Traumatic Brain Injury And Neuroinflammation Flashcards Preview

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Flashcards in Traumatic Brain Injury And Neuroinflammation Deck (57)
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1
Q

Traumatic Brain injury

A

Injury to the brain caused by a trauma to the head, Not of degenerative or congenital of nature requires external physical force.

2
Q

Frontal for healthy and injured brain

A

Concentration, Problem Solving, Speech
TBI
Lack of focus, irritability, language difficultly

3
Q

Parietal for healthy and injured brain

A

Sense of touch, Pain, Temperature
TBI
Difficulty with reading, spatial misperception

4
Q

Occipital for healthy and injured brain

A

Healthy vision
TBI
Blind spots, blurred vision

5
Q

Temporal Healthy and injured brain

A

memory and organisation
TBI
Problems with short-& long-term memory

6
Q

Cerebellum Healthy and injured brain

A

Balence & coordination
TBI
Difficulty walking, Slurred speech

7
Q

Brainstem

A

Breathing, steady heart rate
TBI
Changes in breath, difficulty swallowing

8
Q

Open head injury

A

penetrating injury in the head

9
Q

Closed head injury

A

Blunt injury to the head

Concussion or contusion

10
Q

Coup

A

The region where the head is hit.

11
Q

Contra-Coup

A

After you hit you head and then the brain hits again from the fall back if its a hard hit.

12
Q

Subdural haematoma

A

Bleeding under the dura matter

13
Q

White matter injury

A

Axonal damage - twisting and tearing of the brain inside the skull

14
Q

Secondary damage

A

Changes in blood flow, oxygen levels, glucose levels change and excitotoxic cell damage (inflammation)

15
Q

The leaky brain

A
Cascade of neurochemical events 
- Glutamate 
- Chloride 
- Potassium and sodium 
Swelling and inflammation from tissue damage
16
Q

The swelling of the brain

A

Craniotomy release the pressure,

Ice slows down the swelling.

17
Q

X-ray

A

See if there is any fractures in the skull

18
Q

CT scan

A

Something looks abnormal then they will go for an MRI

19
Q

MRI

A

Expensive to get an MRI

20
Q

EEG

A

Electrical waves - memories or recall, not the first port of call, secondary

21
Q

PET (positron Emission Tomography)

A

It is big and expensive

22
Q

DTI (Diffusion Tensor Imaging)

A

It can image the axons, there will be more blackened areas if there is damage to the axons

23
Q

Second impact syndrome

A
  • Rare but potentially serious
  • Life-threatening condition
  • Results in a loss of auto-regulation of the blood supply
    -Vascular engorgment
    -Increased intracranial pressure
    Rapid brain stem failure.
24
Q

Second impact syndrome is caused by

A

A second injury in which the brain swells uncontrollably, chemical flood it damaging the cells, with rest the brain can heal, but if there is no time for the brain to heal, there can be permanent brain damage.

25
Q

Chronic Traumatic Encephalopathy

A

Progressive degenerative brain disease, causing aggression and lack of impulse control.
Depends on the make up, if they have a ApoE are at a higher risk for having the disease.

26
Q

How is Chronic Traumatic Encephalopathy caused?

A

Caused by repetitive hits to the head, they know about Tal in the brain and the amount meaning they will have the disease, they are currently looking at how to diagnose living people.

27
Q

Dementia Pugilistica

A

Associated with slurred speech, memory impairment and Parkin-like syndrome
Thought to be the same as CTE.

28
Q

Gliovascular complex

A

Is formed around the BBB

29
Q

Different types of glia

A
Ependymal cells 
Oligodendrocytes 
Satellite cells 
Astrocytes
Microglia 
Swann cells
30
Q

Astrogliosis

A

Healthy astrocyte which is activated, turns reactive, (the cytokines being released) causing massive proliferation of these cells, they migrate to the site of injury. Its starts to surround the gliovascular componant and block anything from coming in. (glial scar)

31
Q

What are the immune cells of the brain

A

Monocyte that can go through the blood brain barrier.

Microglia can be ramified or rod microglia.

