TRAUMATIC

BRAIN INJURY
N E U R O R E H A B I L I TAT I O N
 INTRODUCTION

• Trauma is the commonest cause of death under the age of 35 years.

• Head injury is the commonest cause of accidental death.
• Head injury or traumatic brain injury are terms used to describe a physical injury to the brain by an
external mechanical force or projectile that results in loss of consciousness, post traumatic amnesia and
neurological impairments.
• TBI most commonly caused by road accidents, industrial and sporting accidents, attempted suicides
and interpersonal violence.
• The sequelae can have devastating effects on the life of the person affected. Creating general health
and social problems, causing disruption for family members and marital strain, affecting role
relationships and fostering economic hardships.
• The systematic study of the effects of TBI can be traced back to WWII. Here the first effects of TBI
were seen in servicemen with gunshot wounds.
• Majority of TBI individuals seen in hospitals these days are classified as “Closed TBI” i.e. the skull is
not actually penetrated.
• The type of trauma sustained in road accidents (e.g. blunt impact or acceleration-deceleration injuries)

usually results in diffuse brain damage with a variety of physical, behavioral and cognitive problems.

• Rehab role is critical in order to maximize QOL by improving function and participation.

• TBI follows a period of unconsciousness then combination of physical and cognitive impairments

which vary as a consequence of the severity of lesion, the nature of brain damage and medical

complications.

• Behavior, mood and personality changes after TBI have been documented and considered by many

clinicians to be the most difficult to manage effectively.

• Behavior problems ranging from minor irritability and passivity to disinhibited and psychotic behavior.

• Cognitive, behavioral and personality changes are far more frequently associated with long term

functional disability and family stress than are physical impairments.

 EPIDEM IOLOGY

A. The five most prevalent neurological conditions affecting the central nervous system. TBI is one of
them:
1. Cerebrovascular disease
2. Epilepsy
3. PD
4. Migraine
5. TBI
• Males outnumber Females by 2:1. And also suffer severe Injuries.
• Predisposing factors are DUI/Alcohol Consumption
• Mortality amongst those Hospitalized is high. Approx. 24% die and 20% survive with persistent and
severe disability.
• Surviving individuals have outcome defined by global categories listed on the 5-point GCS or the 8-point
GLASGOW OUTCOME SCALE EXTENDED (GOSE).
• Only about 20% of people with moderate to severe TBI are employed 1-year post-injury.
• Vast majority of TBI patients suffer a brief loss of consciousness (<_ 20 minutes) and post traumatic
amnesia (PTA) less than 24 hours.
 PATHOPHYSIOLOGY

TBI may occur as a result of:

1. Direct blow to the head
2. Head may be injured indirectly from an impact to other parts of the body.

• Direct injury may be BLUNT or PENETRATING.

