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TBI Flashcards

1
Q

what is traumatic brain injury (TBI)?

A

external physical injury to brain caused by trauma to head after birth also called as concussion.

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2
Q

what kind of trauma takes place in TBI?

A

it has to be external physical force, not degenerative or congential nature

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3
Q

what is the function of following in a healthy individual?

  1. frontal
  2. parietal
  3. occipital
  4. temporal
  5. cerebellum
  6. brainstem
A
  1. frontal - concentration, problem solving, speech (PCS)
  2. parietal - sense of touch, pain, temperature (TPT)
  3. occipital - healthy vision
  4. temporal - memory + organisation
  5. cerebellum - balance + coordination
  6. brainstem - breathing, steady heart rate
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4
Q

how is the function impaired in these following regions of TBI individual?

  1. frontal
  2. parietal
  3. occipital
  4. temporal
  5. cerebellum
  6. brainstem
A
  1. frontal - lack of concentration, language difficulty, irritability
  2. parietal - difficulty with reading, spatial misperception
  3. occipital - blurred vision, blind spots
  4. temporal - short and long term memory impairment
  5. cerebellum - difficulty walking + slurred speech
  6. brainstem - changes in breath + difficulty swallowing
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5
Q

what are the types of TBI and its causes?

A
  1. open head injury caused by penetrating injury

2. closed head injury caused by blunt injury

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6
Q

what are the types of penetrating injury and blunt injury?

A

penetrating - gunshot wound, knife, fracture, hair/bone going into head
blunt - falling over, stroke(internal head injury)

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7
Q

when are the open head injuries fatal?

A
  • severity depends on the areas affected
  • if involvement and damage to both
    1. hemispheres
    2. ventricles
    3. multiple lobes
    4. brain stem
    then they are usually fatal
  • if the person survived those areas then complete recovery with secondary symptoms
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8
Q

what are the two closed head injuries?

A

coup and contra coup

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9
Q

what is the difference between coup and contra coup?

A

Coup - occurs on the brain directly under the point of impact
Contra coup - occurs on the opposite side of brain from where the impact occurred

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10
Q

what are the characteristics of TBI?

A

bleeding, tearing and sheering

  1. subdural haematoma - bleeding under the dura matter
  2. white matter injury - axonal damage, twisting and tearing of brain inside the skull
  3. secondary change - changes in blood flow, oxygen levels and excitotoxic cell damage (inflammation)
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11
Q

what causes the secondary damage in TBI?

A

due to excessive tearing and shearing force, there is NTs leakage

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12
Q

which are the neurochemicals released in the leaky brain?

A
  1. glutamate
  2. chloride
  3. pottasium and sodium
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13
Q

what does the leaky brain result in?

A
  • swelling and inflammation from tissue damage

- increasing the pressure resulting in more damage

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14
Q

how does the chilling the brain helpful?

A
  • excess bleeding in brain -> pressure
  • no drug can stop the Its leakage resulting in swelling of brain
  • therefore, the brain undergoes hypothermia
  • since neurons and glutamate are temperature sensitive and prefer high temperature
  • the cold temperature slows down the process of injury and inflammation
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15
Q

what are the diagnostic imaging of TBI?

A
  1. x-ray - skulls damage
  2. CT scan - bleeding (first choice for TBI)
  3. MRI scan (functional/resting state)- changes in fluid
  4. EEG - faulty signalling (epileptic seizure)
  5. PET scan
  6. DTI - location of injury, areas affected, white matter tracts
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16
Q

what is second impact syndrome (SIS)?

A
  • back to back concussions without time to heal
  • when there is second head injury before the damage from the first injury has cleared or recovered
  • rare but potentially serious
  • life threatening condition
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17
Q

what is SIS result in?

A

results in loss of auto regulation of blood supply

  1. vascular engorgement
  2. increased intracranial pressure
  3. brain herniation (side effect of high pressure within skull)
  4. rapid brain stem failure
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18
Q

how do the brain cells die in SIS?

A
  • Incapacity of the BV to dilate and conduct blood flow to those areas, damage to BV
  • exacerbation of first injury
  • individuals who survive usually have memory loss or develop dementia
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19
Q

what is the chronic traumatic encephalopathy (CTE)?

A

CTE is a secondary injury ; progressive degenerative brain disease, caused by repeated hits to the head

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20
Q

what is genetic background of CTE?

