Traumatic Brain Injury (TBI)
Acquired Brain Injury (ABI) vs. Traumatic Brain Injury (TBI)
Acquired Brain Injury (ABI):
Umbrella term for any brain damage after birth.
Causes include stroke, cerebral aneurysm (subarachnoid or intracranial hemorrhage), arteriovenous malformations, brain surgery, infections (brain abscess, meningitis, encephalitis), brain tumors (causing mass effect, pressure, swelling, oedema, inflammatory reactions).
Also caused by alcohol/drug use or hypoxia (oxygen deprivation).
The tumor causes mass effect (brain being pushed to the side), swelling and oedema which leads to chemical inflammatory pathways and reactions at the neurons.
Traumatic Brain Injury (TBI):
A type of ABI caused by mechanical injury to the head (object striking, violent stop).
Definition: Alteration in brain function or other evidence of brain pathology caused by an external force.
Definition of Traumatic Brain Injury (TBI)
Alteration in brain function includes one or more of the following:
Period of loss of consciousness or decreased level of consciousness.
Loss of memory immediately before or after the injury (post-traumatic amnesia).
Neurological deficits.
Alteration in mental state at the time of injury.
Other evidence of brain pathology:
Neuroradiologic or laboratory tests confirming damage.
Caused by an external force:
Head striking an object (wall, ground).
Rapid acceleration/deceleration without direct external trauma (brain hitting the skull's interior, shearing forces).
Head struck by an object (punch, sports ball).
Foreign object penetrating the skull (bullet, shrapnel).
Forces from blast or explosion.
Epidemiology of TBI
Major causes: unintentional accidents or events.
Transport accidents and falls are most common (1/3 to 1/2 of incidents).
Motor vehicle accidents: major cause of severe TBIs.
Incidence peaks:
Younger males (15-24 years): motor vehicle accidents, risk-taking behavior, sports-related incidents.
Older adults (75+ years): falls, possibly driving accidents.
Greater incidence overall in males vs. females.
High risk in very young (0-4 years): playing, falls, other hazards.
Head injury is a disease of men between the ages of 15 and 24, and then there's another upwards tilt as people get older and sometimes they tend to fall more frequently.
Severity of TBI
Classified as mild (concussion), moderate, or severe.
Diagnosed by:
Clinical symptoms.
Duration of loss of consciousness.
Depth of coma (Glasgow Coma Scale).
Duration of post-traumatic amnesia (PTA).
Brain imaging results.
Mild TBI (Concussion):
Brief loss of consciousness (seconds or minutes).
Post-traumatic amnesia (PTA) less than 1 hour (if present).
Normal brain imaging results (CT, MRI not sensitive enough).
Moderate TBI:
Loss of consciousness for 1-24 hours.
Post-traumatic amnesia (PTA) for 1-24 hours.
Abnormal brain imaging results (CT, MRI).
Severe TBI:
Loss of consciousness/coma for more than 24 hours.
Post-traumatic amnesia (PTA) for more than 24 hours.
Abnormal brain imaging results.
Mild TBI/Concussion
Causes short-lived neurological impairment.
Repeated concussions can have cumulative effects.
Symptoms should resolve without medical intervention.
Treatment: rest, gradual return to activity.
Community concussion guidelines exist for sports.
Pathophysiology of TBI
Extracranial Mechanisms:
Occur outside the brain/skull, causing damage.
Examples: insufficient oxygen (lung pathology), insufficient blood flow.
Intracranial Mechanisms:
Divided into primary and secondary brain damage.
Primary Brain Damage:
Localized damage at the time of injury (direct consequence of trauma).
Types: Closed/blunt injury and open/penetrating head injuries.
Closed/Blunt Head Injury:
Acceleration/deceleration injury.
Brain hits the skull, shearing/rotational forces damage tissues.
Membrane remains intact, even with skull fracture.
Causes: motor vehicle accidents, falls, sporting injuries, assaults.
Can occur with or without impact to the head.
Open/Penetrating Brain Injury:
Skull and membrane disrupted, exposing the brain.
Increases risk of infection.
Rare (2% of all TBIs).
Focal vs. Diffuse Axonal Injury:
Focal Injury: Localized tissue damage.
Lacerations, contusions/bruising.
Hemorrhages/hematomas.
The inside of the skull has ridges and sharp edges that can damage the brain if it moves around too much inside the skull.
The dura mater also has edges or folds, including the tentorium cerebelli, which the hemispheres then sit on top of. It also has to have an edge where the brain stem goes down into the spinal cord.
