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Anatomy > Peripheral nerves > Flashcards

Peripheral nerves Flashcards

1
Q

Transport mechanisms within axons

A

Axons need to maintain and renew themselves which is the role of the cell body (soma)

  • Some synthesis components requires for structure and function
  • This body could be very remotely located by the synapse therefore need fast transport systems
    • Anterograde transport (cell → terminal) O2, energy and cell components
    • Retrograde transport (terminal → body) communication and reuse
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2
Q

Connective tissue layers of nerve

A
  • Endoneurium
    • Surrounds and separates axons
    • Loose CTP
  • Perineurium
    • Lamellar (layered) sheath around each fascicle
    • Dense Irregular CTP
    • Type 1 and 2 collagen + elastic fibres in circular, oblique and longitudinal orientation
    • Acts as a biochemical diffusion barrier
  • Epineurium (has both interfascicular and epifasicular)
    • Interfascicular (loose) - cushioning and compression
    • Epifasicular (DICTP) - tension resistance
  • Mesoneurium
    • lose CTP surrounding nerve, facilitates sliding in nerve bed
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3
Q

Blood vessels and lymphatics within nerves

A

Nerves relay on adequate O2 and energy to function

  • Anastomotic (plexus) network of blood vessels and their relative tortuosity (slack) accommodates strain and gliding
  • Endoneural capillaries act as blood nerve barrier (control what substances cross
  • Epineural arterioles have smooth muscle to modify diameter but perineurial arterioles have much less
  • Lymphatics as present only in the epineurium mean there is no lymphatic drainage within the fascicles
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4
Q

How can nerve structure vary only the length of the nerve

A
  • The structure of a nerve changes only its length meaning there is a variation in:
    • Number of fascicles (fascicle size inversely related to this)
    • Fascicle and interfasicular epineurium contribution to total CSA, areas of compression often have increased interfascilar epineurium
    • Endothelia capillary density, relates to oxygen and energy supply
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5
Q

Nerve excursion principles

A

Excursion is displacement or gliding of nerve relative to the surrounding nerve bed.

  • Direction and magnitude depends on the anatomical location in relation to the moving axis within the joint
  • Elongation of the nerve bed will cause the adjacent segments of nerve to glide toward the moving joint and shortening will cause nerve to glide away from moving joint
  • Neve excursion occurs first in the nerve segments immediately adjacent to the moving joint and progressively more distal with more movement
  • Magnitude of excursion is largest at these adjacent points
  • Elongation of the nerve bed will cause strain, magnitude of this is greatest in segment closest to moving joint
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6
Q

Excursion examples for 90 elbow flexion to 0 and wrist ext from 0 to 60

A
  • 90 flexion → 0 flexion
    • Median nerve in arm and forearm glide towards elbow
    • Ulna nerve in arm and forearm will move away
  • Wrist extension from 0 → 60
    • Both the nerves beds will elongate meaning both nerves glide towards wrist with more movement occurring in forearm than the arm
    Remember that both nerves are anterior to wrist joint while median is anterior to elbow and ulna is posterior
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7
Q

Excursion with modified SLR

A
  • Distal excursion with DF (greatest at the ankle)
  • Proximal with hip flexion (greatest at the hip)
  • Can move nerves through beds
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8
Q

Nerve tensioning steps and key points

A
  1. Nerve straightens
  2. Fascicle straighten meaning the perineurium is tensioned (not axons)
  3. Axons straight and tension
  4. Some axons rupture (increase of 4% strain after tensioning)
  5. Some fascicles rupture
  6. Once critical number of fascicles rupture there is failure of entire nerve and rapid plastic deformation
  • Perinerium is the main structure to provide resistance to further tension
  • Axons rupture before rupture of perineurium (fasicles)

With excursion and strain there will initially be undulating of fascicles within the nerve then axons within fascicles. It occurs in this order as the axons are longer than the fascicles

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9
Q

Endonureal pressure

A

As fasicle is elongates CSA decreases → increasing intrafasicular pressure which resists further contraction and also compromises intrafasicular microcirculation

This is not constant along a nerve, as the nerve is not homogenous. Transverse contraction is greatest in the middle of the nerve.