A
  • Genetics and age of exposure can play a role
  • CTE can only be diagnosed after death
  • caused by the deposition of tau protein. in hippocampus (temporal lobe)
  • The accumulation goes on for hyperphosorylated tau and it undergoes several stages
  • also involved ApoE gene (associated with the risk of getting AD)
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21
Q

There is higher risk of developing of CTE for those with ApoE genotype?
A. True
B. False

A

A. True

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22
Q

what are the characteristics of dementia pugilistic/ boxing dementia?

A
  • slurred speech (temporal lobe is affected)
  • memory impairment and Parkinson like syndrome
  • also called as punch drunk syndrome
  • thought to be similar to CTE
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23
Q

what are the structural changes in brain in healthy and TBI/AD?

A

Healthy individuals - smoother surface of brain + chunkier gyrus
TBI/AD - gyrus and sulcus becomes prominent due to shrinkage of brain matter

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24
Q

what are the three stages for rate of cognitive decline?

A
  1. ageing only with no injury
  2. additive effects of age and injury
  3. synergetic effects of age and injury
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25
Q

what are the complex neurotoxic cascades after TBI secondary pathological insults?

A
  1. BBB disruption (due to disruption emotion)
  2. cerebral oedema
  3. ischemia (due to lack of oxygen)
  4. energy failure (due to lack of glucose)
  5. excitoxicity
  6. cell death cascade
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26
Q

what is the role of BBB?

A

astrocytes + capillary

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27
Q

what are the types of glia cell found in CNS and PNS?

A 
CNS - 
1. ependymyal cells 
2. oligodendrocytes 
3. astrocytes 
4. microglia 
PNS - 
1. satellite cells 
2. Schwann cells
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28
Q

what is the gliovascular complex?

A
  • BBB + astrocytes surrounding it and the receptors that go within that membrane TGBF, NTs
  • Microglia is surrounding the gliovascular
  • microglia decides what goes in and out
  • In TBI whole complex gets disrupted
  • The endothelial cells which shear apart for exposing areas that come in and out
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29
Q

what is astrogliosis?

A
  • it is the abnormal increase in the number of astrocytes due to destruction of astrocytes
  • Healthy astrocytes will turn into reactive astrocyte
  • proliferate, migrate to point of injury and release cytokines and cytotoxins and form the glial scar
  • load of astrocytes in the affected injury area and more of toxins are secreted as well
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30
Q

what are the insults that induces astrogliosis?

A
  1. IL-1beta
  2. TNF-alpha
  3. ROS
  4. oxidative stress
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31
Q

which gene is responsible for the astrocytes proliferation and migration?

A

astrocyte elevated gene -1

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32
Q

outline the steps of astrogliosis

A
  1. release of inflammatory cytokines like IL-1beta, TNF-alpha and ROS due to oxidative stress due to mild/severe tissue damage and cell death
  2. the release of this mediators activate healthy astrocytes into reactive astrogliosis
  3. injurer increases AEG-1 localisation to cytoplasm and nucleus of astrocytes
  4. the change is localisation of AEG-1 in astrocytes results in in increased proliferation and migration during reactive astrogliosis
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33
Q

what are the causes of destruction of neurons in astrogliosis?

A

CNS trauma, infection, neurodegenerative, injury etc

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34
Q

what is microgliosis?

A

increase in activated microglia at the site of lesion (injury)

35
Q

outline the steps involved in microgliosis

A
  1. resting microglia - surveying function
  2. after TBI -> chemokine produced which attracts peripheral monocyte to CNS
  3. microglia upregulates M1 and M2 cytokines, phagocytic and rod microglia and surface markers
36
Q

what is the role of microglia in resting conditions?

A

Microglia in their resting state are constantly surveying the environment and maintaining homeostasis

  • maintain synapses
  • immune surveillance
37
Q

what is the role of M1 and M2 in TBI

A

M1 - pro-inflammatory and neurotoxic

M2 - neuroprotective

38
Q

what are the downstream effects of M1 and M2 activation in TBI?

A

M1 - release of proinflmmatory cytokines like IL-1beta, TNF-alpha, CCL2, NADPH oxidase
M2 - up regulation of chitiniase and Arginase

39
Q

what is role of phagocytic and rod microglia?

A

phagocytic microglia/M1 - pro-inflammatory

rod microglia/M2 - protective in vitro

40
Q

what are structural definitions of phagocytic and rod microglia?

