Traumatic Brain injury (TBI) Flashcards
LO
- Compare and contrast the causes, outcome, cost, and impact of TBI (and SCI)
- Describe the biological processes that determine the outcome of TBI (and SCI)
- Compare and contrast the molecular and pathological mechanisms of TBI (and SCI)
- Describe symptoms and tissue changes in CTE
TBI facts (do not need to remember)
Acute trauma to head and brain with or without skull fracture
- 213,752 – Total UK admissions to hospital for head injury in 2011-12
- 33.5% - Increase in UK head injury admissions in the last decade
- 10,000-20,000 – Number of severe (fatal or person ends up with paralysis if they survive)traumatic brain injuries per year in the UK
- 2X – More likely for men to sustain a TBI than women. This is because they are more susceptible to injury because they are more likely to take risks
- 15–24-year-old males & over 80-year-olds – Groups at most risk for TBI
- Acute trauma is something which occurs instantaneously
What are common causes of TBI?
- Motor vehicle accidents
- Cycling accidents
- Sports injuries
- Violence
Tell me facts about cycle helmets, and their ability to reduce brain injury
- Pedal cyclists accounted for 6% of total road deaths in 2016; with 18,870 reported pedal cycling casualties (killed, seriously injured, slightly injured) in 2017
- Wearing a cycle helmet? Reduces the risk of brain injury by up to 88%
Tell me some potential effect of head injury and an example for each
Behaviour and personality changes – Anxiety, depression, loss of motivation, difficulty controlling anger, and impulsivity
Cognitive Impairment – Problems with memory, attention and concentration, low tolerance for noisy or stressful environments, loss of insight and initiative
Physical changes – Loss of coordination, muscle rigidity, epilepsy, difficulty speaking, sight/smell/taste loss, fatigue, sexual problems, paralysis
TBI is a heterogenous condition
Frontal lobe damage is what contributes to personality changes
What has been created to diagnose TBI?
The Glasgow Coma scale
What does the Glasgow coma scale monitor ?
How is it scored?
GCS is an indicator of severity of head injury used clinically.
- Monitors changes in consciousness (coma).
- Monitors motor response, verbal response, and eye opening
- Scoring ranges from 1 (no response) to maximum 4-6; scores summed to between 3 and 15.
- This is the standard of care if someone comes into clinic with TBI in order to assess them
What is the prognostic value of the Glasgow coma scale?
Scores immediately after injury and 24 hours post-injury correlate with degree of long-term impairment
What do the Glasgow coma scores mean?
<8 is a severe head injury (coma)
9-12 is a moderate head injury
>12 is a mild head injury
With TBI, you can get different injuries, explain each of these
Open/penetrating injury: When an object goes through the skull and enters the brain.
Closed head injury: A trauma causes the brain to be violently shaken inside of the skull, such as a blast injury. No visible wound.
Crush injury: When the head is sandwiched between two hard objects.
With TBI, one can also get coup or contrecoup injuries. Tell me about each of these
Coup Injury: Primary Injury caused when the head stops suddenly, and the brain rushes forward. Brain incurs a primary impact injury at the site of skull strike as well as surrounding tissue.
Contrecoup Injury: Secondary Injury caused when the brain bounces off the primary surface of impact and goes on to impact the opposite side of the skull. The brain incurs a focal area of damage as well as damage to the nearby surrounding tissue.
Tell me what happens in whiplash
Hyperextension of the neck, followed by hyperflexion. Major area of damage done to anterior longitudinal ligament, but vertebrae can also become dislocated and/or fractured.
Hyperextension
Sudden backwards acceleration of skull. Once skull stops moving, the frontal lobe strikes the front of skull.
Hyperflexion
Head recoils forward and stops. Occipital lobe strikes back of skull.
Tell me the key events that occur in primary injurt (complete at time of impact) in TBI
Skull fracture (open injury)
Contusions (bruising of brain on impact, damage to blood vessels)
Haemorrhage – (bleeding from ruptured blood vessels)
Haematoma – localised pooling of blood
Diffuse Axonal injury (DAI) – damage to axons throughout brain
Concussion – (temporary) neuronal dysfunction
Tell me the key events of secondary injury (Intracranial)(evolves over hours, days, weeks after impact) in TBI
*Brain swelling, Cerebral Oedema, Hydrocephalus- fluid caused by inflammation or rupture of blood vessels
*Increased Intracranial Pressure
*Intracranial haemorrhages, Traumatic haematomas, infections
Blood flow changes and metabolic changes
Epilepsy
Hypoxia-ischaemia (reduced oxygen to brain)
* relate to image
Tell me the neuropathology of TBI
T1-weighted MRI: TBI (severe);
Atrophy and increased ventricles
Top panel looking at coronal view of cortex and middle of brain. Black regions are ventricles housing CSF.
Middle panels show normal ventricles. Those with TBI show an increase in area in which ventricles are covering. Issue with this is that CSF is being produced too quickly or not being drained properly
Whats the equation to calculate the cerebral perfusion pressure?