Diffuse Axonal Injury: Widespread damage from rotational/shearing forces.
Bending/stretching of nerve axons.
Common in high-speed accidents.
May occur without focal injuries.
Associated with long-term disability.
Initial scans may show little, but brain shrinking occurs over time.
Prevalent in cortical white matter, corpus callosum, junction of pons and midbrain.
Cranial nerve damage (I, VII, III) can occur due to strain.
Secondary Brain Damage:
Damage that occurs after the initial injury.
Potentially preventable.
Consequences of edema/hypoxia following trauma.
Cellular, chemical, tissue, and blood vessel changes contribute to further destruction.
Types and extent depend on the primary injury.
Intracranial Mechanisms of Damage
Hematomas:
Massive bleeding in/around the brain after damage to major blood vessels.
Blood accumulates, pressing on the brain (mass effect).
Can cause shifting of internal structures, damage to the brain stem, increased intracranial pressure.
Often require emergency surgery.
Subdural Hematoma:
Between dura and brain surface.
Rupture of small veins causes slow bleeding and accumulation.
Symptoms may appear hours to weeks later.
Epidural Hematoma:
Between skull and dura.
Associated with skull fractures that damage an artery.
Rapid bleeding, requires emergency surgery.
Intracerebral Hematoma:
Small blood vessels within the brain rupture and bleed into the tissue itself.
Effect depends on location and volume.
Often associated with contusions.
Diffuse Axonal Injury (DAI):
Created by rotational and shearing forces; common in car accidents.
Can occur in the absence of focal injuries or with them.
More closely associated with long-term disability than contusions/hemorrhages.
Microscopic damage; initial scans may not show much, but shrinkage can occur over time as damaged nerves die off.
Most prevalent where long fiber tracts are prone to twisting/tearing (cortical white matter, corpus callosum, junction of pons and midbrain).
Cranial nerve damage can occur (I, VII, III).
Secondary Brain Damage
Occurs after the injury, not a direct result of trauma.
Potentially preventable.
Complex cascades of chemical and cellular changes initiated within the contusion and surrounding brain tissue.
Can persist for days to years, contributing to poor outcomes.
May relate to brain swelling/edema and chemical changes due to damaged neurons.
Brain tissue swells as part of the inflammatory process.
Craniectomy (bone flap removal) sometimes performed to decrease intracranial pressure.
Brain Herniation:
Intracranial pressure normally 5-15 mmHg; herniation can occur around 40-45 mmHg.
Subfalcine, transtentorial, or tonsillar herniation (coning).
Intracranial pressure is measured by drilling a bur hole into the skull and attaching a monitor, but they also have another method now by which they put in a shunt or a tube to measure the pressure. Not only can they monitor the pressure, but they can also release fluid and try to decrease the pressure.
Disruption of the blood-brain barrier and effect on microglia can occur.
Some secondary changes last for 12+ months.
Altered Level of Consciousness
Three main types: coma, vegetative state, minimally conscious state.
Coma:
Not obeying commands, not uttering words, and not opening eyes.
Eyes remain closed, no normal sleep-wake cycles.
Lasts 2-4 weeks.
Glasgow Coma Scale score less than 8.
Vegetative State:
No signs of cognition; awake but not aware.
Eyes are open, but not looking and paying attention or responding.
If persists for more than 12 months after traumatic brain injury, it is considered permanent.
Minimally Conscious State:
More than one sign of awareness.
Often emerges from coma or vegetative state.
Glasgow Coma Scale (GCS)
Three components: eye opening, verbal response, motor response.
Highest score: 15 (spontaneous eye opening, normal conversation, normal motor response).
GCS Scale:
Eye Opening:
4 - Spontaneous
3 - To speech
2 - To pain
1 - No response
Verbal Response
5 - Orientated
4 - Confused
3 - Words
2 - Sounds
1 - None
Motor Response
6 - Obeys commands
5 - Localizes to pain
4 - Withdraws to pain
3 - Abnormal Flexion
2 - Extension
1 - None
Localizes to pain: attempts to remove painful stimulus.
Withdraws to pain: stereotype response to pain.
Decorticate posture: flexion of arms and extension of legs.
Decerebrate posture: extension of arms and legs (more severe).
Injury classification based on GCS:
Mild: 13-15.
Moderate: 9-12.
Severe: less than or equal to 8.
Clinical Assessment of Consciousness
Steps involve: Check, Observe, Stimulate, and Rate.
Local factors could cause a lack of capacity to respond.
