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ANAT2012 > Peripheral Nerves > Flashcards

Peripheral Nerves Flashcards

1
Q

Where are the cell bodies of sensory neurons found?

A

dorsal root ganglia

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2
Q

Where are the cell bodies of motor neurons found?

A

ventral horn

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3
Q

Where are the cell bodies of autonomic neurons found?

A

lateral horn

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4
Q

What does it mean to say that neurons are post-mitotic?

A

they are not capable of dividing and therefore if lesioned they cannot be replaced and need to be maintained/renewed themselves

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5
Q

Why do neurons have bidirectional axonal transport?

A

because they are post-mitotic, the neurons must maintain and renew themselves by producing components in the cell body (or soma) and transporting them down the length of the axon while also receiving messages from the end of the axon to inform what is needed

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6
Q

Bidirectional axonal transport relies on what substances?

A

oxygen & energy

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7
Q

What are the connective tissue layers of a nerve (from outer to inner)?

A

mesoneurium (separates from other anatomical structures)
epineurium (containing all fasicles)
interfascicular epineurium (between fascicles)
perineurium (around fascicles)
endoneurium (axons)

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8
Q

What is the perineurium layer of connective tissue important for?

A

maintaining intrafascicular pressure (or ‘endoneurial pressure’) and the strength of the axon

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9
Q

Where does most of the resistance to stretch come from in a nerve?

A

the perineurium

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10
Q

What kind of connective tissue is interfascicular epineurium? How and why does this differ from epifascicular epineurium?

A

loose connective tissue vs dense irregular connective tissue proper (interfascicular epineurium is for cushioning whereas epifascicular epineurium is for surrounding)

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11
Q

True or false… lymphatic drainage is only possible in the epineurium layer of connective tissue

A

true

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12
Q

True or false… the structure of a nerve is consistent along its length

A

false

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13
Q

What variations in structure can be seen along the length of a nerve?

A

number of fascicles
fascicle vs interfascicular epineurium cross sectional area
endoneurial capillary density

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14
Q

What is excursion?

A

displacement or gliding of a nerve relative to its surrounding nerve bed

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15
Q

Elongation of the nerve bed during the movement of a joint will increase strain.

Is the magnitude of strain more significant closer or away from the moving joint?

A

closer to the joint (either significantly increased or decreased)

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16
Q

The movement of a joint creates excursion on its surrounding nerves.

Is the magnitude of excursion greater or lesser at the joint compared with away from the joint?

A

greater

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17
Q

Does nerve excursion first occur adjacent to the moving joint or distal to the moving joint?

A

first occurs adjacent and then occurs more distally

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18
Q

During elongation of a nerve, does the perineurium or axons straighten/tension first?

A

the perineurium

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19
Q

Would axons or fascicles rupture first with excessive elongation?

A

axons would rupture first

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20
Q

Once axons have straightened, how much more strain can they take before rupturing?

A

4%

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21
Q

A critical number of … must rupture to see the failure of an entire nerve

A

a critical number of fascicles

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22
Q

How does endoneurial pressure contribute to nerve stiffness during elongation?

What effect does this have on the blood vessels?

A

as the fascicle is elongated the cross-sectional area is reduced which increases intrafascicular pressure

it can impede on intrafascicular microcirculation

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23
Q

What happens to the stiffness of a nerve if blood vessels serving the nerve are severed?

A

it will decrease

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24
Q

How much tension are nerves typically under at rest?

A

~10%

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25
Q

Is the modulus of elasticity the same along the length of a nerve?

A

no- it varies

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26
Q

How much strain is a nerve typically under when the perineurium reaches its elastic limit? What about its rupture point?

A

~20%

~an additional 8-20%

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27
Q

What will happen if you increase the strain rate on a nerve?

A

increase in stiffness (modulus of elasticity)

the nerve will rupture sooner but at a higher load (increased ultimate stress + decreased ultimate strain)

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28
Q

Is the maximum tensile stress for a nerve related to the fascicular cross-sectional area or the combined total cross-sectional area of the nerve?

Why?