Cerebral Perfusion Pressure = Mean Arterial Pressure – Intracranial Pressure
Cerebral perfusion pressure (CPP) is the net pressure gradient that drives oxygen delivery to cerebral tissue
Mean arterial pressure (MAP) is the average arterial pressure throughout one cardiac cycle, systole, and diastole
Intracranial pressure (ICP) is the pressure exerted by fluids such as cerebrospinal fluid (CSF) inside the skull and on the brain tissue
What are the ICP and GCS scores for the following situations
- Normal
- Drowsy and confused
- Severe brain swelling
Normal ICP = 7-15mmHg
Drowsy and confused patient (GCS 13-15); ICP=20mmHg
Severe brain swelling (GCS <8); ICP=30mmHg (near coma state)
Cerebral perfusion pressure is the ability of the brain to deliver oxygen to the tissues?
Larger ICP can cause severe damage if not relieved
The CPP should not fall below what else theres a risk for what?
CPP should not fall below 70mmHg, otherwise at risk for hypoxia and ischaemia.
What is the Monroe Kellie Doctrine in regard to ICP?
Skull is a rigid structure
3 components:
Brain: 80% of total volume, tissues, and interstitial fluid
Blood: 10% of total volume = venous and arterial
Cerebrospinal fluid: 10% of total volume
Vintracranial = Vbrain + Vblood + VCSF
An increase in one component results in the compression of another
What do the following diagrams show about ICP and homeostasis?
A: Normal.
B: With some increase in ICP, venous volume can decrease through increased release of venous blood into the jugular veins. CSF volume can decrease through increased release of CSF through the foramen magnum into the spinal canal. Body compensates as wants to maintain homeostasis.
C: The intracranial mass is much larger, beyond the pressure-buffering capacity of venous blood and CSF; there is a net rise in ICP. Could lead to long term damage.
What are some treatments for ICP?
Medically induced coma
*Brain diuretic (reduce fluid/water) (e.g., Mannitol – osmotic diuretic)
*Placement of shunt (placement of tube to drain fluid)
Craniectomy (partial skull removal)
*more moderate cases
What are some key events that occur after TBI primary injury…
Secondary Injury - Neurochemical Injury:
- Excessive production of free radicals- things that will oxidise cells and kill them
- Excessive release of excitatory neurotransmitters- could lead to epilepsy
- Alterations in glucose metabolism
- Decreased cerebral blood flow
- Neuroinflammation
–>
Late/delayed Injury (long-term)
- White matter degeneration and cerebral atrophy- axons and neurons are dying off
- Posttraumatic hydrocephalus- swelling of brain?
- Posttraumatic seizures
What are the key events that occur in TBI secondary injury in regard to neuroinflammation
Activation of microglia (i.e., DAMPS), astrocytes, neurons
Activation and recruitment of macrophages
Microglia secrete pro-inflammatory modulators to degrade BBB, release cytokines (in response to DAMPs/damage-associated molecular patterns)
Neuropatholgoy of TBI?
Fluid takes up space in brain cavity
TBI –> neurodegeneration
What happens during diffuse axonal injury (DAI)?
Brain tissue immunostained with beta amyloid precursor protein (BAPP) (above).
BAPP is produced by neurons in response to injury.
Accumulates at points of axonal damage (constriction/transection). Some axons have multiple swellings (‘beaded’ appearance).
Axonal swellings may persist for years.
Diffuse axonal injury by TBI
Tell me about Chronic Traumatic Encephalopathy (CTE) what is is, whats is it AKA, and what are the symptoms?
‘Young person’s disease’ as usually caused by sports
CTE is a progressive and degenerative brain condition that has been linked to repeated head injuries and repeated concussions.
Also known as ‘dementia puglistica’ or ‘punch-drunk syndrome’
Symptoms
- Begins gradually, years after initial trauma(s)
- Memory loss, confusion, impaired judgment, impulsive control problems, aggression, depression, suicidality, parkinsonism, progressive dementia
- These symptoms are mirrors in our neurodegenerative diseases
What are the molecular/ cellular changes found in CTE?
- Abnormal Tau accumulation (and neurofibrillary tangles)
- Microgliosis, astrogliosis
- Brain atrophy (both grey and white matter) (stages 3-4)
- Enlarged ventricles
- Abnormalities in TDP-43 (phosphorylated 43kDa TAR binding protein; prominent in frontotemporal dementia and ALS)
What makes woodpeckers immune to TBI?
The head of a woodpecker moves at 7 m/sec when striking a tree. Their eyes must be closed to save them from popping out. How do they avoid TBI?
Less CSF! (Less fluid surrounding the brain limits motion)
Stronger bones, yet thinner skull bones
Tongue has a bone in it. It wraps around the back of the skull and acts like a spring dampening force on the brain.
Woodpeckers are immune to TBI due to anatomy of their brain/ skull