The patient is rated in each component by matching findings with the corresponding criterion.
There are four criteria for eyes, five for verbal, and six for motor score.
For eye opening:
verbal stimulus is used by introducing yourself clearly and requesting eye opening, if necessary by shouting.
Physical peripheral stimulus is then applied by pressing on the nail tip and is applied with increasing intensity for up to ten seconds until the patient demonstrates a response or until maximum stimulus has been applied.
Verbal response, ask the patient to tell you their name, where they are, and what month it is.
Motor assessment uses central stimulus which may be first applied by the trapezius pinch.
Second location for central stimulus is the supraorbital notch.
If different responses are exhibited between limbs, right and left sides, recall the better side response as the best index of overall responsiveness.
Westmead Post-Traumatic Amnesia (PTA) Scale
Requires daily testing at the same time with the same examiner.
Total of 12 points.
Seven questions.
Remembering face/name of examiner (2 points).
Remembering three standard pictures.
Scoring: Green person (12/12 three days in a row) is out of PTA; a person with four out of twelve will be judged as still being in post traumatic amnesia.
Top score on three consecutive days = out of PTA.
Likely implemented by occupational therapists, nurses, or doctors.
Prognosis of TBI
Main determinant of survival: time to arrive at the emergency department.
Tools to predict the outcome after surviving:
Glasgow Coma Scale.
Post-traumatic amnesia (PTA).
Longer PTA = poorer outcome.
Other factors:
Younger age = better outcome (more neuroplastic potential).
Good cognitive reserve = better outcome.
Females may do better than males (hormonally related, oestrogen as protective).
Strong family/friend support = better outcome.
Recovery is generally slow; most improvements in the first six months, but can improve over years.
Relationship of PTA duration to outcomes:
PTA 1 day or less: quick and full recovery.
PTA 1 day - 1 week: prolonged recovery (weeks/months), full recovery possible.
PTA 1-2 weeks: recovery over many months, residual problems may remain.
PTA 2-4 weeks: prolonged recovery (1+ year), permanent deficits likely.
PTA more than 4 weeks: permanent deficits, significant disability; focus on long-term strategies.
Acute Management of TBI
Respiratory Function:
Improve respiratory function and prevent complications (secondary brain damage).
Comatose patients often put on controlled ventilation.
Hypoxemia and intracranial pressure must be carefully monitored.
Some interventions may be contraindicated (suctioning, coughing).
Managing Intracranial Pressure:
Medical interventions include mannitol (diuretic) and hypertonic saline.
Pressure Care:
Regular turning and skin inspection to prevent pressure areas.
Positioning:
Minimize contracture, foot drop, support injuries, consider respiratory function.
Sensory Stimulation:
Patients may respond to touch/voice, but can't filter information.
Intensive care units are brightly lit and noisy.
May need graduated controlled sensory stimulation.
Musculoskeletal Integrity:
Minimize soft tissue changes from immobilization.
Passive range of motion, stretching, and positioning.
Load bone and cartilage as possible.
Task-related training (if awake/alert enough).
Anti-gravity positions (sitting on the edge of bed or tilt tabling).
Early use of standing patients on tilt tables can be used to try and get a little bit of loading down through their joints, as well as start to adjust the body hemodynamically to being upright again.
Recovery From Coma
Minimally Conscious State: Re-establishing swallowing (speech pathology), weaning off ventilators, developing effective coughing/breathing techniques.
*Focus on communication and establishing means of effective communication (verbal/non-verbal).
Management of Patients in Post-Traumatic Amnesia (PTA)
Confused state with limited ability to take on new information.
Short attention span, easily distractible, restless/fidgety.
Fatigue easily (cognitively and physically).
Easily overstimulated and possibly can't filter information.
Possible agitation, irritability, aggression, perseveration, disinhibition.
May exhibit psychotic behavior.
The patient will not know they are doing any of this or remember this behavior once they are out of PTA
Strategies:
Quiet, consistent environment (low stimulation room).
Remove distractions and triggers for aggression.
Team meetings to discuss contributing factors and behavioral issues.
Behavioral diary to track behaviors and links to triggers.
Minimize active therapy and focus on whole tasks (getting out of bed, walking, dressing).
Concrete goals reinforced daily.
Minimize talking/instructions and hands-on contact.
Demonstrate rather than explain.
Short sessions.
Avoid sensory overstimulation (light, noise, visitors).
Consistent therapist.
Familiar cues/prompts.
Screens/separate rooms as needed.
