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TMS exam > 7 - traumatic brain injury and neuroinflammation > Flashcards

7 - traumatic brain injury and neuroinflammation Flashcards

1
Q

what does TBI stand for

A

traumatic brain injury

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2
Q

define TBI

A

injury to the brain caused by trauma to the head
not of degenerative or congenital nature
commonly requires external force

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3
Q

effects when frontal cortex affected by TBI

A

lack of focus/concentration
irritability
speech/language difficulty

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4
Q

effects when parietal lobe affected by TBI

A

difficulty with reading
spatial misperception
loss of sense of touch/pain/temperature

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5
Q

effects when occipital lobe affected by TBI

A

blind spots and blurred vision

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6
Q

effects when temporal lobe affected by TBI

A

problems with long and short term memory

hearing difficulties

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7
Q

if TBI causes difficulty walking, lack of balance and slurred speech which area has been affected

A

cerebellum

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8
Q

if TBI causes changes in breathing patterns and difficulty swallowing, which area has been affected?

A

brainstem

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9
Q

2 categories of traumatic head injury

A

open head injury

closed head injury

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10
Q

features of open head injury

A

penetration into the skull
–> dura mater (outer meninges layer) is breached

severity dependent on areas affected
–> fatal if brainstem, both hemispheres, ventricles or multiple lobes are damaged

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11
Q

example of open head injury

A

gun shot wound

knife stab

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12
Q

features of closed head injury

A

hit with a blunt object
local impact onto skull

(skull/dura mater remain intact)

skull impacts nerve tissue

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13
Q

coup injury

A

injury occurs under first impact point

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14
Q

contrecoup injury

A

injury occurs on the side opposite the area that was hit

can lead to subdural haematomas

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15
Q

motor-action caused by closed head injury

A

back and forth/rotational motion within the skull

bleeding, tearing and sheering in the brain

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16
Q

subdural haematoma

A

collection of blood outside the brain

bleeding under the dura mater (between cortex and axons)

causes increased pressure on the brain

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17
Q

white matter injury

A

axonal damage

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18
Q

secondary damage caused by closed head ijnury

A 
leakage of neurotransmitters
lack of glucose to the brain
changes in blood flow and oxygen levels
 --> excitotoxic events
--> inflammation
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19
Q

examples of closed heady injury

A

hitting head when falling over

–> causes concussion or can lead to stroke

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20
Q

neurotransmitters involved in neurotoxic cascade

A

glutamate
Cl-
K+
Na+

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21
Q

changes in the brain due to CTE

A

large ventricles affected
loss of matter
gyri become chunkier and more prominent

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22
Q

common name for dementia pugilistica

A

boxing dementia

punch drunk syndrome

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23
Q

features of dementia pugilistica

A

progressive symptoms
slurred speech
memory impairment

similar to CTE

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24
Q

chronic traumatic encephalopathy (CTE)

A

progressive condition
caused by repeated hits to the head
involves memory loss and lack of concentration

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25
Q

subtype of CTE

A

dementia puglistica

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26
Q

secondary impact syndrome (SIS)

A

rare
life-threatening
caused by consecutive concussion
leads to loss of auto-regulation of the blood supply

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27
Q

why does SIS cause lack of blood supply control

A

damage to blood vessels is exacerbated at second impact
rapid brain stem failure
vascular engorgement
increased intracranial pressure

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28
Q

proteins underlying risk of developing CTE

A

Tau protein is excessively hyperphosphorylated

Apolipoprotein E

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29
Q

why did the american footballer die of SIS

A

he had two head impacts in quick succession (knee to the head then impact to his chin)
he then collapsed as his cells didnt have time to repair and left permanent damage

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30
Q

pathological effects of the neurotoxic cascade after secondary TBI

A 
Blood brain barrier disruption
cell death cascade
excitotoxicity
energy failure --> lack of glucose
ischemia --> lack of oxygen 
cerebral oedema
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31
Q

features of the BBB

A

tight junctions formed between endothelial cells
only allows water, oxygen and lipid soluble proteins to move through
–> restricts immune cell migration

surrounded by pericytes and glial cells

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32
Q

importance of pericytes for BBB maintenance

A

monitor nutrient load across membrane

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33
Q

role of glial cells for BBB maintenance

A

surround and support complex
(astrocytes and microglia)

help make CSF
help prevent immune cell migration

34
Q

role of glia in CNS

A

responsible for monitoring metabolsim and maintenance

make up 70%

35
Q

which glia are in CNS

A

ependymal cells
astrocytes
oligodendrocytes
microglia

36
Q

which glia are in PNS

A

schwann cells

satellite cells

37
Q

what is the gliovascular complex

A

made up of the BBB and the astrocytes surrounding it and their receptors

interface between brain vessels and astrocytes

ensures sufficient blood supply to brain regions

38
Q

effect of TBI on endothelial tight junctions

A

tight junctions become sheered apart

brain exposed to other neurotransmitters

39
Q

astrogliosis

A

response to CNS insult
astrocytes become “reactive” after injury
abnormal increase in number of astrocytes due to destruction of nearby neurons

40
Q

overall effects of astrogliosis

A

increased proliferation and migration of astrocytes towards point of injury
secretion of cytokines and cytotoxins
glial scar formation

