Traumatic Brain Injury (TBI)

Upper Motor Neuron condition

TBI is a type of ABI that results from:

- A blow to the head/ blunt impact

- A penetrating head injury

- Violent acceleration-deceleration

TBI causes:

Permanent brain damage, resulting in partial or total functional disability and or psychosocial impairment.

Metabolic and circulatory changes.

Alterations in neurotransmitter and neuroendocrine function (behavioural and arousal).

TBI is the main cause of death and disability in adolescence and YA.

Males: Females 2:1

10% classified mod-severe

Mechanisms of injury - need to know!

Closed Head Injury

- MCA (Motor Car Accidents)

- MBA (Motor Bike Accidents)

- Cycling accidents

- Pedestrian injury

- Falls from a height

- Assault

- Sporting injuries

Open Head Injury

- ‘penetrating’ trauma or blow to the head

- Typically, from a gunshot, stabbing, vehicular or workplace injury

- Infection following initial injury or surgery

Risk factors

- Alcohol and drug use

- Using transport (50%)

- Not using seatbelts, motorcycles and helmets

- Contact sports

- Unsafe workplace practices

Classification of mechanisms of brain damage post-trauma

INTRA-CRANIAL

Primary damage:

- Diffuse axonal injury (DAI)

- Contusions

- Lacerations

- Haemorrhage (subdural, epidural, subarachnoid, intra-ventricular)

Secondary damage

- Brain swelling

- Vasogenic oedema – extracellular accumulation of fluid resulting from disruption of the blood-brain barrier and movement of proteins

- Cytotoxic oedema – cellular swelling, intracellular fluid accumulation, disruption of cell metabolism – can cause cell death.

- Cerebral blood vessel constriction

EXTRA-CRANIAL

- Hypoxia

- Hypotension

- Usually due to SCI and or haemorrhage

- Fractures

- Internal organ damage

TBI Primary Lesions

Diffuse axonal injury (DAI) – breaking and stretching of the myelin sheath; microscopic damage to neurofilaments.

Contrecoup lesions – point of impact in initial damage and head is flung in opposite direction where there is another contact injury. E.g. whiplash, falls, physical assault. (multiple points of impact)

Intracranial/ intracerebral Haemorrhages – raises intracranial pressure which can cause ongoing and secondary damage.

- Coup-contrecoup: Primary damage occurs directly beneath (“coup”) and opposite to (counter-coup), the site of impact. Usually associated w Haemorrhages.

- Rapid acceleration and deceleration of gelatinous brain matter within the skull results in neural tissue laceration by irregular bone structures or dural edges.

TBI Secondary Lesions

Primary injury decreases blood flow and O2 delivery causing hypoxia; meaning there will be a metabolic issue (cerebral-metabolic uncoupling, loss of blood flow means loss of nutrients too which can impair CV autoregulation. Meaning the brain is a lot more vulnerable to secondary damage.

- Release of toxic neurotransmitters (e.g. glutamate)

- Impaired calcium homeostasis

- Increased inflammatory markers and reactive oxygen species (ROS) (superoxides, hydrogen peroxide) which can cause extensive tissue and neuron damage.

- Intracerebral oedema (vasogenic or cytotoxic) —>

- Increase intracranial pressure (ICP), compression of tissue leads to ischemia and decreased cerebral blood flow (further ischemia)

- —> leading to inflammation and further necrosis

TBI symptoms

• TBI damage is usually more diffuse, with more generalized impairments, compared to stroke.

• Traumatic injury & loss of consciousness

• Post-Traumatic Amnesia (PTA)

• Orientated/Persistent Amnesic state

Concussion – Transient TBI

• Traumatically induced, transient disturbance of brain function & involves a complex

pathophysiological process.

• Subset of mild traumatic brain injury (MTBI) which is generally self-limited & at the

less-severe end of the brain injury spectrum. Metabolic changes within brain tissue.

• Concussed brain is less responsive to neural activation.

