Traumatic Brain Injury

Rehabilitation
 Definition
Traumatic brain injury is a non degenerative, non-
congenital insult to the brain, from an external
mechanical force, possibly leading to permanent or
temporary impairments of cognitive, physical and
psychosocial functions with an associated diminished
or altered state of consciousness
 Epidemiology
• Incidence
– Varies in different areas
• Age distribution is bimodal
– Peaks in 15-25yrs, secondary peak in 65-75yrs
• Sex
– Male: female --> ~3:1, mortality is ~4times
common in males
 Causes of Injury
• Motor vehicle accidents related injuries (M.C)
• Falls
• Violence related injuries
• Work related
• Alcohol: Single largest indirect cause
 Pathophysiology
• Primary Mechanisms
– Contusions and lacerations of brain surfaces
– Diffuse axonal injury
– Diffuse vascular injury/Multiple petechial
hemorrhages
– Cranial nerve injury
 Contusion
• Occurs on the undersurface of the frontal lobe
(inferior frontal or orbitofrontal area) and anterior
temporal lobe, regardless of the site of impact

•May produce focal,

cognitive, and
sensory-motor deficits
•May occur from
relatively low velocity
impact, such as blows
and falls
 Diffuse axonal injury
• DAI is seen exclusively in TBI
• Damage seen most often in the corpus callosum and
other midline structures involving the parasagittal
white matter, the interventricular septum, the walls
of the third ventricle and the brain stem
• High impact MVA
• A/D injury
• LOC
 Pathophysiology
Secondary mechanisms
• Most of them occur during first 12-24 hrs might
occur upto 5-10 days post-injury also
– Intracranial hemorrhage(epi,sub,intra)
– Brain swelling/brain edema
– Hypoxia
– Intracranial infection
– Excitotoxicity
– Production of free radicals
 Pathophysiology
• Other factors that may result in secondary brain injury
include
– Hypotension, hyponatremia, electrolyte imbalance,
hyperthermia, hyper and hypoglycemia, hypercarbia,
seizures, anemia
 Recovery mechanisms
• The damaged brain has the capabilities to repair
itself by means of morphologic and physiologic
responses
• Plasticity is influenced by the environment,
complexity of stimulation, repetition of tasks, and
motivation
• It occurs via 2 mechanisms:
– Neuronal regeneration/neuronal (collateral) sprouting
– Unmasking/ functional reorganization
 Terminologies
Coma
– It is a state of unconsciousness from which the
patient cannot be aroused, there is no evidence of
self- or environmental awareness
– Eyes remain continuously closed
– No sleep-wake cycles on EEG
– Universal in severe TBI
 Terminologies
Vegetative state
– Loss of capacity to interact with the environment
despite the preserved potential for spontaneous
or stimulus-induced arousal(loss of cortical func.)
– Patient opens eyes (either spontaneously or with
noxious stimuli)
– VS is characterized by the presence of intermittent
wakefulness evidenced by sleepwake cycles
 Terminologies
Minimally conscious state
• Severely altered consciousness with minimal but definite
behavioral evidence of self or environmental-awareness
• There is evidence that the following behaviors are
reproducible (or sustained), but inconsistent
– Simple command following
– Object manipulation
– Intelligible verbalization
– Gestural or verbal yes/no responses
• Patient may also show
– Visual fixation
– Smooth pursuit tracking
 Predictors of outcome after TBI
• Glasgow Coma Scale
• Duration of coma
• Duration of posttraumatic amnesia (PTA)
• Sustained ICP >20mm Hg
• Age(>55yrs)
• Brain stem reflexes
• Time
• DRS score at admission
• Presence of medical complications
• Post traumatic use of phenytoin, phenobarbitones
 Glasgow Coma Scale
• Eye opening, Verbal response, Motor
response
• 15/3, <8= comatose, lower the score deeper
the coma
• Best motor response is the best acute
predictor of outcome of the three
– Severe TBI = 3 - 8
– Moderate TBI = 9 - 12
– Mild TBI = 13 - 15
 Glasgow Liege Scale
• These are the brainstem reflexes, have been tested
for reliability and prognostic power and shown to
amplify the information provided by GCS
1. Fronto-orbicular reflex
2. Vertical oculocephalic and horizontal
oculocephalic or oculovestibular reflex: “Doll’s
eye” maneuver
3. The pupillary light reflex
4. The oculocardiac reflex
 Posttraumatic Amnesia
• PTA is the interval of permanently lost memory that
occurs following the injury
• Galveston Orientation and Amnesia Test (GOAT) is a
standard technique for assessing PTA (0-100)
• The period of PTA is defined as the number of days
beginning at the end of the coma to the time the
patient attains the first of two successive GOAT scores
≥ 75
• TPP, Pre/post injury memories, hospitalization
Posttraumatic Amnesia