• BLUNT or ACCELERATION-DECELARATION injuries commonly result in multiple
injuries of the body as well as widespread brain damage.
• The impact to the head may cause scalp injuries, deformation of the skull with or without
fractures, or depressed fractures which may lacerate and perforate the Dura mater and brain.
 MECHANISM OF BRAIN DAMAGE
• Mechanism is varied and complex and include both intracranial and extracranial factors.
• Intracranial are typically divided into:
1. Primary damage: in which the effects are largely immediate, and delayed. In general
primary brain damage produces an immediate effect on level of consciousness.
2. Secondary damage: that occurs sometime after the injury. Produces a late deterioration in
the level of consciousness and development of focal signs.
• Hypoxic and ischemic brain damage can be minimized by effective and early resuscitation.
• Secondary brain damage is potentially preventable or treatable. Its treatment has advanced in
the past decade.
• Extracranial brain damage are many: including fractures to the extremities, spine(w/wo/SC)
and pelvis, damage to the underlying organs, rupture of abdominal viscera and facial injuries
 PRIMARY BRAIN DAMAGE
• Primary neuropathology of TBI, occurring at the time of injury is classified as:
1. Focal (contusion, laceration and hemorrhage due to contact).
2. Diffuse (diffuse axonal injury due to acceleration/deceleration).
• Diffuse axonal injury, or microscopic damage to the neuro-filament subunits within the axonal cytoskeleton, is a
predominant feature of TBI due to MVA and other high-speed causes of injury. Diffuse axonal injury can occur in the
absence of focal injuries, mild, moderate and severe TBI, and is primarily responsible for initial loss of consciousness.
• Main regions affected are the parasagittal white matter of the cerebral cortex, corpus callosum, and the pontine-
mesencephalic junction adjacent to the superior cerebellar peduncles.
• Concussion: A clinical syndrome characterized by immediate and transient alteration in brain function, including alteration of
mental status and level of consciousness, resulting from mechanical force or trauma.
• Cerebral laceration and Contusion (or cortical bruising) occur principally at the crests of gyri and expands to variable
depths depending on the severity of the injury.
• Contusions may occur where the brain strikes the skull at the site of the externally applied force(coup) or at a point
180degree from the site of impact, where the brain strikes the skull(contra coup).
• Contusion also occurs on the under surface of the frontal lobes and at the temporal tips due to translational movements of
the brain on the bony contours of the floor of the anterior and middle cranial fossae.
• Contusion may occur in contrast to diffuse with low impact injuries such as blow to head and falls. They do not cause
LOC but are predisposing factors for seizures and may produce focal cognitive and sensorimotor impairments.
CONT…
Hemorrhage may occur in three areas of the brain:
1. Subdural hemorrhage (forceful strikes to the skull/commonly associated w/ skull fracture)
2. Epidural hemorrhage
3. Subarachnoid and intraventricular.
Laceration following penetration of the brain by a projectile or skull fragment.
The primary injury may cause a reduction of blood flow and oxygen supply to the brain, cerebral
metabolic-flow uncoupling, and impairment of cardiovascular autoregulation, leaving the brain
vulnerable to secondary damage.
 SECONDARY BRAIN DAMAGE
• Neuropathologic processes involved in secondary damage include release of excitotoxic levels
of excitatory neurotransmitters(e.g. glutamate), impaired calcium homeostasis, generation of
oxygen free radicals(e.g. superoxide) and inflammatory processes.
• The consequences of these neuropathic processes include cerebral edema, cerebral vasospasm
and hypoxia to critical reduction in cerebral blood flow, leading to ischemic death.
• Cerebral oedema is common after brain injury and is classified as:
1. Vasogenic brain edema (caused by cellular damage to the BBB. The damaged barrier
allows uncontrolled ion and protein transfer from the intravascular to the extracellular brain
components leading to water accumulation in the extracellular space)
2. Cytotoxic brain edema (intracellular water accumulation in neurons, astrocytes and
microglia. It is caused by cell membrane permeability for ions and ionic pump failure.
• Both types lead to ICP and potentially ischemic neuronal death.
CONT…
• As ICP rises cerebral blood flow falls. The relationship b/w ICP and cerebral blood flow can be
described by the following equation:
Cerebral perfusion pressure(CPP) = mean arterial BP - Intra Cranial Pressure(ICP)
• Therefore, an in ICP or BP will CPP causing ischemic damage cerebral edema.
• Treatment to ICP is recommended when it reaches 20mmHg. If ICP to 40-45mmHg it can
lead to “Foramen magnum herniation” or “Tentorial herniation”.
BEFORE TBI
AFTER TBI
 MEASURES OF SEVERITY
Indices of severity (TBI):
1. Depth of initial Coma.
2. Duration of Coma
3. Length of Post-traumatic Amnesia (PTA)