41
Q

immune cells of the brain

A

microglia

monocytes

42
Q

role of monocytes in acute brain injury

A

get through BBB and become active

43
Q

overall functions of microglia polarisation states

A

M1: neurotoxic and pro-inflammatory
M2: neuroprotective

44
Q

microgliosis

A

the process of microglia becoming “reactive”

excessive production of microglia

45
Q

microglia receptor enhanced in inflammatory states

A

TREM2

46
Q

why do microglia need to remain active for quite a while

A

ratio of M1/M2 important for brain homeostasis

enhanced inflammatory response within the brain to cope with neurotoxic cascade

47
Q

how do microglia remain active

A

secrete more cytokines and interleukins

48
Q

overall effects of neuroinflammation

A

microglia activated
glial scar formation
immunotoxicity

49
Q

when is TBI acquired

A

after birth

50
Q

symptoms of concussion

A

sadness
balance problems
sleeping more/less than usual
memory loss

51
Q

axonal injury

A

white matter injury
caused by tearing and shearing
result of acceleration and rotation of the brain

52
Q

how does axonal injury result in neuronal death of grey matter

A

cells are engulfed by cytotoxins released by tearing

53
Q

symptoms of CTE

A 
memory loss
depression
suicidal thoughts
explosive or aggressive behaviour
trouble walking or speaking
54
Q

which groups of people commonly suffer from CTE

A

athletes in contact sports (boxing, american football)
military veterans
victims of domestic abuse

55
Q

role of Tau in CTE

A

protein becomes tangled and accumulates

Tau collects around blood vessels and deep into the sulci of brain cortex

56
Q

what is a NG2 glia cell

A

oligodendrocyte precursor cell

57
Q

function of NG2 glia

A

actively secrete proteoglycans and form synaptic contacts

inhibit further development of axons
prevent axon regeneration

58
Q

what is a glial scar

A

structural formation of reactive glia around an area of severe tissue damage

59
Q

hallmarks of astrocyte reactivity

A 
increased homeostatic and trophic functions
secretory activity
proliferation 
migration 
glial scar formation
BBB repair
60
Q

extracellular hallmark of glial scar formation and BBB repair

A

variety of different cell types line up around damaged area

61
Q

intracellular hallmark of glial scar formation and BBB repair

A

NF-kB signalling

dictates M1 or M2 polarisation depending on cytokines secreted by astrocytes

62
Q

3 main events occuring in glial scar development

A
  1. BBB leakage
  2. increase in numbers of microglia
  3. neurogenesis
63
Q

importance in rebuilding of blood vessels after injury

A

allows healing of vascular leakage of the meninges

64
Q

definition of BBB

A

semipermeable membrane separating blood from the CSF

prevents harmful substances reaching brain while still allowing passage of nutrients

65
Q

what features of the CNS environment make it unique

A
  • different ionic composition for neuronal function
  • specialized neurotransmitter pool
  • low protein concentration, to minimizecell proliferation
  • low exposure to systemic toxins, to minimize neuronal damage
  • reduced traffic ofinflammatory cellsand molecules, to
    minimize local inflammation.
66
Q

effect of cytokines on BBB

A

cytokines are secreted by cells of the CNS (e.g. BBB endothelium) in response to trauma or inflammation

increase its permeability by re-organising actin cytoskeleton

act as chemotactic agents recruiting more immune cells which increases inflammation

67
Q

why are adhesion molecules important

A

for adherence of leukocytes to the brain endothelium

cytokines can increase production of adhesion molecules

68
Q

what is connexin 43 (cx43)

A

immuno-regulating factor

- a gap junction protein highly expressed by astrocytes at the BBB interface

69
Q

absence of astroglial cx43

A

endothelial activation and immune cell recruitment

70
Q

morphological changes to astrocytes after injury

A

extend their processes to form a dense web to fill the empty space left by dead neurons (astrogliosis)
produce more GFAP

71
Q

molecules secreted during astrocyte proliferation

A

lamins

proteoglycans

72
Q

microglia expression of molecules dependent on location

A

the closer the microglia are to the site of injury, the more they express the biologically active molecules

73
Q

role of microglia in immune function

A

sensitive to stimuli due to K+ channels
survey CNS for plaques, damaged neurons and pathogens
initial responders and initiate inflammation
remove damaged cells by phagocytosis

74
Q

microglia state under healthy/normal conditions

A

maintained in immunosuppressed ‘resting’ state due to inhibitory signalling from cell-surface and soluble ligands from surrounding neurons

contribute to brain homeostasis by remodelling synapses, monitoring neural firing and surveillance of the environment for pathogens

75
Q

microglia activation upon brain insult

A

detect PAMPs such as LPS or IFN-y from a bacterial cell wall which activate PRRs
- inhibitory signalling is removed
- microglia retract their processes and transform into an amoeboid shape
- recognised and engulf pathogens and present antigens
(antibodies are too big to cross BBB)
- adopt one of their two possible phenotypes
- secrete cytokines, bioactive lipids, coagulation factors, ROS and neurotrophic factors
- try to break down plaque build-up of proteins
- contribute to glial scar formation

76
Q

why is glial scar formation important

A

for repair of the BBB and revascularisation the blood capillaries

77
Q

microglia plasticity

A

ability to change phenotype depending on local conditions or environment –> necessary to
perform the large variety of functions

78
Q

acute neuroinflammation

A

Characterised by rapid activation of microglia

No peripheral immune damage/response

79
Q

chronic neuroinflammation

A

Microglia continually activated by pro-inflammatory stimuli

Continuous production of pro-inflammatory cytokines and ROS
–> ROS recruit peripheral cells to contribute to immune response

Neuronal death
–>Degradation of tissue and BBB

80
Q

effects of volume loss of brain matter

A

Damage to neurons restricts communication within and between different brain
areas
- Most abilities result from the cooperative action of multiple brain regions

81
Q

role of oligodendrocytes

A

support nerves and axons

produce myelin sheath for axon insulation

TMS exam (22 decks)

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