A

related to the fascicular cross-sectional area therefore strength increases as the number of fascicles increases

this may be due to the increased amount of perineurium

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29
Q

Spinal nerve roots do not contain perineurium & their fascicles are arranged longitudinally as opposed to in a plexus. What would this mean for the stress & strain rate?

A

they have a lower safety factor (they fail at lower stress & strain than other nerves)

30
Q

When does most of the relaxation happen when a nerve is under strain? (thinking about the stress-strain reaction)

A

first 20 minutes

31
Q

How are the contents of nerves displaced during uniform circumferential compression (cuff)?

Where is the damage greatest during this type of compression?

A

contents are displaced transversely & longitudinally

damage is greatest at the edges of the compression where shear forces are greatest

32
Q

Lateral compression of a nerve does not cause damage, why is that?

A

there is no volume change during lateral compression, therefore no increase in pressure and no damage

33
Q

In general, how much do fascicules contribute to the cross-sectional area of a nerve?

A

30-70%

34
Q

Why is it advantageous for a nerve often under compression to have a greater proportion of interfascicular epineurium tissue?

A

because it is loose connective tissue proper, it provides cushioning to the fascicles and acts as a shock absorber

35
Q

Axons in the PNS are capable of regeneration after injury, is this regeneration often complete or incomplete?

A

incomplete therefore often leaving the individual person with a neuropathic condition

36
Q

Experiments looking at the effects of immobilization on nerves found that myelin degeneration occurred how soon?

When was a disruption in collagen deposition seen?

A

~3 weeks

~6 weeks

37
Q

How does Seddon & Sunderlands classification of nerve injury differ?

A

Seddon’s classification has three categories: neurapraxia, axonotmesis & neurotmesis whereas Sunderland’s classification has 5 types

Type 1= neurapraxia (local myelin damage)

Type 2, 3 & 4= axonotmesis + connective tissue damage (damage to axons +/- endoneurium & perineurium respectively)

Type 5= neurotmesis (complete nerve disruption)

38
Q

Are motor neurons or sensory neurons more susceptible to apoptosis following transection?

A

sensory ‘are more sensitive’

39
Q

Whether a neuron dies or not depends on the location of axonal transection. Is the cell more likely to die if the transection is close to or further away from the cell body?

A

close to

40
Q

What happens to the nucleus of a nerve cell after axonal transection?

A

it swells and moves to the edge of the cell body and focuses on producing structural materials for repair rather than neurotransmitters as it would normally

41
Q

What is Wallerian degeneration?

How soon does it occur?

A

a degenerational breakdown of the axon and myelin sheath distal to the point of transection

within 2-4 days of injury

42
Q

How soon do macrophages infiltrate a nerve which has experienced an acute transection?

A

1-4 days

43
Q

What happens to Schwann cells after acute axonal transection?

A

they de-differentiate, detach from axons, proliferate & help recruited macrophages clear cellular & myelin debris

44
Q

Why must myelin debris be removed from the site of acute nerve injury as soon as possible?

A

it slows the process of regeneration

45
Q

After de-differentiation, how do Schwann cells help to regenerate injured nerves?

A

they align longitudinally & express stimulating factors to direct nerve regrowth toward the target organ

46
Q

How quickly do regenerating axons grow?

A

1-3mm/day

47
Q

Muscle atrophy occurs following axonal transection due to deinnervation… how long do muscle cells remain viable for reinnervation?

A

~2 years

48
Q

True or false… the longer between axonal transection and reinnervation the better functional outcome

A

false… the earlier the better

49
Q

What does primary (surgical) repair of nerve transections entail?

A

suturing the nerve back together, either by stitching the epineurial or fasicular ends together

50
Q

In the case that primary repair cannot be carried out on a nerve, what can be done?

A

nerve grafting surgery

either autografting (from the patient) or allografting (from a donor)

synthetics are being researched currently

51
Q

How soon ideally should a primary repair of a nerve transection be done?

A

within 24 hours

52
Q

Where kind of damage typically occurs first during chronic nerve compression?

A

local myelin sheath damage & intraneural oedema

53
Q

How soon is macrophage infiltration seen in chronic nerve compression?

How is this different to an acute nerve injury?