Expect quick and full

recovery with adequate
management
Recovery prolonged
Very prolonged
Recovery, perm. deficits
 Outcome Measurements
• The pattern and severity of injury and resultant
outcomes are highly variable
• Most survivors emerge from coma and achieve
remarkable progress to preinjury functional abilities
• Deficits in cognition are nearly ubiquitous after
moderate or severe TBI
• Limitations in activities related to self-care, toileting,
mobility, basic communication, and feeding
commonly occur in severe TBI
• Changes in behavior, mood, and personality after
TBI have been documented
• In those with less severe injuries, limitations and
restrictions may not be revealed until more complex
community-oriented skills are attempted, such as time
and money management, community mobility, and
school or vocational tasks
• Restrictions in vocational, educational, and
interpersonal domains are widespread
• There is frequently loss or diminution of friendships
and intimate relationships and a devastating impact on
the family system
 Commonly used Scales
• Glasgow outcome scale
• Disability Rating Scale
• FIM scale
• Rancho Los Amigos Levels of Cognitive Function Scale
• Coma recovery scale
 Glasgow outcome scale
• Five categories
– Dead, Persistent vegetative state, Severe disability,
Moderate disability, Good recovery
• Widely used scale, repeated at 6 and 12 months
• Cons: categories are broad, not sensitive enough, not
real indicator of functional abilities
 Disability Rating scale
• The DRS was developed specifically for brain injury
• It provides a quantitative index of disability
• It is more sensitive to clinical changes than GOS
• This is a 30-point scale covering the following eight
dimensions:
– Eye opening
– Verbalization/communication
– Motor responsiveness
– Feeding
– Toileting
– Grooming
– Overall level of functioning/dependence
– Employability
 Ranchos Los Amigos Scale of Cognitive
Functioning
• Eight level scale that focuses on cognitive recovery
and behavior after TBI
• Lower validity and reliability than DRS
 Grading
• Mild Brain Injury
– Any period of loss of consciousness
– Any loss of memory for events immediately before or after the accident
– Any alteration in mental state at the time of the accident
– Focal neurologic deficits, which may or may not be transient
• Moderate Brain Injury
– Length of stay of at least 48 hours
– GCS score of 9-12 or higher
– Operative intracranial lesion
– Abnormal CT scan findings
• Severe Brain Injury
– GCS 8 or Less
– Coma - >6-8 hours
 Investigations / Tests
• Routine
• Radiography
– CT Scan
– MRI
• Neurophysiological tests
– EEG, Evoked potentials
• Neuropsychological testing
 Levels Of Management
• Acute management
• Sub acute management
• Day care
• OPD follow up
• Community reintegration
Rehabilitation assessment after TBI
• Serial neurologic, medical and functional
examinations
• Monitoring participation and progress in formal
therapy and nursing care
• Ensure appropriate prophylactic care
• Assessment of patient preinjury and current social
support systems
• Assessment of patient resources for rehab
• Adequate communication with team members
 Management
• Look out for
– Associated Injuries, Elevated ICP, Hypertension,
Pressure Ulcers, DVTs, Posttraumatic Hydrocephalus,
Posttraumatic Seizures, Posttraumatic Agitation,
Endocrine complications, Spasticity, Nutrition,
Bowel/Bladder
 Management Program for Patients
with Disorders of Consciousness
1. Neuromedical stabilization
2. Preventive therapeutic interventions may be
implemented:
– Manage bowel and bladder function
– Maintain nutrition
– Maintain skin integrity
– Control spasticity
– Prevent contractures
 Management Program for Patients
with Disorders of Consciousness(cont.)
3. Pharmacologic treatment/intervention
– Elimination of unnecessary medicines
– Addition of neurocognitive drugs (efficacy not
proven) like methylphenidate,
Dextroamphetamine, Amantadine, Bromocriptine
4. Sensory stimulation—widely used despite little
evidence of efficacy
– Stimulate one SS at a time, Avoid overstimulation
 Bladder and Bowel management
• Frontal lobe lesions can impair inhibitory control over
bowel and bladder evacuation, leading to urgency and
incontinence
• Slowed mobility, poor communication, and impaired
initiation also contribute indirectly to incontinence,
making this issue a significant one in persons with brain
injury
– Prevention of UTI
– Catheterization(Acute), Timed voiding
– Anticholinergic drugs
– High fibre diet to prevent constipation
– Diarrhea (spurious, C. difficile, osmotic)