GCS is the widely used measure of severity of Coma. Injury severity is as follows:
4. Less than or equal to 8(severe)
5. Moderate 9-12
6. Mild 13-15
The commonly accepted criteria for classifying severity of trauma using the duration of coma are:
7. >6 hours for severe
8. 20 min to <6 hours moderate
9. <20min mild
PTA is the period of impaired consciousness that extends from initial injury until continuous memory for ongoing events is restored. It is
characterized by several cognitive and behavioral disturbances, including:
10. Anterograde amnesia
11. Restlessness
12. Agitation
13. Fatigue
14. Confabulation
• Duration of PTA can be measured by (MOPTAS), (GOAT) and the Westmead PTA scale.
• Commonly accepted criteria for classifying severity is: >4wks extremely severe, 1-4 wks very severe, 1-7 days severe, 1-24 hrs moderate and
<1hr mild.
RANCHO LOS AMIGOS LEVELS OF
COGNITIVE FUNCTIONING (LOCF)
 MANAGEMENT OF ACUTE TBI
• Preservation of life and prevention of secondary brain damages are first priorities in the
emergency treatment of the injured brain and multi injured individual. Improvements in acute
care management over the past 30years have contributed to a dramatic reduction in mortality.
• 1st priorities for pre-hospital staff are resuscitation, assessment of airways and prevention of
aspiration. Hypotension and hypoxemia must be avoided to minimize the risk of secondary
brain damage. GCS is also conducted to assist with categorizing the severity of injury and to
triage the patient.
• CT scan should be done immediately when patient arrives at the ED.
• Monitoring of Vitals signs and coma are performed routinely. Recommended to monitor ICP in
all patients with severe TBI and abnormal CT scan. Enables early recognition of raised ICP and
prevention of secondary brain damage.
• Any patient whose level of consciousness deteriorates should be considered to have a
hematoma and requires immediate investigation.
 1. RESPIRATORY FUNCTION
• Management of respiratory function is complex in the comatose TBI patient.
• Early control of the airway by endotracheal tube and controlled ventilation is paramount to reduce the
likelihood of hypoxemia, hypocapnia, or hypercapnia, to protect the airway from aspiration(e.g. vomitus)
and reduce ICP.
• In the TBI patient, injury can cause abnormalities or dysfunction of any or all of the mechanisms that
provide for adequate oxygenation and ventilation. E.g. lung function may be compromised by damage to
the lung or chest wall(e.g. pulmonary contusion or fractured ribs) or damage to respiratory center of the
brain.
• Brain function may be compromised if the respiratory system is damaged by changing the arterial blood
oxygen and carbon dioxide content delivered to the damaged brain tissue. This can affect cerebral auto-
regulation, alter cerebral perfusion pressure and potentially cause ischaemia.
• Patients with mild or moderate brain injuries GCS>8 having adequate arterial blood gases, no respiratory
dysfunction or signs of deterioration, are usually not ventilated but their inspired oxygen concentration is
increased since the oxygen requirements of the damaged brain are greater than the undamaged brain.
• Severe brain injured patient GCS<8, hypoventilation or apnea may be present, reflected by hypercapnia
(PaCO2 >45mmHg) and severe hypoxemia(PaCO2<60mmHg). Requires immediate intubation,
oxygenation and ventilator support.
CONT…
• Pulmonary complications(e.g. pneumonia, atelectasis, adult respiratory distress syndrome) are the most
frequent medical complication associated with TBI, dramatically contributing to mortality.
• Major aims of Pulmonary physiotherapy intervention as part of the team involved in the initial
management of the person with TBI are to:
1. Improve respiratory function.
2. Prevent respiratory complications and secondary brain damage.
3. Ensuring adequate ventilation.
4. Clearing of excessive secretions.
Major respiratory problems amenable to intervention are hypoventilation, impaired mucociliary clearance,
hyperventilation and ventilation/perfusion mismatch.
PT management(positioning, percussion, manual hyperinflation and suctioning can affect intracranial
variables(ICP and Mean arterial pressure) with adverse events more likely to occur when these variables are
not normal.
Benefits and risks of intervention need to be carefully weighed, intracranial variables(ICP and CPP) closely
monitored and intervention modified or shortened according to need. E.g. postural drainage CI in
Trendelenburg due to Increase in ICP
Secondly prevention of muscle and soft tissue contractures in order to maintain MSK integrity.
 2. MUSCULOSKELETAL INTEGRITY
• Impaired motor control and coma effectively immobilize the individual following TBI, who is
then vulnerable to MSK disorders associated with bed rest, reduce physical activity and disuse.
• These conditions are likely to impede rehab. By interfering with active and intense training
designed to improve motor performance.
• Immobilization induces both muscle atrophy and impairment of contraction. Muscle tissue
responds selectively and differentially to demands placed on it, altering it structure(length,