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10
Q

Nerve response to tension

A
  • Remember that nerves are under a resting level of strain (not stress!) due to anatomical body position.
  • With initial increase in stress there will not be a large increase in strain due to the toe region. Caused by fascicles undulating (fasicles straighten first)
  • Further elongation will show stress and strain increases at constant rate, linear elastic region where the axons are undulating. Damage to axons can occur in the later portions of this region
  • Modulus of elasticity is varied along a nerve due to different structure
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11
Q

How will an increase in strain rate change a nerves response to tension

A

Nerves are visco elastic:

Increase in strain rate will causes increase in modulus of elasticity (stiffness), increase in ultimate failure stress and decrease in ultimate strain.

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12
Q

Total stress resistance in different areas of the nerve

A
  • The total stress a nerve can resist is not related to TCSA but instead total fascicular area (combined area of perineurium, better at resisting tension)
  • For total fascicular area, strength increases as number of fascicles increase, each fascicle is bound by perineurium which is better at resisting tension
  • Important to note for spinal roots as they don’t have perineurium meaning the elastic fail limit will occur at lower stress and strain
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13
Q

Stress relaxation (creep) curve of peripheral nerves

A
  • Most relaxation occurs in first 20 mins

- Repeated strains increase compliance (less stress for strain)

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14
Q

3 modes of compression for peripheral nerves

A

3 modes of compression:

  • Lengthening nerve will causes transverse contracture which will causes compression
  • Uniform circumferential
    • Displace transversely and longitudinally
    • Greatest damage at the edges of where compression is applied (cuff), where shear forces are largest
  • Lateral compression (two parallel structures)
    • The actual volume of the nerve doesn’t not change as the shape can change
    • Movement of components but not large increase in pressure

Important to remember that contributions of interfascicular epineurium and fascicles change. Interfascicular epineurium tissue are better for resisting compression.

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15
Q

Response to immobilisation

A

Peripheral nerves need enough mechanical stimuli for mechanotransduction.

3 weeks - myelin degeneration

6 weeks - deposition of endoneurial collagen, increased ratio or large fibers

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16
Q

Seddon classification of nerve injuries

A
  • Neurapraxia - local myelin damage (usually secondary to compression)
  • Axonotmesis - Loss of continuity if axons and varying amounts of damage to endo and perineurium. Epineurium intact
  • Neurotmesis - Complete disruption of entire nerve trunk
17
Q

Sunderland’s classification of nerve injury

A

Sunderland:

  • Type 1 - local myelin damage (normally secondary to compression)
  • Type 2 - Loss of continuity of axons, endo, peri and epi intact
  • Type 3 - Loss of continuity of axons and endo, peri and epi intact
  • Type 4 - Loss of continuity of axons, endo and peri, epi intact
  • Type 5 - Complete disruption of entire nerve trunk
18
Q

Related points to nerve classification types

A
  • Neurapraxia will causes temporary decrease in conduction, Schwan cells will regenerate
  • Although Sunderland’s classification provided a more accurate description it has limited clinical utility. It is hard to differential which structures are injured and these structures also vary along the length of the nerve.
19
Q

Cell body reaction in response to transection (acute nerve injury)

A
  • Primary sensory neurons are more vulnerable to apoptosis than motor neurons meaning that transection more distally has a decreased risk of apoptosis. (location and type).
  • The cell body swells and the nucleus moves peripherally → change in metabolic action, change from production of neurotransmitters to production of structural materials needed for growth and repair.
20
Q

Responses to axonal transection (acute)

A
  • Wallerian degeneration, distal axonal disintegration and myelin fragmentation (starts 2-4 post injury)
  • Macrophage infiltration, this is immediate (1-4 days)
  • De differentiation of Schwann cells = detach from axons to proliferate and help the recruited macrophages clear cellular and myelin debris (these inhibit growth)
  • Schwann cells align longitudinally where they express stimulating factors to direct growth towards target organ
21
Q

Regeneration after transection

A

Axons from proximal stump grow 1-3 mm per day

During this time the muscle will atrophy and undergo interstitial fibrosis, viable for 2 years. Sensory nerves target sensory organs which can release chemicals to attract. These sensory end organ also degenerate over time and a viable for reinnervation for 1-several years.