 Nutrition
• Patients experience a significant increase in
metabolism and catabolism that peaks 48-72hrs after
injury(hormonal response)
• Additional energy demand after TBI is 40-69% of
normal
• Recommended diet after significant TBI is 2-2.5g
protein/kg/day , 23-35 non protein kcal/kg/day
• Dysphagia is seen in 60% and aspiration in ~40%
 Nutrition
• Nasogastric feeding does not prevent aspiration risk,
increases ulcer risk and may alter sleep hygiene and
behaviours
• Percutaneous endoscopic gastrojejunostomy tubes
are recommended if non oral nutrition and hydration
cannot be achieved by 2-3 weeks post TBI
• Initiating proper nutrition as soon as possible after
TBI has been shown to improve outcome
 Secondary Injuries
• Delayed diagnosis of limb and axial # are common in
TBI as multiple and complex acute issues, altered
consciousness, communication skills and cognitive
impairment can hinder detection
• Focused reexamination for occult injuries should be
under taken
• May present as swelling, pain, deformity, agitation
• Prompt diagnosis and management is necessary to
speed up the rehab process
 Elevated Intracranial Pressure
• ICP is between 2 to 5 mm Hg reclining with the head
and the trunk elevated to 45°
• Upto 15mm Hg harmless, Elevated if >20 for 5min
• >40mm Hg: neuro dysfunction, >60mm Hg: fatal
• Increase ICP in
– Loud noise
– Turning head, especially to left side
– Vigorous physical therapy, Chest PT, Suctioning
– Elevated blood pressure, fever, seizures
 Elevated Intracranial Pressure
• Monitoring
– Papilledema : usually B/L, develops 12-24 hrs after TBI
– CT scan
– Cysternography
• Management
– Non-pharmacological (Head-end Elevation, Hypothermia
Hyperventilation)
– Pharmacological (Mannitol, Frusemide, Acetazolamide)
– Surgical
 Hypertension
• 10-25% cases
• Related to sympathetic hyperactivity usually seen in
severe TBI
• Posttraumatic hypertension usually resolves
spontaneously
• If medication needed, propanolol recommended
• Cases of HTN have been reported secondary to
hydrocephalus several years after TBI
 Venous Thrombo-embolic States
• 10-20%
• The most significant complication of TBI as they are
related to ↑ mortality in the rehabilitation setting
• DVT occurs most commonly in the lower limbs and is
traditionally associated with immobility, paresis,
fracture, soft-tissue injuries, and ages > 40yrs
• Look for swelling, rise of temp, tenderness
• Diagnostic- doppler, D-Dimer assay, Impedance
plethysmography (IPG), I125 fibrinogen scanning
and contrast venography
• Prophylaxis in all TBI
– ROM Ex, encourage early ambulation
– Pneumatic Splints
– Compression boots
• Treatment
– Unfractionated heparin
– LMW heparin
– Warfarin
– IVC filters
 Pressure Ulcers
• Proper positioning
• Change of posture; bed-2h, Sitting-30 min
• Hygiene / Skin care
• Support surfaces
• Overlays: Foam, Water, Gel, Air
• Replacement mattress
• Wheel chair modification
 Cranial Neuropathies
• Most frequently affected cranial nerves in blunt
head trauma:
– Olfactory nerve (CN I)
– Facial nerve (CN VII)
– Audiovestibular/vestibulocochlear nerve (CN VIII)
• More common with occipital than with frontal
blows
• Anosmia is often associated with ↓ appetite/
altered feeding behavior
 Prevention of contractures
• Stretching Exercises
• ROM exercises
• Positioning
• Change of posture
• Use of splints
 Heterotopic Ossification
• HO is the formation of mature lamellar bone in
soft tissue
• Common in TBI, with an incidence of 11%–76%
• Risk factors
– Prolonged coma (> 2 weeks), Immobility, Limb
spasticity, Associated long-bone fracture, Pressure
ulcers
• Pain, restricted ROM, local swelling, erythema,
warmth joint, muscle guarding, low-grade fever
 Heterotopic Ossification
• Hips> Knee> Elbow/shoulder
• DDs: DVT, septic joint, hematoma, cellulitis, fracture
• Diagnosis
– SAP, USG, Xray, CT Scan
– Is a sensitive method for early detection of HO, can be
seen within the first 2–4 weeks after injury in Phase I
(blood-flow phase) and Phase II (blood-pool phase) of a
triple phase bone scan, and in Phase III (static
phase/delayed images) in 4–8 weeks with normalization
by 7 to 12 months
 Heterotopic Ossification
• Management
– ROM exercises
– Control of muscle tone
– Non Steroidal Anti-inflammatory Drugs
– Etidronate
– Perioperative Radiation
– Surgery
 Management of Spasticity
• Oral- Baclofen, Tizanidine
• Stretching, ROM / FES Exercises / Postural care
• TENS
• Orthosis
• Chemical neurolysis-Phenol
• Chemodenervation-Botulinum toxin
• Relaxation techniques
 Pyramid of spasticity treatment

