TBI

1. ETIOLOGY /EPIDEMIOLOGY
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M>F
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15-25-1.0
① Falls (elderly)
② MVA
③ Assnalt
④ contact sports

II. MECHANISMS OF INJURY

① Acceleration
② Deceleration
③ Coup injury
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④ Counter-coup injury

III. PATHOPNYnoway
A. PRIMARY IMRURY B. SECONDARY INJURY
① DAI ① hypoxic ischemic
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injury
② cerebral /cortical ② elevated ICP
contusions
③ brain herniation
④ hydrocephalus
 TRAUMATIC BRAIN INJURY
PATHOPHYSIOLOGY OF HEAD TRAUMA

→ Sullivan: An alteration in brain function, or I. CONCUSSION

other evidence of brain pathology, caused by → Brief alteration of consciousness (e.g.<6
an external force. hours), may be unconscious or dazed
→ No gross, microscopic parenchymal
INCIDENCE abnormalities
→ No or minimal CT/MRI abnormalities
→ Occurs in almost 2 million people per year → Confusion, amnesia, loss of
→ Estimated 5 million people living with TBI consciousness
caused disability → Due to transient functional disruption of
→ M>F the Reticular Activating System, caused
→ Average age is 29 y/o by rotational forces on the upper
→ Most at risk: Low income inner city dwellers brainstem
→ Peaks at 3 age levels:
 1-2 y/o ( due to child abuse)  American Academy of Neurology
 15 24 y/o (risk taking behaviors e.g. Classification for Concussion
bicycling w/o helmet)
 Elderly (most likely to be hospitalized; MC  No LOC but with transient signs
due to Falls) GRADE 1 of confusion
 Symptoms resolve in 15 min
ETIOLOGY  Athlete must be removed from
competition and return only if
1. Falls leading cause of TBI (32%) symptom free after 1 week of rest
2. MVA (19%) secondary in TBI ; primary su
- in

3. Struck by/ against events (18%) sports

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 results from a moderate head

4. Assaults ( 10%) GSW
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GRADE 2 injury with transient confusion

5. Alcoholic abuse that lasts longer than 15 mins
 Most common indirect cause of TBI  Patient exhibits poor
concentration, retrograde or
anterograde amnesia
 Athlete must be removed stat
from competition and receive
medical evaluation
 CT Scan indicated if symptoms
worsen
 Return to play deferred until pt is
asymptomatic for 2 weeks at rest

 results from head injury with LOC

GRADE 3  Pt requires transport to ER for full
neuro evaluation
 Hospitalization is warranted if
altered consciousness or mental
status persists.
 Athlete withheld from competition
until symptom free for min of 1
month.
 This concussion can be
secondary to DAI (diffuse axonal
injury)
 Can result to coma
 II. DELAYED DETERIORATION
→ 5% of patients who are normal initially will
deteriorate in a delayed fashion
→ 75% of delayed deterioration are 2ry to
hematomas (EDH,SDH, contusion)
→ Other causes:
 Posttraumatic diffuse cerebral
edema
 Hydrocephalus
 Tension pneumocephalus
 Seizure V. BASILAR FRACTURES
 Metabolic abnormalities → frequently missed by standard skull Xray
 Vascular event (carotid dissection, → best identified by CT bone windows
SAH) Meningitis → often associated with cranial nerve injury

III. POST-TRAUMATIC BRAIN SWELLING

→ Increased cerebral blood volume, result PATHOPHYSIOLOGY II
from loss of vascular autoregulation. In
extreme cases it is called “malignant  Primary Brain Damage
cerebral edema”  Diffused Axonal injury
 Coup, Contra-coup injury
Note! TRUE CEREBRAL EDEMA: classically at  Closed or Open injury
autopsy, brains “weep fluid”.; Both vasogenic and
cytotoxic cerebral edema can occur within
hours of head injury.

IV. SKULL FRACTURES

Linear Depressed Comminuted

(80%); occurs 1 or more multiple
commonly in the fragments of shattered bone
temporoparietal bone are fragments may  Secondary Brain Damage
area displaced or may not be  Hypoxic Ischemic Injury
inwardly; 85% displaced.  Concussion
are open fxs  Blast Injury

HEMORRHAGIC CONTUSION
Traumatic Delayed Traumatic
Intracerebral Intracerebral
hemorrhage Hemorrhage (DTICH)
 Considered as high  Usually occur within
density area on CT 72 hours after the
 Occur in areas trauma
Raccoon’s sign where sudden  “Talks and
Frontal
lobe
deceleration of the deteriorate”
head causes the  Due to local or
brain to impact on systemic
bony prominences coagulopathy,
in coup or hemorrhage in
Temporal countrecoup fashion necrotic brain
lobe  Follow up CT often tissue, coalescence
show minimal or no of microhematomas
encephalomalacia  Same treatment but
outcome poor
Battle’s sign CSF otorrhea Hemotympanum Treatment
 Surgical decompression may sometimes be
considered if herniation threatens
IV. IMPAIRMENTS

① spasticity (neuromuscular)
② cognitive
③ neurobehavioral
④ dysantmomia
⑤ post traumatic seizure
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⑥ post traumatic
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amnesia

⑤ others :

V. SCALES
① Severity of TBI ( LOC PTA, ,
GCS)
② GLASGOW scales
a. GCS -
assess levetofcomatose
b. GLS -
assess level of comatose + brainstem reflexes

c. G 05

③ RLA help decide when apt is ready for rehabilitation

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.

