Traumatic Brain Injury (TBI)

Acquired Brain Injury (ABI) vs. Traumatic Brain Injury (TBI)

• Acquired Brain Injury (ABI):
  • Umbrella term for any brain damage occurring after birth.
  • Causes include:
    • Stroke
    • Cerebral aneurysm (subarachnoid or intracranial hemorrhage)
    • Arteriovenous malformations
    • Brain surgery
    • Infections (brain abscess, meningitis, encephalitis)
    • Space-occupying lesions (brain tumors) - Mass effect: Brain is pushed to the side causing pressure and swelling, leading to inflammatory reactions at the neurons.
    • Alcohol and drug use
    • Hypoxia (oxygen deprivation)
• Traumatic Brain Injury (TBI):
  • A type of ABI caused by a mechanical injury to the head. External force.

Definition of Traumatic Brain Injury (TBI)

• Alteration in brain function or evidence of brain pathology caused by an external force.
• Alteration in brain function includes one of the following:
  • Loss of consciousness or decreased level of consciousness.
  • Loss of memory from immediately before or after the injury (post-traumatic amnesia).
  • Neurological deficits.
  • Alteration in mental state at the time of injury.
• Evidence of brain pathology:
  • Neuroradiologic or laboratory tests confirming damage.
• External force events:
  • Head striking an object (wall, ground, car).
  • Rapid acceleration/deceleration movements of the brain within the skull.
    • Brain hits the skull's front or back.
    • Shearing forces and rubbing against the skull's inner surface.
  • Head struck by an object (punch, ball).
  • Foreign object penetrating the skull (bullet, shrapnel).
  • Forces generated from events like blasts or explosions.

Epidemiology of TBI

• Major causes are unintentional accidents.
• Transport-related accidents and falls are the most common causes.
• Motor vehicle accidents are a major cause of severe TBIs.
• Incidence by Age and Gender:
  • Younger males (15-24 years): Motor vehicle accidents, risk-taking behavior, sports-related incidents.
  • Older adults (75+ years): Falls, driving accidents.
  • Greater incidence overall in males compared to females.
  • Very young (0-4 years): Playing and related incidents (falls, hazards).

Severity of TBI

• Classified as mild (concussion), moderate, or severe.
• Traditionally diagnosed by:
  • Clinical symptoms.
  • Duration of loss of consciousness.
  • Depth of coma using scales like the Glasgow Coma Scale (GCS).
  • Duration of post-traumatic amnesia (PTA).
  • Brain imaging results.
• Mild TBI (Concussion):
  • Brief loss of consciousness (seconds or minutes).
  • Post-traumatic amnesia (PTA) for less than one hour (if present).
  • Normal brain imaging results (CT, MRI may not detect microscopic damage).
• Moderate TBI:
  • Loss of consciousness for 1-24 hours.
  • Post-traumatic amnesia (PTA) for 1-24 hours.
  • Abnormal brain imaging results (CT or MRI).
• Severe TBI:
  • Loss of consciousness/coma for more than 24 hours.
  • Post-traumatic amnesia (PTA) for greater than 24 hours.
  • Abnormal brain imaging results.

Mild TBI/Concussion Details

• Causes short-lived neurological impairment.
• Repeated concussions can have cumulative effects.
• Symptoms should resolve without medical intervention.
• Treatment: Rest and gradual return to activity.
• Community concussion guidelines should be followed, especially in sports.

Pathophysiology of TBI

• Extracranial Mechanisms: Factors outside the brain that can cause damage.
  • Insufficient oxygen (hypoxia) due to lung pathology.
  • Insufficient blood flow.
• Intracranial Mechanisms: Divided into primary and secondary brain damage.
  • Primary Brain Damage: Localized damage at the time of injury.
    • Closed/Blunt Injury:
      • Acceleration/deceleration injury (brain hits skull).
      • Shearing and rotational forces that damage tissues.
      • Membrane remains intact even if skull is fractured.
      • Causes: Motor vehicle accidents, falls, sporting injuries, assaults.
    • Open/Penetrating Head Injury:
      • Skull and membrane disrupted, exposing the brain to the environment.
      • Increases risk of infection.
      • Relatively rare (2% of TBIs).
  • Secondary Brain Damage: Damage that occurs after the initial injury (potentially preventable).
    • Consequences of edema or hypoxia.
    • Cellular, chemical, tissue, and blood vessel changes that contribute to further brain tissue destruction.
    • Types and extent depend on primary injury severity.