• If premature cognitive or physical activity occurs before complete recovery, the brain

may suffer prolonged dysfunction. Cumulative effects from multiple concussions.

• ≈ 50% are not reported! Athletes under-report symptoms to coaches & medics

• increased concussions happen to front & top of head (increased risk). US college football showed increased side & top impacts.

Evidence of concussion-related deficits

• Short-term memory loss, headaches & migraines 10 - 20 yr post-concussion.

• 5 x increase in mild cognitive impairments.

• Earlier onset of Alzheimer’s Disease and dementias.

• Mood disturbances, attention deficit/ learning disorders

• Visual disturbances & de-coupling of vision from action.

• Motor issues (ataxia).

• Impaired movement planning & execution.

• Changes in autonomic function, HR variability etc.

• Decreased Cerebral blood flow up to 8 days post-injury (can cause hypoxic damage)

• Repeated concussions can cause Chronic Traumatic Encephalopathy (CTE)

CTE

- Any activity involving repeated blows to the head or recurrent concussions increases risk.

- Pattern of repeated minor head injuries increases the risk.

- Causes: Shrinkage of brain and loss of brain function over time

Symptoms:

- 5 x increase in mild cognitive impairments: attention deficit/ learning disorders.

- Mood and behaviour changes

Highest at risk:

- athletes w Hx of repeated head injuries

- military vets w repeated head trauma – blast events

- Associated w shrinking of the brain (atrophy) and neurofibrillary tangles that contain a tau protein (can lead to early onset dementia)

Neurological Symptoms of Concussion

• Vertigo

• Auditory symptoms

• Vestibular ocular reflex dysfunction

• Nystagmus (repetitive, uncontrolled eye movements)

• Nausea & vomiting

• Ataxia & general lack of coordination, poor reaction time, bradykinesia (slowing of movement)

Concussion Assessment Tools

• Sport Concussion Assessment Tool (SCAT3).

• Standard Assessment of Concussion (SAC).

• ImPACT Post Concussion Scale (PCS).

1. Common Acute TBI Impairments *

• Cognition & information processing

• Speech & Language

• Memory

• Attention

• Reasoning & problem solving

• Abstract thinking

• Judgement

• Sensory, perceptual & motor abilities

• Behaviour / mood / personality changes

• Physical functions (balance, coordination, paralysis, weakness, timing)

Physical impairments usually include:

• Movement & control problems in all 4 limbs, neck and/or trunk.

• Upper motor neuron damage may cause spasticity, clonus & abnormal involuntary posturing.

• Brainstem & cranial nerve damage may affect vital functions (respiration, heart rate, swallowing).

• Cerebellum damage - imbalances, decreased coordination, difficulties with movement control & timing.

Long term consequences of TBI *

• Altered tonal state

• Spasticity

• Ataxia

• Dyspraxia

• Paralysis

• Muscle & Joint contractures

• Reduced balance & co-ordination

• Heterotrophic ossification

• Ventilatory support & pulmonary complications

CONSIDERATIONS for OUTCOMES

From EP perspective: trying to get people firstly functioning for ADL’s but also:

Purposeful movements.

Communication.

Recovery is measured in months & years.

Population generally young so outcomes are extremely important.

Glasgow Coma Scale

Mild Head Injury 13 - 15

Moderate Head Injury 9 - 12

Severe Head Injury 8 or less

TBI Medications

• Anti-convulsants (Neurontin, Topiramate, Carbamazepine, sodium valproate).

• Anti-depressants (Amitriptyline, Paroxetine, Sertraline, Citalopram & other SRIs).

• Anti-psychotics (Quetiapine)

• Pain management (NSAIDS, acetaminophren, paracetamol).

• Motor control, anti-spasticity (Baclofen, Tizanidine, Cyclobenzaprine).

• Memory & cognition (Donepezil, Modafinil, Methylphenidate).

• Migraine (Amitriptyline, Gabapentin, tryptans, Topiramate).

• Sleep Disorders (Melatonin, Trazedone [SSRI], diazepam)