A

several weeks as compared to 1-4 days in actue injuries

54
Q

How does Schwann cell response in chronic nerve compression differ from an acute nerve injury?

How soon does this response kick in during prolonged compression?

A

there is an increase in proliferation and apoptosis of schwann cells resulting in a net turnover

this is mediated by the mechanosensitivy of the schwann cells (as opposed to mediated by macrophage infiltration during an acute injury response)

starts ~2 weeks after maintained compression & peaks at ~4 weeks

55
Q

Describe the timeline of demylination and remylination in a chronic nerve compression injury.

Is the new myelin sheath comparable to the original?

A

focal demylination occurs over 7-10 days with remyelination occuring over 2-4 weeks

the new myelin sheath is thinner resulting in a slower conduction velocity

56
Q

Is muscle atrophy seen in both acute & chronic nerve injuries?

A

No- it is only generally seen in acute injuries due to deinnervation following wallerian degeneration.

In a chronic injury the muscle cells remain innervated albeit with slower conduction velocity due to the now thinner myelin sheath.

57
Q

What effect does intraneural oedema due to chronic nerve compression have on the nerve?

A

an increase in pressure in the fascicles impairs intraneural blood flow and axoplasmic flow disrupting the normal function of the axon

this results in the activation of fibroblasts & fibrosis (scarring)

58
Q

What type and size of nerves are predisposed to chronic nerve compression injuries?

A

sensory more susceptible than motor

large more susceptible than small

59
Q

What are the 3 levels of severity of chronic nerve injuries?

A 
1= sensory impairments (parasthesia, pain)
2= sensory & motor impairments without muscle wasting
3= sensory & motor impairments with muscle wasting
60
Q

What are the most common upper limb compression/entrapment neuropathies?

A

carpal tunnel syndrome & cubital tunnel syndrome

61
Q

What are some less common upper limb compression/entrapment neuropathies?

A

ulnar nerve compression @ Guyon’s canal

median nerve compression in the forearm

radial tunnel syndrome

62
Q

What are some predisposing factors to carpal tunnel syndrome?

A

high repetition wrist and/or finger activities leading to fibrosis/scarring

occupational exposure to vibration (i.e. hand tools)

63
Q

What movement of the wrist increases carpal tunnel pressure?

A

wrist flexion

64
Q

Other than wrist flexion, what else could increase the pressure within the carpal tunnel?

A

oedema (swelling, i.e. during pregnancy)

incursion of muscles into the tunnel (i.e. lumbricales during MCP flexion or extrinsic flexor muscles during wrist extension)

65
Q

What is a normal pressure measurement (mmHg) of the carpal tunnel while in neutral wrist position?

How does this change during wrist extension?

A

3-5 mmHg

dramatically increases to 63 mmHg at 40 degrees of wrist extension

66
Q

What is an expected pressure (mmHg) within the carpal tunnel in some with carpal tunnel syndrome, in neutral wrist position?

How does this change during wrist extension?

A

~30 mmHg

dramatically increases to 110 mmHg @ full wrist extension

67
Q

What are neurodynamics and how can they help people with chronic nerve compression?

A

a manual therapy technique that uses nerve elongation & excursion to facilitate the movement of oedema within a nerve and reduce symptoms

68
Q

How do neurodynamic exercises help with scar formation within a nerve following chronic compression?

A

these exercises encourage normal nerve excursion and may limit fibroblast activity and therefore minimise scar formation

69
Q

How does electrical stimulation increase sensory & motor neuron regeneration?

A

the electrical stimulation of the muscle attracts the regenerating nerve towards it assisting in regeneration

70
Q

Why is someone with diabetes more vulnerable to nerve pathologies?

A

they experience an increase in collagen deposition and therefore nerve sectional area, which makes the nerve more susceptible to compression injury (larger fibres are more susceptible than small fibres)

71
Q

Describe the ‘double crush phenomena’.

Why does the presence of a nerve disorder predispose someone to developing a secondary nerve disorder?

A

a nerve injury may result in an additional injury elsewhere along the same nerve or in the same area due to:

disruption in axonal transport
altered ion channels
neuroinflammation
central sensitisation
altered neural biomechanics

ANAT2012 (10 decks)

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