Intracranial Mechanisms in Detail

• Primary Brain Damage:
  • Focal Injury: Localized tissue damage.
    • Lacerations, contusions (bruising).
    • Hemorrhages or hematomas.
    • Brain is prone to damage from bony landmarks inside the skull.
    • Dura mater (outermost meningeal layer) has edges and folds that can cause damage.
  • Hematomas: Massive bleeding in or around the brain.
    • Blood accumulates and presses on the brain, causing further damage.
    • Severe compression can shift internal brain structures (mass effect).
    • Can raise intracranial pressure.
    • Often require emergency surgery.
      • Subdural Hematoma: Between dura and brain surface; rupture of small veins; slow bleeding.
      • Epidural Hematoma: Between skull and dura; associated with skull fractures damaging an artery; rapid bleeding.
      • Intracerebral Hematoma: Small blood vessels within the brain rupture and bleed into the tissue.
  • Diffuse Axonal Injury (DAI):
    • Widespread damage due to rotational and shearing forces.
    • Common in high-speed injuries like car accidents.
    • Can occur without focal injuries.
    • More closely associated with long-term disability.
    • Microscopic damage may not be initially visible on scans.
    • Over time, brain shrinking may be seen on imaging as damaged nerves die off.
    • Most prevalent in cortical white matter, corpus callosum, and junction of the pons and midbrain.
    • Cranial nerve damage (I, VII, III) can occur due to strain on the nerves.

Secondary Brain Damage Details

• Occurs after the initial trauma and is not a direct result of the trauma itself.
• Potentially preventable.
• Complex cascades of chemical and cellular changes are initiated, leading to ongoing damage.
• Can persist for days to years.
• May relate to brain swelling/edema and chemical changes due to damaged neurons leaking substances.
• Brain tissue swells as part of the inflammatory process.
• Craniectomy: Bone flap removed to decrease intracranial pressure (ICP).
• Brain Herniation: Occurs if ICP gets too high.
  • Normal ICP: 5-15 mmHg.
  • Herniation occurs around 40-45 mmHg.
    • Subfalcine herniation.
    • Transtentorial herniation.
    • Tonsillar herniation (coning): Brainstem pushed down through foramen magnum.
• Intracranial Pressure (ICP) Monitoring:
  • Burr hole with monitor.
  • Shunt/tube to measure and release fluid.
• Disruption of blood-brain barrier and effects on microglia.

Altered Level of Consciousness

• Coma:
  • Not obeying commands, not uttering words, not opening eyes.
  • Eyes remain closed, no normal sleep-wake cycles.
  • Usually lasts 2-4 weeks.
  • Glasgow Coma Scale (GCS) score < 8.
• Vegetative State:
  • No signs of cognition; awake but not aware.
  • Eyes open but not focusing or responding.
  • If persists >12 months after TBI, considered permanent.
• Minimally Conscious State:
  • More than one sign of awareness.
  • Often a transition state emerging 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).
• Motor Response:
  • Localizes to pain: Attempts to remove painful stimulus.
  • Withdraws to pain: Generalized withdrawal from pain.
  • Decorticate posture: Flexion of arms and extension of legs.
  • Decerebrate posture: Extension of arms and extension of legs (more severe).
• Injury Classification (based on GCS score):
  • Mild: 13-15
  • Moderate: 9-12
  • Severe: <=8

Glasgow Coma Scale - Assessment (4 Steps)