Rhizotomy
Motor point/Nerve
blocks
Casting and Orthosis Medication
Physical Modalities
Positioning & handling Stretching
techniques programe
Prevention of nociception Reassurance and Education
 Post traumatic seizures
• Serious complication
• Incidence- 5% of TBI
• Types: Generalized / Partial
– Immediate(<24hrs)
– Early(24hrs to 1week)
– Late(after first week)
• Risk factors include penetrating injuries, IC
Hematoma, Early seizure, Depressed skull #, PTA>
24hrs
 PTS
• Diagnosis:
– Clinical
– EEG
• Standard, sleep deprived, 24hr
– Prolactin level
• Prophylaxis
– Controversial-Surgeons / Physicians
– Prophylactic use has not been proven
– Phenytoin prophylaxis proven effective only during 1st
week (to prevent early seizures in GCS <12)
• Carbamazepine and Valproic acid are DOC for Partial
and generalised seizures respectively
 PTS
• Anticonvulsant medications are usually started once
late seizures occur
• All anticonvulsants may cause some degree of
sedation and cognitive deficits(Esp Phenobarbitones)
• One to two year seizure-free interval is used more
often as time frame for withdrawal of anticonvulsant
therapy
 Agitation
• A subtype of delirium unique to TBI survivors, in
which the survivor is in a state of posttraumatic
amnesia, and there are excesses of behavior,
including a combination of aggression, disinhibition
and/or emotional lability
• Seen in 1/3rd of patients
• Pain is overlooked cause
• Treatment:
– Medication(usually not required,)
– Floor beds can eliminate need for restraints
– Use physical restraints only if patient is a danger to self
or others; should be applied only to minimal degree
 Agitation (contd..)
• Patient should be maintained in a safe, structured,
low-stimulus environment
• Limit the length and number of therapy sessions
• Minimize contact with unfamiliar staff
• Tolerate restlessness when possible
• Craig Bed
 Post TBI Hydrocephalus
• Ventriculomegaly is common after TBI(cerebral atrophy
and focal infarction)
• Hydrocephalus is most often Communicating
type/normal-pressure type
• Triad of Gait disturbance, Urinary incontinence, dementia
(is of little help in severe TBI)
• Diagnosis:
– Clinical: vomiting, confusion, drowsiness
– Routine, CT scan, LP, Cisternography
• Treatment: Shunting
 Endocrine complications
• 20% post TBI
• DI, Cerebral Salt Wasting, SIADH, Thyroid
dysfunction, Hypogonadism, Adrenal
insufficiency
• CF: Lethargy, Seizures, Weakness, fatigue,
Anorexia
• Investigation: Hormonal evaluation, serum
and urine osmolality, CT brain
• Treatment: Hormonal replacement
 Fluid restriction ~1lt/day
Hydration/ fluid
Hypertonic saline , correction HR-> Desmopressin
replacement
Treatment not > 10mEq/24hr Chlorpropamide Na+ correction
Demeclocycline in Chronic
 Motor and Balance Recovery
• Prognosis of functional recovery of
coordination and motor function is generally
favourable, even in severe TBI
• Damage to visual or vestibular pathways can
lead to array of deficits that impair balance
• Cerebellar insult -> ataxia, Basal ganglia ->
tremors and bradykinesia
• Drug induced
• Vestibular system -> BPPV, dizziness
 Motor and Balance Recovery
• Most rapid recovery takes place in 2-3 months
• Improving function with upperlimb ataxia, myoclonus,
and tremors are difficult
• Use of weighted instruments for ADL might be of some
help
• Strength must be preserved for these aids to have
utility
• Splinting of proximal joints may be carried out to
improve fine motor function
• Beta blockers and dopaminergics may be of some help
 Motor and Balance Recovery
• Slowness of movement and response is often a
persistent complication after TBI that has clear
functional and vocational implicatiions
• If natural recovery, repetitive tasking and cognition
enhancing medications do not have the desired impact
then patient and employer education regarding
persistence of these deficits is imperative to ensure
successful community reintegration
 Autonomic Disturbances
• Diagnosis of exclusion
• D/D: Neuroleptic malignant syndrome, Serotonin
syndrome, Malignant hyperthermia, Thyroid storm
• CF: Hypertension, Fever, Tachycardia etc
• Causes: Injury to one or more parts of brain
• Treatment: Medical management
– Clorpromazine, Bromocriptine, Propronolol, clonidine
Attention and Concentration problems
• Try reducing distractions in environment (ear plugs, sit
facing wall)
• Avoid interruptions(use do not disturb signs)
• Schedule regular breaks throughout the day to reduce
fatigue
• Alternate B/W cognitively challenging and less
demanding tasks
• Set goals to sustain attention for longer periods of time
• Avoid multitasking wherever possible
• Consider psychostimulants if required
 Memory impairments
• Usual pattern
Trauma