A

phagocytic microglia - amoeboid morphology, jellyfish phenotype
rod microglia - align with neuronal structures

41
Q

outline the evidence for microglial priming in TBI

A
  1. surveying microglia - at rest carrying outs usual function
  2. active microglia - astre TBI, microglia produce cytokines and chemokines
    3a. resolved - this immediate response resolves the inflammation and some microglia reign to their original activity
    3b. unresolved, primed - but some microglia develop a primed/ pro-inflammatory profile
  3. hyper activated - following a secondary insult (e.g. immune challenge) these primed microglia become hyperactive and produce amplified and prolonged pro-inflammatory response
42
Q

describe profile of each of these microglial forms in microglial priming

  1. surveying
  2. activated
  3. primed
  4. hyper-activated
A
  1. surveying - immune surveillance
  2. activated - increased IL-1beta, TNF-alpha, CD14, CCL2, iNOS
  3. primed - increased MHCII + CD68
  4. hyper-activated - high expression of IL-1beta, TNF-alpha, CD14, iNOS
43
Q

monocytes convert into macrophages following TBI?
A. True
B. False

A

A. True

44
Q

activated microglia and arched macrophages are almost identical in which aspects following the conversion off monocytes to macrophages in TBI?

A
  1. morphology

2. cell surface markers

45
Q

what are the four types of animals of TBI?

A
  1. blast injury
  2. fluid percussion
  3. weight drop injury
  4. controlled cortical impact injury
46
Q

what are the features of controlled cortical impact (CCI) model?

A
  1. easily reproducible
  2. mimics conditions like
    a. concussion
    b. axonal injury
    c. BBB dysfunction
47
Q

how many model exist in weight drop injury model?

A
  1. marmarou’s

2. shohami’s

48
Q

what is the difference between marmarou’s and shohami’s weight drop model?

A

marmarou’s - metal disk placed over skull prevents bone fracture from the weight drop, model is mainly associated with diffuse injury
shohami’s - weight drop delivered to one side of unprotected skull, model is mainly associated with focal injury

49
Q

what is marmarou’s and shohami’s model mainly associated with?

A
  1. marmarou’s - diffuse injury (general concussion like car crash)
  2. shohami’s - focal point injury
50
Q

what are the features of FPI model?

A
  1. can mimic clinical TBIs without skull fracture

2. present pathophysiological features like brain swelling and intracranial haemorrhage

51
Q

what are the features of blast injury model?

A
  1. ideal for investigating how blast waves affect brain by inducing mainly diffuse injuries
    e. g. military personnel exposed to blast often suffer from tBIs even without external injuries
52
Q

what are imaging techniques of glia and TBI?

A
  1. 2 photon imaging?
53
Q

what is the diagnosis for TBI?

A
  1. optical coherence tomography for retina variation
54
Q 
what happens to brain during concussion? 
A. axonal injury 
B. tearing and shearing 
C. bouncing 
D. neuronal death 
E. fracture
A

A. axonal injury
B. tearing and shearing
the tearing and shearing causes axonal injury affecting the white matter

55
Q

what is the cause of CTE?

A

repetitive mild traumatic brain injury

56
Q

who is most likely to get affected with CTE?

A

athletes, contact sports scubas boxing, football, ice hockey, military veterans, victims of domestic abuse, headbangers

57
Q

what are the CTE symptoms?

A

memory loss, depression, suicidal thoughts, explosive or aggressive behaviour and in some cases trouble walking or speaking

58
Q

what is the pathology of CTE?

A
  1. tau protein tangles accumulation in brain’s cortex

2. tau collection around blood vessels and deep in cortical sulci of brain

59
Q

what are the structural changes of brain in CTE?

A

decreased volume due to neuronal and axonal loss

60
Q

which mouse models would you use for penetrating injury?

A
  1. weight drop injury model

2. blast injury model

61
Q

which mouse model would you use for diffuse/blunt injury?

A
  1. fluid percussion
62
Q

how many types of microglia are present based on

a. location
b. function and morphology

A

a. location - two
1. ramified/branching/outward projections
1. bipolar /rod shaped
b. structure and morphology
1. ramified
2. bipolar/rod shaped
3. amoeboid

63
Q

what are the characteristics of ramified microglia?

A
  1. numerous processes with filopodia like protrusions
  2. acts as surveillance cells to main homeostasis of neuronal microenvironment
  3. directly remove dysfunctional synaptic terminals to main neuronal integrity of neuronal circuitry
64
Q

what are the characteristics of bipolar/rod shaped microglia?

A
  1. elongates cell bodies with processes extending towards the two ends
  2. from end to end alignments adjacent to neuronal processes
  3. phagocytic in nature, involves the internalisation of degenerating neurones after CNS injury
  4. potentially involved in neuronal reorganisation via synaptic stripping
65
Q

what is synaptic stripping?

A

the removal of dysfunctional synapses by activated microglia in a pathological event

66
Q

what are the characteristics of amoeboid microglia?

