused by an
external traumatic force that may lead to loss
of consciousness, other complication and even
death

Head injury may happen from superficial inward:
Scalp skull brain
Scalp
Has 5 layers:
S- skin
C- subcutaneous tissue
A- aponeurotic layer
L- loose connective tissue
P- pericranium (superficial covering of the skull)
Bleeding: most common problem in scalp
Scalp is highly vascular
Skull Fracture
Occurs when elastic tolerance of skull bone is
exceeded
3 types:
A. Linear skull fracture:
80% of all skull fractures and is the most common
Starts from a point of impact and extends into the
base of the skul
B. Basilar skull fracture:
located parallel to petrous bone or along the
sphenoid bone and towards the sella turcica and at
the ethmoidal groove
Cant be seen on X-rays but maybe based on
findings:
1. CSF leak (rhinorrhea) leak in nose
2. Pneumocephalus
3. Hemotympanum blood behind tympanic
membrane
4. Battle sign delayed eccyhmosis over mastoid
process
5. Racoon sign bluish discoloration around the eyes
Subtypes:
1. Sellar fracture:
Neuroendocrine injuries (injury to pituitary
gland)
Associated with CN palsies 6 (gaze
paralysis), 7 (bells palsy) and optic nerve
injuries
Air fluid level in the sphenoid sinus:
suggestive of sellar fracture


2. Petrous Fracture
- Disruption of ear ossicles

3. Frontal Fracture
- Loss of sense of smell
C. Compound/Depressed fracture:
Compound Fracture
Pericranial tissues are torn so that there is
direct communication from outside and inside
of brain
- Severe brain damage
Depressed Fracture
- Pericranium is intact but fragments of
fracture is depressed
- Brain is not penetrated
Brain
degree of damage depends upon the force
applied, speed of force, area of application
and whether the head is fixed or movable.
Critical aspect:
Inflammation brain swelling if massive
herniation (foramen magnum)death
Epidemiology:
Trauma is the leading cause of death in
the U.S for persons under 34 years of
age. Each year, there are 22 fatal head
injuries per 200,000 persons and over
500,000 injuries are significant enough to
require hospitalization.
Accidents are the fourth most common
cause of death for all ages. 50%of all
accidental deaths result from motor
vehicle accidents.
Gunshot and falls are the most leading
causes.

Head injury occurs more frequently in
men than women, largely d/t alcohol
intoxication at the time of accident.
The typical patient is between the ages
of 15 and 24 years

Etiology:
The most common cause of TBI is
vehicular accidents. May also be seen in
such traumatic events like gunshots
wounds, falls, or mauling incidents

The vast injury of TBI in hospitals are
classified as close-head injuries, wherein
the skull is not usually penetrated. The
nature of injury sustained in vehicular
accidents (e.g blunt impact, acceleration-
deceleration0 often results in multi focal
lesions and diffuse brain damage with a
variety of physical, cognitive, and
neurobehavioral impairments.
Pathophysiology/Pathogenesis:
Depending on the nature, direction, magnitude,
of the forces applied to the skull, primary
damage can be any or all of the following
types:
I. Primary damage
A. Local brain damage
B. Polar brain damage
C. Diffuse brain damage

II. Secondary injury
The energy requirements of the brain are
extremely high following severe head injury,
numerous conditions conspire to decrease
the energy supply, causing secondary injury
to the brain.
A. Hypoxic-ischemic injury
B. Intracranial hematoma
C. Intracerebral pressure

Other causes

Intracranial infection
Cerebral artery vasospasm
Postraumatic epilepsy
Clinical signs and symptoms:
According to degree of severity:
1. Mild head injury most frequent of all TBI
syndromes
Headache
Dizziness
Poor concentration and information processing
Memory loss
Fatigue and irritability
Progressive loss of neurological and cognitive
functions with significant atrophy of cerebral
tissue due to repeated minor injuries (ex.
Dementia pugilistica seen in boxers)
Brief loss of consciousness with GCS of 13 and
higher
No focal neurological findings, no abnormality
of computed tomographic scan or skull
radiographs and discharge from hospital
within 48 hrs.
2. Moderate head injury
Group of patients who are placed mild and
severe head injury
GCS of 9-12, 10-12, 8-12
Admission to hospital for head trauma
associated with a post-traumatic amnesia
lasting between 1-24 hours
3. Severe head injury
Comatose for at least 6 hrs
Patients who have undergone sufficient
amount of recovery will potentially benefit
from intensive rehabilitation while also
having sufficiency from severe and complex
deficits to require medically supported and
multidisciplinary approach to inpatient,
hospital-based rehab program
4. Persistent vegetative state (PVS)
Patient continues to demonstrate no
awareness if surroundings and niether
speaks nor makes volitional movements;
however, other activities (sleep-wake cycle,
yawning, lip-smacking, grimacing,
withdrawing form noxious stimuli and visual
fixation) are presumably mediated
principally by ,lower brain structures
The following factors have positive
prognostic significance for emerging from
unresponsiveness:
Young age
Reactive pupils and conjugate eye
movements
Decorticate posturing rather than
decerebrate or flaccid states
Early spontaneous eye opening
Absence of ventilator dependence or
hydrocephalus
Diffirential diagnosis:
Akinetic mutism & Locked- in
syndrome
hypertonial and posturing are
absent while in PVS there is
preserved conciousness through eye
movements
Deformities/Disabilities
I. Medical problems after TBI
a) Fractures
b) Seizures
c) Hydrocephalus
d) HTN, tachycardia, & increased cardiac
output

e. Cardiopulmonary disorders long term
survivors show decreased lung capacity, vital
capacity, & FEV
f. hypothalamic and endocrine dysfunction
diabetes insipidus (as a result of impairment
of posterior pituitary)
- hypotension & hypothermia
- menorrhea in women
- sexual dysfunction in men

