HEAD INJURY

PATHOGENESIS
• DIFFUSE BRAIN INJURY RESULTS IN
AXONAL INJURY, HYPOXIC DAMAGE,
DIFFUSE BRAIN SWELLING.
• PRIMARY DAMAGE IS THE RESULT OF
FORCES EXERTED ON THE BRAIN AT THE
TIME OF INJURY.
• SECONDARY DAMAGE IS THE RESULT OF
BRAINS REACTON TO TRAUMA MAINLY DUE
TO LACK OF OXYGEN IN THE HIGH O2
DEMANDING BRAIN.
 PATHOGENESIS
• SECONDARY PROBLEMS ARE MAINLY DUE
TO
• INCREASED ICP
• CEREBRAL HYPOXIA OR ISCHEMIA.
• INTRACRANIAL HEAMORRHAGE.
• ELECTROLYTIC IMBALANCES.
• INFECTION
• SEIZURES DUE TO PRESSURE OR
SCARRING.
 PATHOLOGY
• OVER ALL RESULT OF VASCULAR
CHANGES IS DECREASE ABILITY OF
CEREBRAL VESSELS TO MAINTAIN
NECESSARY HOMEOSTASIS.
 IN NORMAL
• ACH. CAUSES VASODIALATION BY
RELEASING ENDOTHELIUM DERIEVED
RELEASING FACTORS ------,WHICH
RELAXES SMOOTH MUSLCE OF
VESSEL WALL WHICH RESULTS IN
VASODIALATION.
 IN TBI
• THIS REACTION IS MISSING
RESULTING IN VASO SPASM.
 IN VASCULAR DAMAGE
• DISTURBED BBB RESULTS IN LEAKING
OF SERUM PROTEINS AND NEURO
TRANSMITTERS INTO PARENCHYMA
RESULTING IN OEDEMA.
 FOCAL INJURY
• DAMAGE CAN BE IN THE FORM OF
HAEMATOMA ,OEDEMA,CONTUSION,L
ACERATION OR COMBINATION OF
FOUR.
• COUP AND COUNTER COUP INJURY.
 DAI- DIFFUSE AXONAL INJURY

• ACCELARATION,DECELERATION,ROTA
TIONAL FORCES CAUSES DAI.
• DAI IS CHARACTERISED BY
WIDESPREAD SHEARING AND
RETRACTION OF DAMAGED AXONS.
 HII- HYPOXIC ISCHAEMIC
INJURY
• RESULTS FROM LACK OF
OXYGENATED BLOOD FLOW TO THE
BRAIN TISSUE.
• HYPOXIA –--- HYPERCAPNIA ----
INCREASED C.O –---- INCREASED
CEREBRAL BLOOD FLOW –----
INCREASE OEDEMA.
 ICP

• INCREASE ICP.

• NORMAL ICP IS 4-15 MM HG.

 SECONDARY CELL DEATH
• SECONDARY CELL DEATH OCCURS
AS A RESULT OF SERIES OF
CELLULAR EVENTS AFTER DAMAGE
---- GLUTAMATE NEUROTOXICITY –-
INFLUX OF CALCIUM IONS --– FREE
RADICAL AND CYTOKINES RELEASE
---RESULTING IN CELL DEATH.
 VASCULAR CHANGES
• IMPACT --- VASCULAR DAMAGE ----
INFARCTION ----- ENCAPSULATION OF
INFARCTION BY GLIAL ELEMENTS ----
FORMATION OF CYSTIC CAVITY.

