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Advanced Neurosciences > PNS Injury And Resprouting > Flashcards

PNS Injury And Resprouting Flashcards

1
Q

What is anterograde transport?

A

Movement of the materials away from the cell body
(Same direction as signal propagation)

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2
Q

What is retrograde transport?

A

Movement of material towards the cell body

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3
Q

What factors influence axonal transport?

A

Neurotubules
Microtubules
Energy

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4
Q

Describe anterograde transport

A

Rapid transport carries mainly membrane bound materials such as plasma membrane proteins and synaptic vesicles
Slow transport carries soluble enzymes and structural proteins (tubulin)
Slow transport rate determines rate of recovery following peripheral nerve injury

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5
Q

Describe retrograde transport

A

It is slow - half that of anterograde
Important in regulating metabolism of the cell
When an axon is cut the signal to induce chromatolysis is carried by retrograde transport

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6
Q

What is the connection between retrograde transport and viruses?

A

Some neurotropic viruses
(Poliomyelitis, herepes, rabies, neurotoxins)
Enter peripheral nerve endings and ascend to infect the cell body via retrograde transport

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7
Q

What is focal demyelination?

A

Conduction block - part of neuropraxia
No axonal degeneration, caused by mild compression or traction to the nerve
(Carpel tunnel syndrome)

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8
Q

What are the classifications of nerve injuries?

A

1st degree - neurapraxia
2nd degree - axonotmesis
3rd degree - axonotmesis
4th degree - axonotmesis
5th degree - neurotmesis

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9
Q

What are the differences between 2nd, 3rd, 4th axonotmesis?

A

2nd - damage to axon only
3rd -damage to axon and endoneurium
4th - damage to axon, endoneurium and perineurium

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10
Q

What is neurotmesis?

A

Complete nerve transaction (+ epineurium)
E.G laceration from knife, gunshot

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11
Q

What is the prognosis of an injury close to the neuronal cell bodies?

A

Poor prognosis for regeneration, reinnervation, functional recovery and neuronal survival

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12
Q

What is the prognosis for an injury close to the target site of the nerve fibres?

A

Good prognosis for regeneration, reinnervation, functional recovery and neuronal survival

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13
Q

What is axotomy?

A

The severing of an axon into two or more parts

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14
Q

What is the first neural response to axotomy?

A

Chromatolysis

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15
Q

What are the steps of chromatolysis?

A

Cell body swells and becomes distended
Nucleus is displaced to periphery
Nissl bodies becomes dispersed into smaller ribosomal groupings
Epigenetic changes switch to a regeneration phenotype

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16
Q

How long does chromatolysis take?

A

Chromatolysis is at its maximum 12-24 hours after injury
Chromatolysis is more prolonged the closer the injury is to the cell body

17
Q

What is Wallerian degeneration?

A

The well orchestrated morphalogic and biochemical changes that occur in axons, Schwann cells and macrophages distal to a site of nerve injury
Results in the establishment of a microenvironment supportive of axonal regeneration

18
Q

What happens during Wallerian degeneration?

A

Myelin surrounding distal parts of axon begin to degenerate
(In the anterograde direction)
Schwann cells and macrophages remove debris by phagocytosis (1-2 months)
Schwann cells proliferate forming new layers of basements membrane

19
Q

What are the bands of Brungner?

A

During Schwann cell proliferation of Wallerian degeneration empty endoneural tubes are formed with the schwann cells and endoneurium known as the bands of brungner

20
Q

What is growth cone formation?

A

Several days after the injury to a peripheral nerve, the proximal axon stump begins to send out very thin axonal sprouts
This specialised amoeba like region is filled with microtubules called a growth cone

21
Q

How quickly does the growth cone progress?

A

It will advance down the empty tube at a rate of 1-4 mm/day
The same rate as slow axonal transport

22
Q

What is the end organ response to peripheral nerve degeneration?

A

Muscle is paralysed and reflexes lost
Hypotonia (little/ no resistance to passive movements)
Atrophy of the muscle and spontaneous contraction set in fasciculations

23
Q

What is synaptic stripping?

A

When the synaptic terminal withdraws from the neuronal cell bodies or dendrites of the chromatolytic neurons and are replaced by the processes of glial cells
Depresses synaptic function and can impair function recovery

24
Q

What glial cells replace synaptic terminals in the CNS and PNS?

A

CNS - microglia and astrocytes
PNS - Schwann cells

25
Q

When is synaptic stripping seen?

A

During transneuronal or transynaptic degeneration

26
Q

Describe anterograde degeneration of the visual pathway

A

Damage of the retinal ganglion
Degeneration of the lateral geniculate nucleus and neurons in the visual cortex

27
Q

Describe retrograde degeneration of the visual pathway

A

Damage to visual cortex neurons
Degeneration of the lateral geniculate nucleus and retinal neurons

28
Q

What is a neuroma?

A

A benign tumor of nerve tissue that is often associated with pain or specific types of various other symptoms
Most commonly arise from non neuronal nervous tissue after trauma or amputation

29
Q

How is a neuroma formed?

A

A scar (connective tissue) may block the advancement of the growth cones and will result in a mass of trapped and regenerating axons

30
Q

What is the surgical method of fixing a peripheral nerve injury?

A

Gap nerve grafts
A small part of the sural nerve in the leg is implanted at the site of repair

31
Q

What is a method of preventing the synaptic terminal from withdrawing from the cell body?

A

Supplying exogenous NGF
Nerve growth factor is an insulin like protein which regulates growth, development and maintenance of sympathetic and embryonic sensory neurons

32
Q

What are two ways that NGF can be inhibited?

A

Anti-NGF antibodies
When microtubules are blocked by colchicine

Advanced Neurosciences (20 decks)

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