Retrograde Posttraumatic
amnesia Coma amnesia

Spared remote Permanent memory gap Variable recent

memory memory
 Memory impairments
• Use assistive devices like memory books, to do
lists, cameras, alarms, calenders, tape recorders
• Establish routine and maintain structure
• Repeat information
• Teach mnemonic strategies, imagery techniques
• Break tasks down into smaller steps and
introduce new steps as earlier steps are
accomplished
 Language problem
• Use short simple sentences to communicate and do
it slowly and clearly
• Instructions in multiple formats
• Be patient and allow patients time to find words and
complete sentences
• Encourage patients to use gestures drawings and
descriptions when speaking
• Educate family members and caregivers about nature
of deficits and techniques
 Sexuality
• Sexual dysfunction is common
• Includes inappropriate behavior, impulsivity,
decreased libido, inadequate sexual performance
• Have more of body image perception problems
• Coexistent depression may affect adversly
• Psychotherapeutic approaches are designed to help
patients and family members to cope up with
impaired performance or disinhibition
 Pediatric TBI
• Causes : abuse, MVA, Accidental injuries, violence inj
• Complex issues are posed by children with TBI because
the injury interacts with the processes of biological,
psychological, and social development
• It is challenging to disentangle neurologic recovery
from normal growth and maturation
• Children may grow into•their educational disability
without the educational system recognizing their prior
injury
 Pediatric TBI
• Have important effects concentration, attention, and
on emotional adjustment in children and adolescents
• Depression, dysthymia, and anxiety disorders have
been noted in increased frequencies