volume, cross sectional area).
• Demineralization of skeleton due to decrease or no load on the muscles and bones.
• Soft tissue contractures are common following TBI, prevalence of 11-81%.
• Muscles at particular risk of shortening due to effects of position and immobilization include
hip and knee flexors, ankle plantarflexors and inverters, shoulder adductors and internal
rotators, elbow flexors, forearm pronators, wrist and finger flexors, thumb flexors and
adductors or any other muscles held persistently at short length.
 CONT…
• Main aim of physiotherapy management in preserving MSK integrity in people with TBI is to
prevent or minimize adaptive changes in soft tissue, in particular to prevent muscle shortening
and increased stiffness by:
1. Applying passive stretch to the at-risk muscles and soft tissues
2. Loading bone and cartilage
3. Task related training that involves active stretching during the lengthening phase of actions.
• Passive stretch used clinically to prevent (or treat) contractures. PROM performed vigorously
will lead to increase in hyperreflexia.
• Passive stretch can be applied for longer periods of time by positioning and using equipment. For
e.g. the calf muscles can be stretched with the support of a tilt table with a wedge placed under
the feet to maximize the stretch. This standing also loads the bones and cartilage of the lower
limbs , providing a weight bearing stimulus to maintain bone mineral density.
• In the first days post injury, the comatose patient can be positioned in side lying or semi prone to help
prevent contractures development.
• A pillow is placed between the slightly flexed legs to prevent the hips from adducting.
• The upper limb may be positioned on a pillow with the shoulder girdle protracted and the elbow extended.
• Inflatable plastic blow up splints or foam splints may be useful in maintaining position.
• As soon as vital signs are stable, in particular blood pressure and ICP, periods of sitting and standing if
necessary with external constraints are instituted.
• The use of serial casting has been found to be effective in both preventing and correcting contractures in
people with TBI.
• Applying casts with muscles in a lengthened or a neutral position stretches the connective tissue elements
and provide a stimulus for the muscle to add sarcomeres to the muscle fiber as reported in animal studies.
• Casting has been more successful when done immediately for patients at risk of developing contractures
then waiting for contractures to occur.
• Casts are applied with minimum padding in order to prevent movement and ensure a sustained stretch.
• When casting a two-joint muscle, a lengthened position is more easily achieved if the cast is applied while
the muscle is not lengthened over the other joint. Circulation monitoring is initiated as soon as casts are
applied. Casts need to be replaced/changed regularly to examine the condition of the skin.
• Regularly changing casts also leads to determine the ROM of joints ensuring that muscle shortening in fact
is being prevented/corrected.
ALTERED LEVELS OF CONSCIOUSNESS
• There are three main disorders of consciousness after TBI.
• Coma is a state of unconsciousness in which there is neither arousal nor awareness.
• Eyes remain closed and there is an absence of sleep/wake cycles. There is no motor response to
command and no speech.
• Coma exists in the early period after injury and usually lasts no longer than 3-4 weeks.
• Vegetative state describes a condition in which the patient demonstrates no signs of cognition
but may return to wakefulness with the eyes open in response to verbal stimuli. The patient is
unable to engage in verbal interaction or produce organized, discrete motor responses. The
patient appears to be “awake but not aware”.
• Minimally conscious state has recently been defined as “a condition of severely altered
consciousness in which minimal but definite behavioral evidence of self or environmental
awareness is demonstrated.
RECOVERY FROM COMA
• Recovery from coma manifests itself with periods of opening of the eyes.
• The minimally conscious state may follow the period of coma.
• During this phase the person with TBI starts to inconsistently demonstrate conscious awareness
of self or their environment.
• Aspen Neurobehavioral Conference Workgroup outlined 4 criteria that characterize entry into
the minimally conscious state. At least one of these criteria needed to be observed:
1. Following simple instructions
2. Gestural or verbal yes/no responses
3. Intelligible verbalizations
4. Purposeful movements or affective behaviors that are contingent on relevant environmental
stimuli(e.g. appropriate smiling or reaching to grasp an object)
• The reestablishment of unassisted breathing, swallowing, effective coughing and
communication through facial expression, gesture and language is essential if the patient is to
resume more normal function.
• Options to augment communication include eye gaze, facial expression, gesture and
communication boards with letters, symbols or pictures.
REHABILITATION AND OVERALL VIEW
1. COGNITIVE AND BEHAVIORAL IMPAIRMENTS