1. Check: Identify any factors that might interfere with the assessment (e.g. local injuries). Observe the patient for spontaneous eye opening, speech, and movement. Observe: for spontaneous behaviours. 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 each component, the top criterion is a normal response, whilst the lowest criterion is no response.
2. Stimulate: If necessary, stimulate the patient, first verbally and then physically. Verbal stimuli is used by introducing yourself clearly and requesting eye opening, if necessary by shouting. If the patient opens their eyes to sound is recorded. If the patient does not open their eyes when you speak to them, a physical peripheral stimulus is then applied
3. Stimulation starts at a low level 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.If the patient opens their eyes record to pressure. If they do not open their eyes record as none.
4. Assess the verbal response: ask the patient to tell you their name, where they are, and what month it is. If they answer correctly, record Orientated. If during conversation the patient is able to speak in phrases or sentences but is unable to give the correct answers to these questions about orientation, record Confused. If they do not talk sensibly, but are to single words, record words. If the patient moans and groans with no recognizable words, record sounds. If the patient makes no sounds at all, then record None. speechlessness may result from factors other than depressed consciousness; presence of an endotracheal tube. In these cases, record Verbal not testable
5. Assess the motor component of the coma scale first ask the patient to perform a two step action by asking them to grasp and release your fingers with their hand or opening their mouth and sticking out their tongue. If the patient does this record obey commands. If the person can't move their arms, for example because of a spinal injury, you should ask them to open their mouth and stick out their tongue.A peripheral stimulus alone is inadequate to assess the motor component of the coma scale and an additional central stimulus is needed.

Post-Traumatic Amnesia (PTA) - Westmead PTA Scale

• Developed at Westmead Hospital in Sydney.
• Requires daily testing (12 points total).
• Same time and examiner each day.
• Seven questions.
• Remembering examiner's face and first name (2 points).
• Remembering three standard pictures.
• Scoring: 12/12 for three consecutive days = out of PTA.

Prognosis of TBI

• Main determinant of survival: Time to arrival at the emergency department.
• Predicting Outcome: Glasgow Coma Scale (GCS) and Post-Traumatic Amnesia (PTA).
• Longer PTA = poorer outcome.
• Other Factors:
  • Younger age = better outcome.
  • Cognitive reserves = better outcome.
  • Females may do better than males (hormonally related).
  • Family and friend support = better outcome.
  • Recovery is generally slow (up to six months for main improvements, but can continue for years).

Duration of PTA and Likely Outcomes

• PTA <= 1 day: Quick and full recovery possible.
• PTA 1 day - 1 week: Recovery prolonged (weeks/months), but full recovery possible with good management.
• PTA 1-2 weeks: Recovery over many months; may have residual problems but optimism for functional recovery.
• PTA 2-4 weeks: Very prolonged recovery (one year or more); permanent deficits likely, less chance of full functional recovery.
• PTA > 4 weeks: Permanent deficits, significant disability; focus shifts to long-term strategies and compensation.

Acute Management of TBI

• Respiratory Function: Improve oxygenation to prevent secondary brain damage.
  • Comatose patients often require controlled ventilation.
  • Some interventions may be contraindicated (suctioning, coughing) due to increased ICP.
• Managing Intracranial Pressure (ICP):
  • Medical interventions: Mannitol (diuretic), hypertonic saline (osmotic effect).
• Pressure Care:
  • Regular turning and skin inspection to prevent pressure areas.
• Positioning:
  • Minimize contractures, foot drop, and support injuries.
  • Consider respiratory function.
• Sensory Stimulation:
  • Patients may respond to touch and voice, even if unconscious.
  • ICUs are brightly lit and noisy, which can be unpleasant.
  • Graduated, controlled sensory stimulation may be needed.
• Musculoskeletal Integrity:
  • Minimize soft tissue changes due to immobilization.
  • Passive range of movement, passive stretching, and positioning.
  • Loading bone and cartilage when possible.
  • Task-related training if possible.
  • Anti-gravity positions (sitting on edge of bed, tilt tabling).
  • Early use of tilt tables can be beneficial.
• Family and Friends:
  • Provide information and support.
  • Listen and validate their thoughts and feelings.
  • Honest about what you know and don't know regarding prognosis.
  • Keep families engaged or calm to integrate this into therapy.

Recovering from Coma

• Emerging from Coma (Minimally Conscious State):
  • Re-establishing swallowing (speech pathology).
  • Weaning off ventilators.
  • Developing an effective cough and breathing techniques.
  • Establishing effective communication (verbal or non-verbal).
  • Promoting time in the upright position.
  • Maintaining range of movement.