A
  1. highly motile with fewer or no processes
  2. involved in the degradation of extracellular laminin
  3. phagocytic in nature, clears cell debris and extracellular protein aggregates like beta amyloid and alpha syncuelin
  4. secrete neurotoxic factors like IL-1B,TNFalpha,NO etc which induce neuronal cell death.
67
Q

when does bipolar/rod shaped microglia convert into amoeboid microglia?

A

lipopolysaccharide (LPS) activation

68
Q

what are the conversional stages in microglial morphologies?

A
  1. ramified can covert into bipolar/rod shaped or amoeboid depending on the type of stimulus
  2. bipolar/rod shaped can covert into amoeboid with LPS activation + chronic activation of microglia in later stages of ND diseases
69
Q

which are the essential cytokines released in M1 and M2 state of microglia and its downstream effects?

A

M1 - pro-inflmmatory: IL-1beta, TNF-alpha, IFN-gamma, LPS -> immune cell infiltration + neuronal damage
M2 - anti inflammatory: IL-4, IL-13 -> resolution of inflammation + neurotropic factors

70
Q

which are three activation pathways in microglia?

A
  1. classical activation - resting to activated microglia via M1 polarisation
  2. alternative activation - resting to activated microglia via M2 polarisation
  3. M1 to M2 state via cytokines release
71
Q

how many types of microglia are present in the inflammatory immune cascade?

A
  1. resting - M0
  2. classical M1
  3. alternative M2 - M2a, M2b, M2c, M2d
72
Q

which of the microglia phenotype are present in

  1. anti-inflammatory/repair
  2. pro-inflammatory
  3. would healing/angiogenesis
A
  1. anti-inflammatory/repair - M0, M2a (IL-4/IL-13), M2b (LPS/IC), M2c (IL-10/GlcH)
  2. pro-inflammatory - M1 (LPS/IFN-gamma/TNF)
  3. would healing/angiogenesis - M2d (A2AR agonist)
73
Q

what is DAM and what is its function?

A
  • DAM - disease associated microglia, a new protective microglia
74
Q

how does DAM acquire its neuroprotective role?

A
  • due to TREM2 molecule
75
Q

what is the cellular response of reactive microgliosis?

A

negative and progressive response

76
Q

how does the scar formation inhibit axon regeneration?

A
  • via NG2 glia (polydensrocytes/precursor of oligodendrocytes)
  • inhibit axon regeneration by
    1. inhibiting NG2 proteoglycan expression
    2. forming synaptic contacts
77
Q

what are the hallmarks of astrocyte reactivity?

A

1, increased homeostatic and trophic conditions

  1. proliferation
  2. migration
  3. secretory activity
  4. glial scar formation and BBB repair
78
Q

Which of the following radioligand would give an indication of microglia activity in vivo using PET imaging?

  1. S100β
  2. Tau
  3. TSPO
  4. GFAP
  5. Microglasis
A
  1. TSPO (traslocator protein)

GFAP and S100B are astrocyte markers

79
Q

what is the aim of therapeutic targets for TBI?

A
  1. to ameliorate/inhibit the pro-inflammatory M1 like response
  2. promote the anti-inflammatory M2 like positive tissue remodelling
80
Q

what are the some clinical examples for therapeutic targets?

A
  1. minocycline targeting microglia after TBI
  2. lipid lowering drugs for immunomodulation
  3. HDAC inhibitors
81
Q

what is the role of HDAC and its inhibitor for TBI?

A

Role of HDAC - remove acetyl group, tighter DNA wrapping around histones, suppressing gene transcription
Role of HDAC inhibitors - activate gene transcription

82
Q

what are the anatomical changes after the application of HDAC inhibitors?

A

Both grey matter and white matter tracts are significantly preserved by HDAC inhibition after TBI

83
Q

what are the genetic biomarkers for prediction of vulnerability to TBI?

A

BDNF, ApoE and TREM2

84
Q

briefly explain the microglial shift in TBI

A
  1. In normal healthy CNS, most of the microglia are displayed as ramified microglia.
  2. In response to the change in the microenvironment, the ramified microglia undergo rapid transformation into bipolar/rod-shaped microglia or amoeboid microglia depending on the types of stimulus.
  3. Bipolar/rod-shaped microglia can quickly transform into amoeboid microglia in response to lipopolysaccharide (LPS) activation.
  4. The amoeboid microglia transformed from bipolar/rod-shaped microglia secrete pro-inflammatory cytokines and degrade extracellular laminin.

TMS (10 decks)

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