• INTERNAL BLEEDING RESULTS IN

RAISED ICP.
 VASCULAR CHANGES
• SHEAR AND TENSILE FORCES AT
TIME OF INJURY.----- DISRUPTION OF
BRIDGING VEINS ---- SUB DURAL
HEAMATOMA.
• RUPTURE OF PLIAL VESSELS IN SUB
ARACHNOID SPACE ---- SUB
ARACHNOID HAEMORRHAGE ------
VASOSPASM-- ----- DECREASE IN
REGIONAL CERERBRAL BLOOD FLOW.
 PARENCHYMAL CHANGES
• AXONAL INJURY ------ SHEAR AND
TENSILE FORCES ------ DISRUPTS
AXOLEMMA ------IMPAIRS TRANSPORT
OF PROTEINS FROM CELL BODY AND
CAUSES SWELLING OF AXON.
 PARENCHYMAL CHANGES
• DIFFUSE BRAIN DAMAGE -----
INCREASE IN EXTRACELLULAR
NEURO TRANSMITTERS ----- AFFECTS
POST SYNAPTIC FUNCTIONS ----
SECONDARY DYSFUNCTION OF
NEURAL MECHANISMS.
 BRAIN DAMAGE
• HYPOXIA -----HYPERCAPNIA-----
INCREASED C.O ------- RAISED B.P
-------- INCREASED CEREBRAL BLOOD
FLOW ----- BRAIN SWELLING ------
FURTHER NEURONAL DAMAGE.
• BRAIN SWELLING ----- RESPIRATORY
CENTRE DEPRESSION ------ HYPOXIA .
 CLINICAL MANIFESTATIONS -
MOTOR
• PARALYSIS , PARESIS.
• CRANIAL NERVE INJURIES – 3,6,7,8,9
RESULTING IN PARALYSIS OF EYE
MUSCLES – 3,6.
• FACIAL MUSCLE PARALYSIS – 7
• VESTIBULAR DISTURBANCES – 8
• SPEECH AND SWALLOWING
DIFFICULTIES -9
 CLINICAL MANIFESTATIONS
• PARALYSIS TONGUE MUSCLES -12
• INCORDINATION,
• LOSS OF BALANCE.
• DECEREBRATE , DECORTICATE
RIGIDITY.
• ABNORMAL MUSCLE TONE.
• LOSS OF BLADDER AND BOWEL
CONTROL.
SENSORY AND PERCEPTUAL
• VISUAL , HEARING – DISTURBANCES.
• VISUO-SPATIAL ABNORMALITIES,
DIZZINESS, AGNOSIA ETC.
 ANS
• CHANGES IN PR, RR,H.R }RATE AND
RHYTHM.
• TEMPERATURE AND B.P CHANGES.
• ABNORMALITIES IN
SWEATING ,SALIVATION,
TEARING,SEBUM,SECRETION.
 COGNITIVE
• INTELLECTUAL DISORDERS, MEMORY
LOSS, CONCENTRATION DEFICTIS,
CONFUSION, MOTIVATIONAL
PROBLEMS, ATTENTION DEFICITS.
• EXECUTIVE FUNCTIONAL LOSS –
CHOOSING A GOAL , DEVELOPING A
PLAN, EXECUTING A
PLAN,EVALUATION OF EXECUTING OF
THE PLAN.
 COGNITIVE
• REDUCED PROBLEM SOLVING SKILLS.
• LACK OF INITIATION ,REASONING
PROBLEM SOLVING.
 BEHAVIOURAL PROBLEMS
• LIABILITY, UNCONTROLLED ANGER,
IRRITABILITY , EUPHORIA,
INTOLERANCE, HYPER OR HYPO
ACTIVITY.
 IMPAIRMENTS ASSOCIATED
WITH TBI
• NEURO MUSCULAR – ABNORMAL
TONE , SENSORY AND MOTOR
IMPAIRMENTS, IMPAIRED BALANCE,
PARALYSIS.
• COGNITIVE ALTERED LEVEL OF
CONSCIOUNESS, MEMORY LOSS,
ALTERED ORIENTATION.
 IMPAIRMENTS -TBI
• VISUAL ,PERCEPTUAL DEFICITS—
RIGHT –LEFT DISCRIMINATION –
APRAXIA.
• DYSPHAGIA.
• BEHAVIOURAL PROBLEMS –
INHIBITION, APATHY, IRRITABILITY,