Management of Patients in Post-Traumatic Amnesia (PTA)

• Characteristics:
  • Confused, disoriented, limited ability to take in new information.
  • Short attention span, easily distractible.
  • Fatigue easily (cognitively and physically).
  • Easily overstimulated.
  • Agitated, irritable, aggressive.
  • Perseveration (getting stuck on a topic or task).
  • Disinhibition (inappropriate behavior).
  • May exhibit psychotic behavior.
• Strategies:
  • Quiet, consistent environment (treat in room or low-stimulation room).
  • Remove distractions and triggers for aggression.
  • Team meetings to discuss contributing factors.
  • Behavioral diary to track behaviors and triggers.
  • Minimize active therapy; practice whole tasks (getting out of bed, walking).
  • Concrete goals reinforced daily.
  • Minimize talking and instructions.
  • Minimize hands-on contact.
  • Short sessions.
  • Avoid sensory overstimulation (brightness, colors, noise, number of people).
  • Consistent therapist.
  • Familiar cues and prompts.

Rehabilitation Stage: Cognition and Behavior

• Cognitive Deficits:
  • 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).
• Behavioral Issues:
  • Impaired drive (dissociation between knowing and doing; lack of initiation, apathy, lethargy).
  • Discontrol/disinhibition, impulsiveness, lability (emotional instability), reduced anger control, aggressiveness, sexual acting out, perseveration, poor social judgment.
• Strategies to Assist:
  • Environmental supports and reminders (written worksheets, photos, videos).
  • Clear cues and concise instructions.
  • Memory aids (lists, sticky notes, diaries, phone reminders).
  • Dual-task practice (if functional and automatic).
  • Simple environment.
  • Clearly specified and agreed-upon treatment goals and schedules.
  • Consistent treatment approach by the whole rehab team.
  • Avoid trigger situations (overstimulation, lack of control, confusion).
  • Address lack of quality sleep, pain, infection, temperature, or need to use the toilet.
  • Behavior modification program (neuropsychologist).

Role of Physiotherapists

• Assessment and treatment of motor deficits.
• Sensorimotor impairments are highly variable.
• Detailed assessment over multiple sessions due to cognition, fatigue, and behavior issues.
• Impairments:
  • Negative Features: Loss of strength and joint range of motion, loss of dexterity and coordination, ataxia, poor balance, vestibular dysfunction, sensory loss, visual changes, fatigue.
  • Positive Features: Spasticity, hypertonus (increased resistance to passive movement).
• Concurrent Injuries: Fractures, spinal and abdominal injuries, which may impact on intervention planning and completion.
• Pain is common and can be a barrier to optimising intervention including communication ability that may not be able to verbally tell you they have pain.
• Clinical Reasoning: RAMP (Remediate, Adapt, Maintain, Prevent).
• Therapy Modalities: Focus on impairments and task-related training (neuroplasticity, motor learning).
• Task-Related Training Modifications:
  • Task modification to enable success.
  • Feedback on biomechanical features of actions.
  • Consistent cues.
  • Clear, meaningful goals.
  • Clear and concise feedback.
  • Slow things down and allow time for processing.
  • Give a sense of control.
• Multidisciplinary Team: Speech, language and communication deficits, swallowing deficits, hearing loss and bladder and bowel issues all require a multidisciplinary team.
  • Physio: motor control, sensorimotor ability.
  • OT: cognitive ability, perceptual ability
  • Neuropsychologist: brain function
  • Speech pathologist: swallowing, speech, communication
  • Social Worker: finances, care, family support/liaison

Evidence for Physiotherapy Management

• SIGN Guidelines for Brain Injury Rehabilitation in Adults (2013).
  • Repetitive task-oriented activities are recommended for improving functional activity.
  • Casts, splints, passive stretching may be considered if progress contractures or deformities.
  • Botulinum toxin therapy could also be considered effective.
• Canadian Guidelines (2016):
  • service requirements, multidisciplinary team, behaviour/cognitive management, communication strategies, ADL retraining, return to vocational activities, vocational activities, controlled stimulation with a graded sensory approach for managing hypersensitivity, fatigue and overstimulation