④ principles of Neuroplasticity
 GLASGOW LIEGE SCALE

① Fronto orbicular reflex

- : contraction of orbicularis oculi
2° to glabellar reflex

② horizontal { vehicular
auto cephalic { ourlorestibu tar reflex doll 's :
eye maneuver

③ ontocardiac reflex : A) Bradycardia dlt pressure @ eyeball

④ pupillary light reflex constriction

:
 ☆ Not related
to stimulus

☆
party

☆ MMMM rearming

☆
  Clinical Assessment
SEQUELAE OF TBI
I. PRIMARY CLINICAL ASSESSMENT
Neuromuscular  Abnormal tone
 Basic brain support Impairment  Decorticate vs.
 Spinal immobilization Decerebrate rigidity,
 Baseline neurological examination spasticity
 Sensory impairment
 Motor control
impairment
 Balance impairment

Cognitive  Retrograde Amnesia

Impairment  Anterograde Amnesia
 Post traumatic Amnesia
 Declarative memory
 Procedural memory

II. SECONDARY CLINICAL ASSESSMENT Behavioral  Disinhibition

Impairments  Impulsiveness
 External signs of injury  Physical and verbal
 Glasgow Coma Scale = (LOC) aggressiveness
 Pupillary size & response to light  Apathy
 Eye movements  Lack of concern
 Important indices of brainstem & reticular  Sexual
activating system functions Inappropriateness
 Cervical spine injury must be first ruled out  Irritability
 Motor power  Egocentricity
 Determination of motor weakness
 Lateralized weakness suggests a possible Altered Orientation
intracranial pathology, either hematoma or
contusion Attention Deficits
 Respiratory pattern Impaired Executive
 Cheyne-stokes respiration Functioning
 Central neurogenic hyperventilation
 Apneustic respiration Visual Perceptual
 Ataxic respiration Deficits
 Vital signs Swallowing
 Cushing response Communication
= rise in blood pressure, bradycardia, Indirect Impairments  Soft tissue contractures
& abnormal respiratory patterns  Pressure ulcers
 Cushing’s TRIAD  DVT
a. BP: 200/100 (increased BP)  Heterotrophic
b. PR: 48 (decreased PR) Ossification
c. RR: 30 irregular (decreased RR)  Decreased Bone
***indicative of increased ICP density
 Muscle atrophy
 Gross sensory examination:  Pneumonia
(suspecting a spinal cord injury)  Decreased endurance
 Epidural vs Subdural Hematoma  Infection

EPIDURAL SUBDURAL
Lucid Interval ++ +/-
Skull Fracture ++++ -
Seizures - ++
CT Scan Lentiform Crescent
shape shape
Prognosis Good if… Poor
 PHYSICAL THERAPY PT INTERVENTION
PATIENT EXAMINATION
1. Motor Strategies
I. Review the medical record for: 2. Restorative vs Compensatory strategies
 Arousal, attention and cognition 3. Task oriented approach
 Integument integrity 4. Locomotor training with Body weight support
 Sensory integrity 5. Constraint induced Therapy
 Motor function 6. Aerobic and Endurance conditioning
 Range of motion 7. Electrical stimulation
 Reflex integrity 8. Dual Task Performance
 Ventilation and respiration / gas exchange 9. Patient/ Family caregiver Education
II. Assess for: 10. Community Reentry Programs
 Behavioral status
 Aerobic capacity/ endurance  Maintain ROM
 Cranial nerve integrity RLA LOCF I, II, III  Maintain skin integrity
 Gait locomotion and balance  Maintain respiratory
 Pain status
 Posture  Provide sensory
 ROM stimulation for arousal
 Self care and ADL skills and elicit movement
 Work/ leisure and community reintegration  Promote early return of
functional mm. strength

 Glasgow Coma Scale  Provide structure and

→ to measure a person's level of RLA LOCF IV, V, VI consistency
consciousness  Engage pt in a task
 Severity of TBI Scales specific training
a. GCS (Glasgow coma scale)  Emphasize safety
b. PTA (Post-Traumatic Amnesia)  Model calm, focused
c. LOC (duration of loss of behavior
consciousness)  Prevent over-stimulation
 Galveston Orientation and Amnesia Test of RLA IV pts
(GOAT)
→ is a measure of attention and orientation,
especially to see if a patient has recovered
from post-traumatic amnesia (PTA) after a  Special Considerations for
traumatic brain injury Confused And Agitated Patients

 Ranchos Los Amigos Level of Cognitive 1. Encourage repetition for consistency

Function 2. Increase safety precautions
→ a renowned clinical tool used to rate how 3. Calm behavior and environment
people with brain injury are recovering. 4. Expect no carryover of learning
→ The 10 levels of recovery noted in the
scale also help to decide when a patient is PROGNOSIS
ready for rehabilitation.
GCS score: >8 GCS score: <8
 Graduated Return to Play Protocol (GRTP) Young adults Adults
→ An athlete should only move to the next (+) VOR: doll’s eye sign (-) VOR: doll’s eye sign
step if they do not have any new PTA <4 weeks PTA >12 weeks
symptoms at the current step. Coma <1 week Coma >2 weeks
 principle of the GRTP is to ensure that
increasing levels of activity do not Note! In examination of VOR, the examiner
provoke a recurrence of the symptoms observes a positive oculocephalic reflex when the
of concussion in the player pt moves their eyes opposite of the rotation of their
→ typically overseen by a PT, certified head (normal reflex is present/intact). Abnormal
athletic trainer, or in some cases, coaching when it stays midline and does not move.
staff, under the direction of a physician. Examination of CN 3,6,8.