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Translational Medical Sciences > Traumatic Brain injury > Flashcards

Traumatic Brain injury Flashcards

1
Q

What is traumatic brain injury

A

Injury to the brain caused by trauma to the head

- not congenital or degenerative in nature but caused by external physical force

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2
Q

What is the healthy frontal lobe associated with

A
  • speech
  • problem-solving
  • concentration
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3
Q

What is the healthy parietal lobe associated with

A
  • sensation of pain
  • temperature
  • touch
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4
Q

What is the healthy occipital lobe associated with

A

healthy vision

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5
Q

What is the healthy temporal lobe associated with

A
  • memory

- organization

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6
Q

What is the healthy cerebellum associated with

A
  • balance

- coordination

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7
Q

What is the healthy brain stem associated with

A
  • breathing

- steady heart rate

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8
Q

What would a TBI in the frontal lobe result in

A
  • language difficulty
  • lack of focus
  • irritability
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9
Q

What would a TBI in the temporal lobe result in

A
  • problems with long and short term memory
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10
Q

What would a TBI in the occipital lobe result in

A
  • blind spots

- blurred vision

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11
Q

What would a TBI in the parietal lobe result in

A
  • spatial misperception

- difficulty reading

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12
Q

What would a TBI in the cerebellum result in

A
  • difficulty walking

- slurred speech

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13
Q

What would a TBI in the brain stem result in

A
  • changes in breath

- difficulty swallowing

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14
Q

What are the two types of traumatic head injury

A
  • Open-head injury (penetrating injury, including fractures and bone segments)
  • Closed head injury (blunt injury, including stroke)
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15
Q

What does the severity of open head injury depend on

A

areas affected

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16
Q

When is open head injury fatal

A
  • when there is damage to both hemispheres, ventricles and multiple lobes
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17
Q

Who is more at risk for open heady injury

A
  • children and infants
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18
Q

What is the process of closed head injury

A
  • consists of a coup and contra-coup

- first point of contact= coup

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19
Q

What does a coup and a contra-coup usually result in

A
  • subdural haematoma due to close head injury
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20
Q

What is a subdural haematoma

A
  • bleeding under dura matter
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21
Q

Name the three types of axonal injury

A
  • Twisted axon pulled away at synapse
  • Torn axon
  • Broken axon
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22
Q

What secondary damage can a closed head injury result in

A

○ Immediate leak of neurotransmitters
○ Lack of oxygen and glucose to the brain
○ Leads to inflammation

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23
Q

Name the outcomes of closed head brain injury

A
  • Bleeding (subdural haematoma)
  • Tearing (tearing and twisting of brain in the skull)
  • Sheering (secondary damage)
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24
Q

Describe the pathology of the BBB in TBI

A
  • secondary damage caused by severe closed head injury
  • disruption of BBB
  • cascade of neurochemical events
    • potassium and sodium
    • chloride
    • glutamate
  • Swelling and inflammation from tissue damage
    • increases pressure on the brain in turn leading to more damage
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25
Q

What are the treatment options available for a leaky brain

A
  • no known drug can stop the leak of neurotransmitter or the swelling of the brain
  • chilling of the brain is the only known treatment that works
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26
Q

Why does chilling of the brain work as an efficient treatment for swelling and inflammation

A
  • Excitotoxicity is temperature sensitive
  • high temperatures are required as a catalyst for neurotransmitters to cascade
  • a lower temperature prevents the aforementioned from occuring
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27
Q

What diagnostic imaging techniques can be used to scan for TBI

A
  • CT scan
  • X-ray
  • PET scan
  • MRI (functional or resting state)
  • Diffusion tensor imaging
  • EEG
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28
Q

What is secondary impact syndrome

A
  • life threatening
  • result of back-to-back concussions
  • results in a loss of autoregulation of blood supply:
    • vascular engoregement
    • increased intracranial pressure
    • rapid brain stem failure
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29
Q

What is Dementia Pugilistica

A
  • punch drunk syndrome
  • boxing dementia
  • similar to CTE
  • associated with memory loss and slurred speech
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30
Q

What is Chronic Traumatic Encephalopathy

A
  • CTE
  • Evidence that there’s a link between traumatic brain injury and neurodegenerative diseases
  • higher risk for people with Apoe4 gene
  • Can be diagnosed by tau protein aggregation
  • Also found in hippocampus (classic area for AD)
  • Repeated hits to the head leads to aggregation of Tau
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31
Q

What do MRI-CT scans of brain injury tend to show

A
  • Change in enlarged vesicles
  • Gyri becomes more prominent
  • Grooves shrink
  • Loss of brain matter
32
Q

