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

7 - traumatic brain injury and neuroinflammation Flashcards

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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
subtype of CTE
dementia puglistica
26
secondary impact syndrome (SIS)
rare life-threatening caused by consecutive concussion leads to loss of auto-regulation of the blood supply
27
why does SIS cause lack of blood supply control
damage to blood vessels is exacerbated at second impact rapid brain stem failure vascular engorgement increased intracranial pressure
28
proteins underlying risk of developing CTE
Tau protein is excessively hyperphosphorylated Apolipoprotein E
29
why did the american footballer die of SIS
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
30
pathological effects of the neurotoxic cascade after secondary TBI
``` Blood brain barrier disruption cell death cascade excitotoxicity energy failure --> lack of glucose ischemia --> lack of oxygen cerebral oedema ```
31
features of the BBB
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
32
importance of pericytes for BBB maintenance
monitor nutrient load across membrane
33
role of glial cells for BBB maintenance
surround and support complex (astrocytes and microglia) help make CSF help prevent immune cell migration
34
role of glia in CNS
responsible for monitoring metabolsim and maintenance | make up 70%
35
which glia are in CNS
ependymal cells astrocytes oligodendrocytes microglia
36
which glia are in PNS
schwann cells | satellite cells
37
what is the gliovascular complex
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
effect of TBI on endothelial tight junctions
tight junctions become sheered apart | brain exposed to other neurotransmitters
39
astrogliosis
response to CNS insult astrocytes become "reactive" after injury abnormal increase in number of astrocytes due to destruction of nearby neurons
40
overall effects of astrogliosis
increased proliferation and migration of astrocytes towards point of injury secretion of cytokines and cytotoxins glial scar formation
41
immune cells of the brain
microglia | monocytes
42
role of monocytes in acute brain injury
get through BBB and become active
43
overall functions of microglia polarisation states
M1: neurotoxic and pro-inflammatory M2: neuroprotective
44
microgliosis
the process of microglia becoming "reactive" | excessive production of microglia
45
microglia receptor enhanced in inflammatory states
TREM2
46
why do microglia need to remain active for quite a while
ratio of M1/M2 important for brain homeostasis | enhanced inflammatory response within the brain to cope with neurotoxic cascade
47
how do microglia remain active
secrete more cytokines and interleukins
48
overall effects of neuroinflammation
microglia activated glial scar formation immunotoxicity
49
when is TBI acquired
after birth
50
symptoms of concussion
sadness balance problems sleeping more/less than usual memory loss
51
axonal injury
white matter injury caused by tearing and shearing result of acceleration and rotation of the brain
52
how does axonal injury result in neuronal death of grey matter
cells are engulfed by cytotoxins released by tearing
53
symptoms of CTE
``` memory loss depression suicidal thoughts explosive or aggressive behaviour trouble walking or speaking ```
54
which groups of people commonly suffer from CTE
athletes in contact sports (boxing, american football) military veterans victims of domestic abuse
55
role of Tau in CTE
protein becomes tangled and accumulates Tau collects around blood vessels and deep into the sulci of brain cortex
56
what is a NG2 glia cell
oligodendrocyte precursor cell
57
function of NG2 glia
actively secrete proteoglycans and form synaptic contacts | inhibit further development of axons prevent axon regeneration
58
what is a glial scar
structural formation of reactive glia around an area of severe tissue damage
59
hallmarks of astrocyte reactivity
``` increased homeostatic and trophic functions secretory activity proliferation migration glial scar formation BBB repair ```
60
extracellular hallmark of glial scar formation and BBB repair
variety of different cell types line up around damaged area
61
intracellular hallmark of glial scar formation and BBB repair
NF-kB signalling | dictates M1 or M2 polarisation depending on cytokines secreted by astrocytes
62
3 main events occuring in glial scar development
1. BBB leakage 2. increase in numbers of microglia 3. neurogenesis
63
importance in rebuilding of blood vessels after injury
allows healing of vascular leakage of the meninges
64
definition of BBB
semipermeable membrane separating blood from the CSF | prevents harmful substances reaching brain while still allowing passage of nutrients
65
what features of the CNS environment make it unique
- different ionic composition for neuronal function - specialized neurotransmitter pool - low protein concentration, to minimize cell proliferation  - low exposure to systemic toxins, to minimize neuronal damage - reduced traffic of inflammatory cells and molecules, to minimize local inflammation.
66
effect of cytokines on BBB
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
why are adhesion molecules important
for adherence of leukocytes to the brain endothelium cytokines can increase production of adhesion molecules
68
what is connexin 43 (cx43)
immuno-regulating factor | - a gap junction protein highly expressed by astrocytes at the BBB interface
69
absence of astroglial cx43
endothelial activation and immune cell recruitment
70
morphological changes to astrocytes after injury
extend their processes to form a dense web to fill the empty space left by dead neurons (astrogliosis) produce more GFAP
71
molecules secreted during astrocyte proliferation
lamins | proteoglycans
72
microglia expression of molecules dependent on location
the closer the microglia are to the site of injury, the more they express the biologically active molecules
73
role of microglia in immune function
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
microglia state under healthy/normal conditions
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
microglia activation upon brain insult
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
why is glial scar formation important
for repair of the BBB and revascularisation the blood capillaries
77
microglia plasticity
ability to change phenotype depending on local conditions or environment --> necessary to perform the large variety of functions
78
acute neuroinflammation
Characterised by rapid activation of microglia | No peripheral immune damage/response
79
chronic neuroinflammation
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
effects of volume loss of brain matter
Damage to neurons restricts communication within and between different brain areas - Most abilities result from the cooperative action of multiple brain regions
81
role of oligodendrocytes
support nerves and axons | produce myelin sheath for axon insulation

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