LACK OF CONCERN.
• INDIRECT IMPAIRMENTS – BED REST.
 EVALUATION
• HISTORY.
• CLENT /FAMILY DATA.
• MDT – MEMBERS REFERRALS AND
TREATMENT.
• VITALS.
• HMF.
• CRAINAL NERVE TESTING.
 EVALUATION
• CVS ASSESMENT.
• INTEGUMENTARY SYSTEM.
• MUSCULO- SKELETAL SYSTEM.
• NERVOUS SYSTEM.
• SENSORY SYSTEM.
• MOTOR SYSTEM- TONE ,MUSCLE
STRENGTH,FLEXIBILITY, MT. RT.,
ENDURANCE, FATIGUE.
 EVALUATION
• BASIC SYNERGIES.
• ANTICIPATORY REACTIONS.
• DISABILITIES.
• ANS
• COGNITIVE AND PERCEPTUAL
DYSFUNCTION.
 DISABILITY LEVELS
• BARTHEL INDEX.
• FIM.
• DRS.
• UE. MOVEMENT PATTERNS AND
FUNCTIONS ARE EXAMINED BY USING
NINE –HOLE PEG TEST, MAS,
FRENCHY ARM TEST.
 IMPAIRMENTS
• STRENGTH., FLEXIBILITY, TONE, SPEE
D OF MOTION.
• REACTION TIME, ENDURANCE,
FATIGUE, SENSORY FUNCTION.,
PROPRIOCEPTION, 2-POINT
DISCRIMINATION., STEREOGNOSIS,
VISUAL AND VESTIBULAR TESTS.
 CLINICAL SCALES
• GCS.
• GOAT – GALVESTON ORIENTATION AND
AMNESIA TEST.
• RLA.
• GOS.
• DRS.
• FIM.
• FAM.
• WESTMEAD POST TRAUMATIC AMNESIA.
 GCS
• DEVELOPED BY TEASDALE AND
JENNETT.
• 3 – 15.
• LESS THAN 8 SEVERE BRAIN INJURY.
• 9- 12 MODERATE BRAIN INJURY
• 13 -15 MILD HEAD INJURY.
 GOAT
• GALVESTON ORIENTATION AND
AMNESIA TEST.
• IT’S A MEASURE OF POST TRAUMATIC
AMNESIA
• SCORE BETWEEN 75 – 100 NORMAL.
• LESS THAN 75 PTA.
 GOS
• PROGNOSTIC VALUE.
• 0 – GOOD RECOVERY.
• 1 – DISABLED MILD.
• 2 - MOD. DISABILITY.
• 3 – SEVERE
• 4 – VEGETATIVE
• 5 – DEAD.
 DRS
• 0 – NONE
• 30 – DEATH
• IT HAS
• EYE OPENING
• VERBAL
• MOTOR
• COGNITIVE LEVEL OF FUNCTIONING.
• EMPLOYABILITY.
 FIM + FAM
• MEASURE OF FUNCTIONAL MOBILITY
AND ADL.
• 1 – TOTAL ASSISTANCE
• 7- COMPLETE INDEPENDENCE.
 RLA – LEVEL OF COGNITIVE
FUNCTIONING - LOCF
• RECOVERY MEASURE OF COGNITIVE AND
BEHAVIOURAL ASPECTS.
• GCS + RLA – MOST WIDELY USED.
• 1- NO RESPONSE.
• 2 -GENERALISED RESPONSE.
• 3 – LOCALISED RESPONSE.
• 4 – CONFUSED AGITATED.
• 5 – CONFUSED INAPPROPRIATE.
• 6- CONFUSED APPROPRIATE.
• 7 – AUTOMATIC APPRORIATE.
• 8 – PURPOSEFUL AND APPROPRIATE.
 TBI CLASSIFICATION
• GRADE- 1 – TRANSIENT LOC- LESS THAN
5MIN ,NOW ALERT, ORIENTED WITHOUT
NEUROLOGICAL DEFICIT. GCS 14-15.
• GRADE 2 – PREVIOUS LOC.LESS THAN MIN
NOW IMPAIRED CONSCIOUNSESS,BUT
FOLLOWS SIMPLE COMMANDS.
• NO NEUROLGICAL DEFICITS GCS – 9 -13
 TBI
• GRADE -3 PREVIOUSLY
UNRESPONSIVE LESS THAN 5
MIN ,NOW NOT FOLLOWING EVEN A
SIMPLE COMMAND .PUPILS
UNEQUAL , INAPPRORIATE WORDS,
GCS LESS THAN 9.