32
Q

What is microglial priming?

A

Staying in M1 state constantly, releasing loads of cytokines and if it can’t be stopped it becomes Hyper-activated microglia, which is what happens in dementia

33
Q

M1 - M2 - M1

Ramified state to an ameboid state

A

Activated because of brain injury is M1- Damage sensing PR profile change branch outgrowth
M2- Reactive markers branch withdrawal
M1- Phagocytosis, phagoptosis ameboid
M2 is trying to counteract what is happening with M1 state,
M2 is trying to get it back into its normal ramified state

34
Q

Marmarous weight drop model

A

Global traumatic injury effect

35
Q

What to consider when picking a TBI Model?

A

Controlled Cortical Impact Injury Model

36
Q

Shohamis weight drop model

A

Focal weight top, to look at it more focussed.

37
Q

Fluid percussion injury models

A

Inject fluid into brain, measure the pressure on the brain and skull and look at the damage occured after that.

38
Q

Blast Injury Models

A

Near an explosion, simulate the blast as it can affect the brain.

39
Q

Oligodendrocytes

A

It is a type of glia which synthesises myelin in the CNS

40
Q

Astrocytes

A

Supply metabolic fuel, as lactic acid to neurones, they also synthesis neurotransmitters, secrete trophic factors that promote neuronal survival, modulate cerebral blood flow and help maintain the brain extracellular K+ concentration.

41
Q

Ependymal

A

Type of glia which lines the ventricles in the brain and central canal of the spinal cord, they have cilia that beat influencing a flow of CSF, they are responsible for the formation of the blood-cerebrospinal fluid barrier.

42
Q

Microglia

A

Type of glia which proliferate following neuronal injury and serve as scavengers to remove cellular debris.

43
Q

What is the leading cause of TBI?

A

Falling

44
Q

Who can suffer from TBI?

A

Everybody

45
Q

Which one of the following is an acquired brain injury?

A

Meningitis - acquired brain injury means not due to a direct hit, something that the brain gets from an inflammatory response/ could also be a stroke for example

46
Q

Which of the following cells are glia in the CNS?

A

Ependymal cells

Astrocytes and the microglia.

47
Q

What are the symptoms of a concussion?

A
Sadness (underlying changes in the frontal lobe)
Balance problems (temporal lobe is affected 
Sleeping more or less than usual and memory loss. Dependent of severity.
48
Q
Which is NOT an example of an experience TBI? 
Blast injury 
Controlled cortical impact 
Cervical dislocation 
Weight drop 
Fluid percussion impact
A

Cervical distortion, - this is the way an animal get uthanised in the lab, this would be a severe traumatic brain injury, but is not a model of one.

49
Q

Is TBI a grey or white matter loss?

A

The tearing sheering of the axons in the white matter, so it is classified as a white matter loss but the damage of the inflammation is inflicted on the grey matter.

50
Q

What is controlled cortical impact model looking at?

A

is a model looking at the focal point that we want to investigate.

51
Q

What is the Blast injury model looking at?

A

The blast injury having impact on the brain, like they would have in soldiers

52
Q

What is weight drop model?

A

It investigated overall impact to the brain.

53
Q

What is fluid percussion impact?

A

Investigating for example sub-dural hematomas/meningitis , investigating the pressure and fluid under the skull.

54
Q

Symptoms: memory loss, depression, suicidal thoughts, explosive or aggressive behaviour, they play football and have had repetitive mild traumatic brain injury.
What is the cause?

A

Chronic Traumatisch Encephalopathy
There is no treatment.
Pathology: Tau protein tangles first accumulate in the brains cortex. Tau collects around blood vessels and in deep cortical sulk of the brain.
Other symptoms include; Troubles walking or talking.

55
Q

What are the diffuse injury?

A

Blunt head trauma
Blast injury
Diffuse axonal activation without focal cell death

56
Q

What are the penetrating/focal injury/

A

Skull fracture
Foreign body
Focal lesion of cell necrosis, leukocyte infiltration, gliosis

57
Q

What models would you look at for diffuse injury?

A

Blast injury model

Fluid percussion injuries