• It has long been realized that it is the cognitive impairments and changes in personality and behavior that have
the most profound consequences in terms of rehabilitation and social reintegration.
• COGNITION: impairments are widely reported, the most common being disorders of learning and memory,
the rate of information processing and attention, and executive function. These are evident early after
moderate to extremely severe TBI and are still present after 5-10 years post injury. Memory has several
components, including working memory, immediate memory(verbal and visual memory), learning rate, use of
semantic knowledge, forgetting rate, sensitivity to interference, retrograde amnesia and prospective memory.
• Memory aids and strategies can also be used by the individual with TBI to cope with everyday life.
• Attention impairments can include difficulty in selectively directing attention to task at hand, in dividing
attention b/w tasks, in sustaining attention over time and overall attention capacity. Task related training is
possible in the presence of attention deficits and slowed processing speeds. Training interesting tasks that are
relevant to the individuals, using clear visual or auditory cues and feedback, and modifying the environment in
order to remove distractions.
• Behavior: impaired regulation of mood and behavior is evident after TBI, and it is
increasingly understood that disorganized behavior seen after frontal lobe damage is related
to impairments in the cognitive domain.
• Behaviors can be broadly classified as impaired drive or dyscontrol.
1. Behaviors allied with impaired drive or arousal include reduced initiation, apathy, loss of
interest, lethargy, slowness, inattentiveness, reduced spontaneity, unconcern, lack of
emotional reactivity, and dullness.
2. Behaviors related to dyscontrol include disinhibition, impulsiveness, lability, reduced
anger control, aggressiveness, sexual acting out, perseveration and generally poor social
judgment.
Rehabilitation for people with TBI with challenging behaviors does not involve the “piecemeal
reductions of behaviors considered unacceptable by others, but rather a comprehensive lifestyle
change, including construction of a meaningful role of personal values”
GOALS OF TREATMENT FOR BEHAVIOR
 2. COMMUNICATION
• Impaired communication is a consequence of TBI.
• Adequate speech is often present but language may be ineffective at a conversation level.
• Individuals with TBI frequently talk better than they communicate.
• Strategies are being developed for optimizing language and communication that involve
training the communication partners of TBI patients and social skills training for the individual.
• Other ways of encouraging communication are summarized:
 3. TASK RELATED TRAINING
• In TBI there may be weakness, loss of coordination, hyperreflexia, rigidity, cerebellar ataxia, tremor,
dyskinesia and sensory loss.
• The physiotherapist needs an understanding of the pathophysiology of the primary sensorimotor
impairments and the adaptations or compensations that emerge as the patient attempts to perform
everyday actions. Major role of PT is to train the individual to perform everyday actions more
effectively, including sitting and standing balance, reaching and manipulation tasks, walking, stair
climbing and running.
• PT evaluation primarily involves observation and analysis of the effects of sensorimotor impairments.
• Information is also gathered about the individuals communication, cognitive and behavioral
impairments and any other relevant information.
• Emphasis should be placed on real world tasks as assessed on the MAS.
4. CARDIORESPIRATORY CONDITIONING
• Etiology of cardiorespiratory deconditioning after TBI is multifactorial with both central and
peripheral adaptations occurring due to initial brain damage, trauma and prolonged and
extreme physical inactivity.
• The consequences of deconditioning and physical inactivity may include increased physical
fatigue, participation restriction in pre-injury work and leisure activities, changes in body
composition and an increased risk of comorbid conditions such as DM and HD.
• Conditioning programs are prescribed to increase physical activity and combat
cardiorespiratory deconditioning.
• The ACSM has developed specific guidelines for implementing a conditioning program for
people with brain injury, however yet to be validated. These guidelines recommend aerobic
exercises three to five times a week at an intensity of 40 to 70% VO2 peak or 13/20 RPE and a
duration of 20-60min using appropriate mode.
• Types of conditioning programs in individuals with TBI include circuit training classes,
individual utilizing gymnasium equipment, aquatic exercise classes, functional retraining
and home based and fitness center based exercise programs
Potential benefits of Exercise program include
Physiotherapy should be biased towards functional performance of concrete tasks with enjoyable activities
and repetitive exercises.
THANK YOU