• GRADE 4 – NO EVIDANCE OF BRAIN

FUNCTION – BRAIN DEATH.
 NEUROLOGICAL RECOVERY
AND FUNCTIONAL RECOVERY
• NEUROLIGICAL DEFICIT SEEN AFTER BRAIN
INJURY MAY BE ATTRIBUTED TO
LOCALIZED BRAIN DAMAGE AND DUE TO
DORMANCY OF ASSOCIATED PARTS OF
BRAIN.

• WITH TIME DORMANCY MAY BE OVERCOME

AND RESULTS IN FUNCTIONAL OR
NEUROLGICAL RECOVERY.
 RECOVERY
• DENDRITIC SPROUTING BOTH
COLLATERAL AND REGENERATIVE
MAY OCCUR IN DUE COURSE OF TIME
AND ALSO CONTRIBUTE FOR
RECOVERY.
 ACUTE CARE
• EVALUATION OF NEUROLOGICAL
STATUS WORKING IN CONJUNCTION
WITH DOCTORS AND NURSES.

• MONITORING OF CRANIAL NERVE

FUNCTION , REFLEXIVE AND
VOLUNTARY MOTOR BEHAVIOUR.
 TREATMENT
• CHEST CARE,PROPER POSITIONING,
ROM EXERCISES, RELAXATION
EXERCISES.

• EARLY FACILITATION OF MOVEMENT.

• CHEST DRAINAGE TUBES ARE KEPT
BELOW LEVEL OF CHEST AT ALL
TIMES.
 TREATMENT
• IF NASOGSTRIC TUBE IS PRESENT
HEAD END OF TUBE IS PRESENT ,HEAD
END OF BED IS RAISED 30 DEGREE TO
AVOID ASPIRATION.

• CLOSE COMMUNICATION WITH OTHER

MEMBERS OF TEAM SHOULD BE
MAINTAINED.
 TREATMENT- ACUTE CARE.
• CHEST , AIRWAYS, SHOULD BE
CLEARED BY CHEST PHYSIO.BUT
CONTRAINDICATED IF RAISED ICP IS
PRESENT.

• MOINTERING OF ABG ANALYSIS.

• PLANNING FOR WEANING WITH
ASSISTNACE OF OTHER TEAM
MEMBERS.
 TREATMENT
• RESTORATION OF NORMAL
MOVEMENT .TASK SPECIFIC TRAINING
PROGRAMME AND FORCED USE OF
LIMB PREVENTS DEVELOPMENT OF
COMPENSATORY MOVEMENT
STRATERGIES.

• SERIAL CASTING,DYNAMIC SPLINTING

IN CASES OF TONE CHANGES .
 TREATMENT.
• DESIGNING OF WHEEL CHAIR.
• SENSATION ,DENTITION ,TONGUE
CONTROL, LARYNGEAL CONTROL, ARE
ASSISTED FOR TRAINING OF SPEECH AND
SWALLOWING.

• COGNITIVE AND BEHAVIOURAL ASPECTS

ARE KEPT IN MIND. AS FUNCTIONAL OUT
COMES ARE LIMITED BY COGNITIVE
DEFICITS.
 PROGNOSTIC INDICATORS.
• GCS 3 -5 MORTALITY RATE MORE
THAN 60%.
• DEVELOPMENT OF PUPILLARY
ABNORMALITY IN PRESENCE OF
PRESERVED BRAINSTEM FUNCTIONS
WORSENS PROGNOSIS.
 VERY , VERY POOR
PROGNOSTIC INDICATORS.
• SBP LESS THAN 95 MM OF HG.
• PAO2 LESS THAN 65MM OF HG.
• GCS LESS THAN 7.
• ICP MORE THAN 30 MM OF HG.
• H.R LESS THAN 50 / MIN.
• C.T SCAN SHOWING MIDLINE SHIFT
OF MORE THAN 10 MM.
EARLY POSITIONING IN BED
• SUPINE: LYING SHOULD BE AVOIDED
WHENEVER POSSIBLE WITH NECK IN
EXTENSION -------RIGID
HYPEREXTENSION TONE
THROUGHOUT THE BODY,FLEXION
CONTRACTURE OF THE ELBOW.
• IN SUPINE ----- VOMITING ------RISK OF
ASPIRATION------- PNEUMONIA WILL
BE GREATER.
EARLY POSITIONING IN BED
• IN SUPINE – PRESSURE OVER BONY
PROMINANCES.
• IN SUPINE – NECK IN EXTENDED
POSITION ------ DIFFICULTIES IN
MOUTH CLOUSURE, EATING,
DRINKING , BREATHING, SPEAKING ,
SWALLOWING.
 SITTING
• NECK EXTENSION ---- DIFFICULTY IN
SITTING AND BALANCING .
• PROLONGED IMMOBILIZATION IN SUPINE
RESULTS IN SCAPULAR RETRACTION .
• IN SUPINE NECK SHOULD NOT BE
POSITIONED IN EXTENSION.
• SIDE LYING --- SPASTICITY IS REDUCED ,
NO PRESSURE ON SACRUM,ASSISTS IN
POSTURAL DRAINAGE.
 TURNING
• PASSIVE TURNING.
• ACTIVE TURNING.
• SIDE LYING – SACPULAR
PROTRACTION – ARM AT RIGHT
ANGLES TO TRUNK. PRESSURE OVER
STERNUM FACILITATES SCAPULAR
PROTRACTION .
 IN SIDE LYING