What can affect the rate of cognitive decline

A
  • TBI can shift the timeline to get dementia towards a younger age
  • TBI in combination with CTE can shift it even further
33
Q

What does the neurotoxic cascade following TBI consist of

A
  • Excitotoxicity
  • Ischaemia
  • BBB disruption
  • Cerebral odeoma
  • Energy failure
  • Cell death cascade
34
Q

What types of glia are a part of the CNS

A
  • Microglia
  • Oligodendrocytes
  • Astrocytes
  • Ependymal cells
35
Q

What role do microglia play in the CNS

A
  • clean up debris and pathogens via phagocytosis
36
Q

What role do ependymal cells play in the CNS

A
  • line the ventricles and central canal

- assist in the production, circulation and maintenance of CSF

37
Q

What role do astrocytes play in the CNS

A
  • form scar tissue
  • provide structural support
  • maintain BBB
  • regulate homeostasis in the brain
38
Q

What role do oligodendrocytes play in the CNS

A
  • myelinate CNS axons

- provide structural framework

39
Q

What types of glia are a part of the PNS

A
  • Schwann cells

- Satellite cells

40
Q

What role do satellite cells play in the PNS

A
  • surround neurons in the ganglia

- regulate O2, CO2, nutrients an neurotransmitter levels around neurons in ganglia

41
Q

What role do schwann cells play in the PNS

A
  • myelinate peripheral axons

- part of repair process after injury

42
Q

What are the different shapes of microglia

A
  • Bipolar/rod
  • Amoeboid
  • Ramified
43
Q

What can move through the BBB

A
  • oxygen
  • water
  • lipid soluble proteins
44
Q

What surrounds the BBB

45
Q

What modulates the transfer of nutrients b/w glial cells and the membrane

46
Q

What is the gliovascular complex

A

the BBB and the astrocytes surrounding it

47
Q

What happens to the gliovascular complex in TBI

A
  • entire complex is disrupted
  • endothelial cells are ruptured
  • greater exposed surface area that allows more materials to exchange
  • disruption of pathways of transport across the BBB allows the flow of neurotransmitters in the wrong direction and may contribute to excitotoxicity
48
Q

What are the pathways across the BBB

A
  • Paracellular aqueous pathway (water soluble proteins)
  • Transcellular lipophilic pathway (lipid soluble agents)
  • Transport proteins (glucose, amino acids)
  • Receptor mediated (insulin)
  • Adaptive transcytosis (albumin and other plasma proteins)
49
Q

How is the structure of the brain affected in TBI

A
  • Bleeding, tearing, sheering
50
Q

What are the stages of TBI

A
  • Mechanical damage
  • Inflammation and angiogenesis
  • Glial scar formation
  • Structural tissue regeneration
51
Q

How does TBI progress

A
  • Acute injury causes secondary damage to the BBB leading to tearing, bleeding and sheering
  • BBB leakage allows monocytes in the blood stream to migrate to the site of injury within the brain parenchyma and trigger the activation of microglia
52
Q

Explain the role of mircoglia during inflammatory events

A
  • First line of defence in the CNS
  • constantly scan the CNS and are very sensitive to changes in the environment
  • Under normal conditions, microglia exist in a resting ramified state wherein they function as debris-collectors for cellular debris and apoptotic cell via phagocytosis
  • Activated microglia can polarize into M1 (pro-inflammatory) or M2 (anti-inflammatory) state depending on the nature of the inflammatory stimulus
53
Q

Name some inflammatory events that can activate microglia

A
  • Neuronal damage
  • invasion by infectious agents
  • presence of pathogenic proteins
54
Q

Describe the polarization states of microglia and their relationship

A
  • M1 state: pro-inflammatory, classical activation
    • respond to injury or infection
    • produce oxidative metabolites and proinflammatory cyokines and chemokines
    • induce infiltration of peripheral leukocytes to clear up the site of injury or infection
  • M2 state: anti-inflammatory, neuroprotective, alternative activation
    • microglia antagonize the M1 pro-inflammatory responses
    • secrete anti-inflammatory cytokines
    • facilitate phagocytosis of cell debris
    • induce reconstruction of the ECM and tissue repair
    • also produce neurotrophic factors to support neuronal cell health and survival
55
Q

Describe the timeline of polarization of microglia

A
  • After an insult to the brain, monocytes, microglia, and rod microglia are activated
  • Monocytes migrate to lesioned areas, whereas gray matter microglia are less likely to displace
  • Microglia change morphology in a time-dependent fashion, sprouting new ramifications soon after injury, and then withdrawing branches to develop an ameboid phenotype
  • In the very early phases after injury, microglia have a M1 phenotype, then, with the recruitment of macrophages, both myeloid populations upregulate M2 markers
  • The peak of M2 marker expression soon vanishes and is followed by upregulation of M1 markers that lasts longer
56
Q

What process occurs with monocytes after TBI?