Physical impairments
1. Cranial nerve dysfunction
a) Olfactory nerve injuries
Test: scratch and sniff odor panel
b) Visual impairment spotty scotoma and optic nerve
lesions
Test: visual acuity test
c) Affectation of extraocular movement
b) Facial nerve injuries disrupted by temporal bone
fracture
Test: SMILE
e) Movements of tongue, pharynx and larynx
Test: cough and gag reflexes

2. Sensory deficits
disorders in the somesthetic sensation
can result from damage of brain
structures and may result to he distortion
of touch, pain, temperature and also the
position sense
3. Heterotrophic ossification
Primarily in the proximal joints of both
UE and LE
may present with pain, warmth,
swelling, and contracture
4. Increased ms. Tone and contractures
Spasticity
Dystonia
Posturing in response to head position, and
cutaneous stimulation
Extrapyramidal syndrome
Contractures

5. Sensorimotor deficits
General deconditioning generalized
weakness and loss of flexibility
Hemeparesis result of direct unilateral
trauma to the cortex; also from bleeding and
hypoxia
Bilateral hemiparesis voluntary movt may
be lacking entirely and movt appear to be
dominated by reflexes
Balance and deficit
Ataxia and incoordination d/t damage
of cerebellum and basal ganglia
Associated injuries fracture, PNI, SCI

6. Nutrition and feeding
Gastroesophageal reflux leads to aspiration
and esophagitis

7. Bowel and bladder dysfunction
particularly in frontal lobe lesion leads to
urgency and incontinence
Cognitive impairments
Impairments of arousal and attention
- Reticular activating system (RAS) primary of
arousal role is control
a.) deficits in tonic arousal
b.) deficit in phasic arousal


Decreased level of consciousness
- acceleration-deceleration type of
injuries with some focal injuries,
persistent vegetative state ( continued
decreased level of consciousness), post-
traumatic amnesia
a.) declarative memory unable to
describe memories
b.) procedural memory carry over skills
that do not require verbal explanation

Impairments of learning and
remembering
a.) retrograde amnesia inability to
recall events preceding injury
b.) manifest in aberrant sexual gesture
and bizarre speech

Impairment of language and
communication
a.) dystonia most common language
disorder in TBI
- a word-finding or object-naming
disturbance
- accompanied by signs of
dysergraphia, dyslexia, and dyscalcula
- damage in dominant parietal lobe
Impairments of visouspatial perception
and construction
a.) prosopognosia
b.) disturbances in body scheme
c.) problems in motor planning
d.) impaired perception of form, spatial
relations, color and figure-ground
relationship
Behavioral deficits
- Most disabling and enduring:
a.) sexual disinhibition
b.) apathy
c.) aggresion
d.) low frustration tolerance
e.) depression
prognosis
The prediction of expected outcome is very
uncertain and difficult. each pt c TBI has a
complex combination of physical, cognitive
and behavioral deficits that present a unique
rehabilitation problem. However , a number of
helpful prognostic variables have emerged for
determining finer distinction of outcome.
I.Two most useful prognostic indicators
1.duration of coma
-coma for only a few hours only subtle
neurophysiological and personality deficits.
-coma lasting for several days to weeks: has
substantial deficits but has the capacity to
become physically indep. And return to gainful
employment.
-coma for a month or two: permanently impaired
to an extent :has potential to produce physical
independence and selfcare
-coma for 3 or more months: dependent in
almost all areas of function.
2. post-traumatic amnesia
-use of galveston orientation amnesia test
-pts. Are cumulatively subtracted from a total
score of 100 for errors in orientation. And the
pts recall is tested at the bedside.
-normal range 100-75 borderline abnormal
scores: 74 to 66
-prolonged post-traumatic amnesia: poor
prognosis.
II.NUEROLOGIC INDICATORS
:decerebration and decortication during the
acute emergency and neurosurgical phase are
indicators of increased severity.
III. Physiological indicators
-ischemic injury- worse prognosis
-level of creatine phosphokinase (CPK) and
lactic dehydrogenase (LDH)- relate to severity
of injury .
-elevation of catecholamines- inc. damage and
outcome.
IV. AGE
-generally the older the pt. the lesser is the
chance of optimum recovery.
V. SEX
-aggresion: M>F
VI. PREMORBID STATUS
-when a head injury occurs in person who has
already lost a seizeable number of neurons
because of previous brain ds. Or injury. The
result of that injury is much worse than in a
person w/out prior brain damage.

VII. SOCIO-ECONOMIC STATUS
-greater degree of family support, higher
economic groups and availabilily of economic
support for pursuing a long-term of
rehabilitation have better outcomes.
DIFFERENTIAL DIAGNOSIS
Mental retardation
-present at birth and is a static condition
-no pre morbid level of function with which to
compare the pts current diminished
functional abilities.
Stroke
-generally occurs in order population in which
decline of functions is a natural event of that
stage of life.
SCI
-less variable and has immediately evident
range of syndromes and outcomes that with
TBI
-process of physiological adjustment is much
easier compared w/ TBI who has a
characterized of memory loss lack of insight
into the deficits.