• IN SIDE LYING WHEN MARKED

EXTENSOR SPASTICITY IS A
PROBLEM – FLEXION OF NECK AND
ARMS INHIBIT MASS EXTENSION.
• TURNING PATIENT EVERY 2-3 HOURS
AND REPOSITIONING OF LIMBS
PREVENTS CONTRACTURES AND
DEFORMITIES AND PRESSURE
SORES.
 IN WHEEL CHAIR
• IN W.CHAIR TO AVOID DEVELOPMENT
OF PRESSURE SORES FREQUENTLY
TOO EXTENSION OF HIPS RELIEVES
PRESSURE ON ISCHAIL
TUBEROSITIES.
• CHANGE OF POSITION WILL PREVENT
STASIS DUE TO PROLONGED
PRESSURE ON WEIGHT BEARING
AREAS.
 DEEP VEIN THROMBOSIS
• PREVENTION
• TREATMENT.
HETEROTOPHIC OSSIFICATION

• Heterotopic ossification is described as

ectopic bone formation in the soft tissue
surrounding the joints
 HO
• Heterotopic ossification generally causes
joint pain and decreases range of motion
(ROM). It is often associated low-grade
fever, peri-articular swelling, peri-articular
warmth, and peri-articular erythema
 HO
• MOST COMMON SITES OF HO ARE
hips, knees, elbows, shoulders, hands,
and spine. Risk factors associated with the
development of heterotopic ossification
after TBI are a posttraumatic coma lasting
longer than 2 weeks, limb spasticity, and
decreased mobility. The risk of heterotopic
ossification is greatest during the first 3-4
months after injury.
 HO
• The mainstay of preventing heterotopic
ossification in patients with TBI is ROM
exercise
 HO
• Heterotopic ossification may result in
functional impairment, and patients may
require surgical excision. To minimize risk
of recurrence, surgical
excision has traditionally been delayed 12-
18 months to allow the heterotopic bone to
mature.
 SPASTICITY
• . Spasticity is defined as velocity-
dependent increase in tone. Rigidity is
also a function of tone, but it is defined as
the non–velocity-dependent increase in
tone.
 SPASTICITY
• Spasticity is most often encountered in
lesions of the upper motor neurons,
whereas rigidity is most common in
disorders of the basal ganglia. The
morbidity associated with spasticity is
variable, because in some people,
spasticity may assist in leg extension for
walking or finger flexion for grasping.
Prolonged low tone after TBI is generally
predictive of poor motor recovery
 SPASTICITY
• Guidelines for the treatment of spasticity
are generally based on (1) any resulting
limitation in function, (2) pain, (3)
prevention of contracture, and (4)
assistance with positioning. First-line
treatments for spasticity are correct
positioning of the involved body segment
and ROM exercises. Second-line
treatments include splinting, casting, and
other modalities
 ANTISPASTIC DRUGS
• . Dantrolene sodium baclofen, tizanidine,
clonidine, and benzodiazepines. Local
treatments for spasticity include chemical
neurolysis with phenol or alcohol injections
and with botulinum toxin type A and type B
injections.