A
  • Adhesion
  • Infiltration from blood
  • Migration
  • Proliferation
57
Q

What process occurs with microglia after TBI?

A
  • Limited migration
  • Damage sensing profile changes branch outgrowth
  • Reactive markers branch withdrawal
  • Phagocytosis, phagoptosis, ameboid
58
Q

Discuss the use of xray in TBI imaging

A
  • for skull bone damage
59
Q

Discuss the use of CT in TBI imaging

A
  • bleeding in the skull area
60
Q

Discuss the use of MRI in TBI imaging

A
  • can identify build up of fluid in brain

- can identify skull fractures

61
Q

Discuss the use of EEG in TBI imaging

A
  • for irregular electrical activity eg seizures
62
Q

Discuss the use of PET in TBI imaging

A
  • Expensive
  • Says about the same as an MRI
  • Useful if you’re looking for a specific protein
63
Q

Discuss the use of diffusor tensor imaging in TBI imaging

A
  • Visualises damage to the brain by isolating white matter tracts
  • Massive equipment which needs a lot of room and is expensive to buy
64
Q

What is the proposed mechanism for excitotoxicity from leaky BBB in TBI

A
  • Disrupted endothelial membrane due to injury from TBI
  • Immune cell circulate in the blood stream and brain and activate microglia and astrocytes
  • Activated astrocytes secrete S100
  • Activated microglia secrete and get activated by:
    glutamate
    Arachadonic acid
    quinolonic acid
    pro-inflammatory cytokines (IL-1B, TNFa, IL2, IL6)
  • This leads to free radical generation of lipid peroxidation and peroxynitrite)
  • This leads to mitochondrial dysfunction
  • Mitochondrial dysfunction leads to accelearated excitotoxicity and synaptic dysfunction
  • ultimately leads to excitotoxicity
65
Q

Which markers give indication of microglia activity?

66
Q

What is the marker for astrocytes?

67
Q

What are the main NEURODEGENERATIVE-ASSOCIATED GENES specifically expressed in microglia?

A
  • APOE4
  • TREM2
  • BDNF
68
Q

What is astrogliosis and how does it occur

A
  • Astrogliosis is the adjustment of astrocytes to insult/injury in the brain
  • Insult to epithelial tissue causes the release of cytokines like IL1B, TNFa, IL2 and ROS
  • This activates resting astrocytes
  • Reactive astrocytes induce recruitment and proliferation of other astrocytes as they migrate to the site of injury to form an astroglial scar
69
Q

What is the evidence for microglial priming in TBI

A
  • microglia are said to be primed for activation after TBI, making individuals prone to secondary impact syndrome
  • Already in active state and producing cytokines
  • If another insult occurs, microglia becomes even more active due to priming
  • Blood monocytes also enter brain after TBI
  • Secrete similar things to microglia
  • Overall increased response and inflammation
70
Q

What are the hallmarks of astrocyte reactivity

A
  • Increased homeostatic and trophic functions
  • Secretory activity
  • Proliferation
  • Migration
  • Glial scar formation
71
Q

What are the models available for TBI

A 
Diffuse injury
- Blast injury
- Weight drop injury
Focal injury
- Fluid percussion
- Controlled cortical impact injury model
- Weight drop energy
72
Q

What is a glial scar formed by

A
  • Migration of myelin-associated inhibitors, astrocytes, oligodendrocytes, oligodendrocyte precursors, and microglia
73
Q

Why does scar formation inhibit axon regeneration?

A

NG2 GLIA (polydendrocytes) may inhibit axon regeneration by:

  • expression of inhibitroy NG2 proteoglycan
  • formation of synaptic contacts
74
Q

What is the controlled cortical impact injury model and what are its advantages

A
  • easily reproducible
  • mimics:
    concussion
    BBB rupture
    axonal injury
75
Q

What is the weight drop injury model and what are its advantages

A

Two models

  • one with a protective disk on top so when weight is dropped there are no skull fractures, associated with diffuse injury
  • one with an unprotected skull so weight is dropped to one side of the skull, associated with diffuse injury
76
Q

What is the fluid percussion injury model and what are its advantages

A
  • mimics TBI without skull fracture
  • pathophysiological features like:
  • intracranial bleeding
  • brain swelling
77
Q

What is the blast injury model and what are its advantages

A
  • military personnel experience TBI without skull fractures

- this model is ideal to study how blast waves induce brain injuries

Translational Medical Sciences (8 decks)

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