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Trauma Sciences > Neurotrauma Science > Flashcards

Neurotrauma Science Flashcards

1
Q

Define anterograde axonal cargo

A

Movement towards synapse -> replaces cell membrane and synaptic/vesicular proteins,

Small vesiculotubular structures, neurtransmitters, membrane proteins and lipids

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2
Q

Define retraction balls

A

Aka axonal balls: are axonal swellings depicted with amyloid precursor protein staining
Pathological hallmark of DAI.

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3
Q

Define periodic varicosities

A

Periodic swellings along axon?

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4
Q

Define Amyloid plaques

A

Amyloid precursor protein (APP) is an integral trans-membrane protein

Becomes amyloid fibrillary form (oligomer/misfolded) when lysed to form amyloid plaques: toxic

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5
Q

Define Wallerian degeneration

A

Programmed axonal death: fundamental intrinsic death process of axons: active cell autonomous death pathway.

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6
Q

Define Calpain and what does it do?

A

Non-lysosomal calcium dependent protease

degrades cytostructural components like spectrin, microtubules and MAP, neurofilaments as well as voltage gated sodium channels - responsible for acute axonal degeneration, limited to area near transection site

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7
Q

Pathophysiology of Alzheimer’s?

A

Amyloid plaques

(These oligomers can ‘seed’ and induce other Aβ molecules to take on these abnormal forms (prion like chain reaction)

Neurofibrillary tangles
Amyloid or tau hypothesis?

(varicosities and microglial activation)

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8
Q

What is the process of Wallerian degeneration?

A

Absence of NMNAT2 (which converts NMN into NAD) -> rise in NMN and decrease in NAD -> sarmoptosis (increase in death molecule: SARM1)

Active dismantling/dying back

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9
Q

Define axon

A

Primary protoplasmic protrusion of a neuron.

Carries action potentials away from cell body.

Other protoplasmic protrusion is a neurite.

Shape and function determines the difference

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10
Q

Define retrograde axonal transport

A

Towards cell body; membrane is recycled

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11
Q

Cells in the brain?

A

Neurons, astrocytes, microglia and oligodendricytes

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12
Q

How differentiate between axon and dendrite?

A

Axon is larger, doesn’t taper, direction of flow is away from cell body not towards.

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13
Q

What are the 3 important structural polymers in cells/axons?

A

Microfilaments/ actin filaments
Intermediate filaments/ neurofilaments
Microtubules

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14
Q

What do microfilaments do?

A

Made of actin.
Actin: important in dendrites/axon growth

Have a + growing end and myosin motors that use ATP hydrolysis to move

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15
Q

What do neurofilaments do?

A

Structural matrix that embeds microtubules

Very tough - left when dissolve a cell
No motor
Maintain flexibility and strength

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16
Q

What do microtubules do?

A

Tubular heterdimer

Strongest, complex, spiral cylinder w positive charge on leading edge -> directional charge allows it to be used as a railroad for motor proteins (inc vesicles and mitochondria, mRNA). Holds a reliable shape

Hollow - so can bend without breaking

17
Q

What is true of microtubules in dendrites but not axons?

A

Microtubules are bidirectional in dendrites but not axons

18
Q

What do neurofilaments do?

A

Structural matrix that embeds microtubules
main structural support (has been used as a marker for injury)

Very tough - left when dissolve a cell
No motor
Maintain flexibility and strength

19
Q

What do microtubules do?

A

Tubular heterdimer

Strongest, complex, spiral cylinder w positive charge on leading edge -> directional charge allows it to be used as a railroad for motor proteins (inc vesicles and mitochondria, mRNA). Holds a reliable shape

AKA: transport

Hollow - so can bend without breaking

20
Q

What carries APP?

A

Kinesin1

21
Q

Types of diffuse traumatic brain injury?

A

Blast, concussion, diffuse axonal injury and abusive head trauma/shaken baby syndrome

22
Q

Focal traumatic brain injury?

A

Contusion
Penetratin
Haematoma - epidural, subdural, intracerebral, intraventricular, subarachnoid

23
Q

Mechanism/pathophysiologoy of DAI

A

High velocity shearing injury from rapid acceleration/deceleration

More coma than concussion, i.e. LOC from moment of head injury. Never walk -> DAI. Only from instant impact.

24
Q

Common DAI mechanisms?

A

Common mechanisms: RTA/fall from height/blast injury

Boxers don’t get DAI: focal injuries, not enough force.

25
Q

Where are duret’s haemorrhages?

A

Brainstem

26
Q

What was the theory behind DAI? And what is it now?

A

Theory was that shearing strains - > snap axons -> cell wall breakdown -> electrolyte imbalances?
When look histopathology: very rare to snap axons, they are quite elastic. Instead, axons stretch and recoil -> leads to dysfunction.

27
Q

What is the blue-tack analogy?

A

Snapping: microtubules, ie train tracks -all cargo falls off (bulging ), repair: undulating process; reform and axon relaxes.
Not the same as primary axotomy: explaining the stretching damage (micro tubular fracture?)

28
Q

Why get LOC?

A

Brainstem - reticular formation damage OR through diffuse cortical injury

29
Q

What happens in primary axotomy?

A

influx of calcium through holes etc -> ROS/calpain/apoptosis.
Calpain is responsible for acute axonal degeneration, but limited to near injury

30
Q

No primary axotomy/macroscopic structural lesion in DAI - why functional impairment?

A

Neuronal death
Axonal disconnection & synaptic loss
Disorders of functional connectivity ‘network issues’

31
Q

Acute axonal degeneration?

A

Mechanoporation - calcium influx, energy failure, ROS, calpaan (and other proteolytic enzymes)

32
Q

Macroglia and phagocytosis - discuss

A

Microglia can engulf and destroy a whole neuron in minutes – primary phagocytosis or phagoptosis (eaten alive)
Their role after WD is slower and can take weeks to ‘clear up’ debris – secondary phagocytosis (eaten dead).
Partially mediated by astrocytes.

33
Q

Eat me signals:

A

Phosphatidylserine, complement etc. Related ‘opsonins’ mediate binding

34
Q

Some explanations of TBI/dementia

A

Single event sufficient
Chronic microglial activation
White matter degeneration.

A single traumatic brain injury is associated with an increased risk of dementia and, in a proportion of patients surviving a year or more from injury, the development of hallmark Alzheimer’s disease-like pathologies

Persistent inflammation and ongoing white matter degeneration for many years after just a single traumatic brain injury in humans

35
Q

Brain trauma and Alzhirmer’s

A

Brain pathology after single severe TBI is similar to early amyloid pathology in AD
Increased brain concentrations of soluble amyloid-β42 (Aβ42) peptides
Deposition of diffuse (not neuritic) Aβ plaques in brain tissue in approximately 30% of patients with severe TBI
Amyloid deposition post TBI is supported by PET imaging studies
Repetitive TBI can produce tauopathy (NFT and neuropil threads) with or without amyloidosis

Trauma Sciences (10 decks)

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