Rehabilitation Stage
Cognition and behaviour are biggest considerations.
Cognitive deficits can be variable:
Disordered learning and memory (most TBI patients have memory problems).
Slow information processing.
Poor executive functioning (planning, decision-making, problem-solving, attention, inhibiting inappropriate responses).
Assisting with Cognitive Issues
Environmental supports and reminders (written worksheets, photos, videos).
Clear cues and concise instructions.
Clear, concise feedback and concrete goals.
Memory aids and strategies (writing things down, lists, sticky notes, diaries, phone reminders, routine).
Dual-task practice (if functional and automatic).
Behavioural Issues
Impaired drive (dissociation between knowing and doing).
Lack of initiation, apathy, loss of interest, lethargy, slowness, unconcern, lack of spontaneity.
Discontrol/disinhibition, impulsiveness, lability, reduced anger control, aggressiveness, sexual acting out, perseveration, poor social judgment.
Strategies for Behavioural Issues
Simple environment (treat in-room).
Clearly specified and agreed-upon treatment goals and schedules (written and on display).
Consistent treatment approach across the rehab team.
Know and avoid trigger situations (overstimulation, lack of control, confusion, cognitive challenges).
Consider lack of quality sleep, pain, infection, temperature, the need to toilet.
Use prompts, visual reminders, clear communication.
Behavior modification program (neuropsychologist).
Physiotherapy Role
Assessment and treatment of motor deficits.
Sensorimotor impairments are highly variable; not always unilateral.
Thorough assessment is needed (may be split over multiple sessions due to cognition/fatigue/behavior).
Impairments
Negative Features:
Loss of strength and joint range of movement.
Changes in muscle/soft tissue length.
Loss of dexterity and coordination, ataxia, poor balance, vestibular dysfunction.
Sensory loss, visual changes, fatigue (cognitive/motor).
Positive Features:
Spasticity is quite common.
Hypertonus.
Concurrent injuries are common (fractures, spinal/abdominal injuries).
Surgical procedures for repair.
Pain is common and needs to be managed.
Clinical Reasoning
Similar processes but with more components to consider.
Therapy principles still follow RAMP (repetition, amount, intensity, specificity) with a focus on impairments and task-related training.
Greater focus at the impairment level than other neurological conditions.
Co-related MSK and trauma issues are prevalent.
Task-related training uses neuroplasticity and motor learning principles.
Younger patients = focus on higher-level activities (return to running/sport/work).
Cognitive and Behavioural Impairments
Incorporate management into physiotherapy.
Addressing cognitive abilities and vision for community navigation.
Task modification to enable success.
Specific feedback given on biomechanical features.
Consistent cues, session to session and task to task.
Clear, meaningful goals.
Simple and not overwhelming feedback.
Slow things down and pause before speaking.
Allow time to process information.
Give the person a sense of control.
No specific therapy modalities for TBI compared to other neurological conditions, but maybe more emphasis on the need for MSK techniques and even cardiorespiratory approaches.
Any of the therapy modalities may be appropriate to the specific patient, depending on their impairments, activity and participation limitations and restriction, as well as their goals.
Fitness Training
Deconditioning is a significant problem.
Fitness training is often well accepted, especially in younger patients.
Problems pushing heart rates up sufficiently for training effect.
Careful monitoring and consideration of medical advice.
Multidisciplinary Team
Speech, language, communication deficits.
Swallowing deficits.
Hearing loss.
Bladder and bowel issues.
Multidisciplinary team is vital (different disciplines addressing the person with the TBI's component deficits and needs).
Evidence for Physiotherapy Management
Fewer well-developed clinical guidelines due to heterogeneity and smaller numbers.
Refer to Scottish Intercollegiate Guidelines Network (SIGN) Guidelines for Brain Injury Rehabilitation in Adults (2013).
SIGN Guidelines:
Repetitive task-oriented activities for improving functional activity.
Casts, splints, passive stretching for contractures/deformities.
Botulinum toxin therapy for focal spasticity.
Canadian Guidelines (2016):
Service requirements (multidisciplinary team).
Behaviour management, cognitive management, communication strategies.
ADL retraining and return to vocational activities.
Recreational and leisure activities.
Controlled stimulation with a graded sensory approach for managing hypersensitivity, fatigue and overstimulation.
Education to patients, families, and carers, and the incorporation of self-management.
Greater tolerance to sitting and standing
*Incorporation of self management as well as the use of many of the therapy modalities.
Individual research articles and systematic reviews otherwise provide additional evidence.