Note that early innervation produces superior functional return for both sensory and motor

22
Q

Primary repair of acute transection

A

Nerve transection primary repair is best within 24 hours. It is either epineural repair or fascicular repair. Brings to ends together.

When there is too much tension for primary nerve repair then grafting can occur, normally sural nerve and limb is immobilised until healing complete (4 weeks)

23
Q

Components of chronic nerve compression

A
  • Axonal integrity persevered in early stages therefore neurapraxia (focal demyelination)
  • Macrophage infiltration is gradual (several week)
  • Schwann cell turnover = proliferation and apoptosis at 2 weeks peaking at 4 weeks.
    • This is from Schwann cell machanosensistivity not macrophage induced
  • Focal demyelination 7-10 days followed by remyelinating 2-4 weeks. This occurs due to changes in the Schwann cells. New sheath is thinner
  • Nerve conduction velocity is decreased but not absent meaning normal neuromuscular action and no atrophy
  • Late stage can lead to axonal damage and this is evident by motor weakness.
    Sensory neurons more susceptible to compression. Larger fibers are more vulnerable to compression and ischemia
24
Q

Process of chronic compression

A
  • pressure causes intraneural oedema
  • Ischaemic damage to endoneural capillary
  • Damage to blood nerve barrier
  • Increase in intraneural pressure from oedema
  • Impairs blood flow and axoplasmic flow (antergrade and retrograde)
  • Activation of fibroblast and fibrosis

The impairment of impulse conduction is directly related to amount of intraneural oedema and myelin changes

25
Q

Classification of chronic nerve compression based on symptoms

A

Sensory only

Sensory and motor weakness without wasting

Sensory and muscle wasting

Compression at one site can increase risk of sensitivity at another. Can get multilevel nerve compression (double crush) pathology

26
Q

Common compression/entrapment neuropathies

A

Most common

  • Carpal tunnel syndrome
    • Predisposing factors include high rep wrist/finger activities→ shear injury → fibrosis or occupational exposure to vibration
    • Wrist flexion increases carpal tunnel pressure
    • Increased volume of contents in carpal tunnel (oedema, incursion of muscles such as lumbricals or FDS)
  • Cubital tunnel syndrome (ulna)

Less common

  • Ulna nerve compression at Guyons canal
  • Median nerve compression in the forearm
  • Radial tunnel syndrome
27
Q

Neurodynamic techniques

A
  • Movement of nerve can facilitate evacuation of oedema due to variations in intraneural pressure
  • Nerve gliding may also limit fibroblastic activity and minimise scar formation
  • Electrical stimulation increases sensory and motor neuron regeneration
28
Q

Factors that predispose individual to nerve pathology

A
  • Systemic factors such as diabetes, thyroid disease
  • Non systemic factors - presence of a nerve disorder is a predisposing factor for another nerve disorder (double crush) due to axonal transport, altered ion channels, inflammation, central sensitisation
29
Q

Determinant or pathophysiology and classification for acute vs chronic

A

Acute
Presence or absence of axonal damage
Seddon = neurotmesis (therefore atrophy)
Pathology = transection. Cell body swells and changes metabolic priority to axon repair. Wallerian in distal stump.

Chronic
Amount and duration of compression
Seddon = Neuropraxia (therefore weakness and decreased velocity)
Pathology = sufficient stimulus to induce intraneural oedema, ischemic damage to endoneural cap (blood nerve barrier) -> further increased pressure. Therefore impaired blood flow and impaired axoplasmic transport

30
Q

Reason for macrophage infiltration in acute vs chronic.

A

Acute
Damage to axon and therefore cytokine and inflammatory factors

Chronic
Many factors released as a result of damage

31
Q

What fibres are more vulnerable to compression

A

Sensory neurons

Larger fibres

32
Q

Classifications to indicate severity of chronic compression

A

sensory only
sensory + weakness without wasting
Sensory and muscle wasting (will required surgical decompression)

Will depend on amount of compression, fibrosis

33
Q

What is double crush

A

Impairments at one site will predispose to another site of compression. Serial constraints to axoplasmic flow

Anatomy (10 decks)

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