FMC Test 2 *Neurotmesis, Neuropraxia, Axonotmesis* Flashcards

1
Q

What is Neurotmesis?

A

The nerve is severed
- Results in loss of axon and connective tissue continuity
(Ex. GSW, Stab wound, avulsion injury)

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2
Q

What is the difference between Klumpke’s Palsy and Erb’s Palsy?

A

Klumpke’s Palsy is a result of injury to the lower brachial plexus. (C8, T1), elbow is flexed, wrist is supinated, “claw-like” hand

Erb’s Palsy is a result of injury to the upper brachial plexus. (C5-C7), this has a classic limb posture of a waiters tip, the arm lies internally rotated at the side, with the elbow extended, the forearm pronated and wrist and fingers flexed. Paralysis in deltoid, bicep brachii, brachialis, brachioradialis

Both are result of Neurotmesis

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3
Q

What are the Clinical Manifestations of Neurotmesis?

A
  • Depends on nerve involvement and injury factors
  • In peripheral nerve distribution distal to lesion:
    –Flaccid paralysis of muscles
    –If left untreated:
    -Health declines in target tissue
    -Rapid atrophy
  • Loss of sensory function
  • Loss of sympathetic function
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4
Q

Do Neurotmesis require surgery?

A

Yes, surgical intervention is required
- Primary repair preferred

Operative delays lead to tissue fibrosis that would preclude repair or reconstruction

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5
Q

What do Surgical repair options include for Neurotmesis?

A
  • Nerve Graft
  • Group Fascicular Repair
  • Epieneural Connective Tissue Repair
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6
Q

After a patient has neurotmesis surgery, what are the next steps?

A

Repair site protection is the most important factor after coaptation or autograft
- Post-operative splinting maintains slack in nerve
- Compressive dressing decreases venous congestion and edema
- ROM exercises with restrictions to allow CT to heal

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7
Q

What is the healing time in the Inflammatory Stage, for Nerve Connective Tissue (Epineurium/Perineurium)? (For Neuropraxia)

A

Up to 3 days (most within 48 hours)

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8
Q

What is the healing time in the Repair Stage, for Nerve Connective Tissue (Epineurium/Perineurium)?
(For Neuropraxia)

A

Day 4-Day 21 (Depends on the extent of the injury)

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9
Q

What is the healing time in the Remodeling/Maturation Stage, for Nerve Connective Tissue (Epineurium/Perineurium)?
(For Neuropraxia)

A

21 days to several months

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10
Q

What does the Rehabilitation looks like once the Connective Tissue conduit is healed (Epineurium/Perineurium)?

A
  • Obtain and maintain full motion
  • Teach safety to compensate for loss of sensation and/or motor function
  • Sensory re-education exercises are initiated early and progressed
  • Sensory stimulation tactics to decrease hypersensitivity
  • Pain increases as healing progresses
    (Expect pain as regeneration of the nerve progresses)
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11
Q

For Nerve (Axon), what is the time frame in the Inflammatory Stage of Tissue Healing?
(For Neurotmesis and Axonotmesis)

A

Up to several weeks associated with Wallerian Degeneration

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12
Q

For Nerve (Axon), what is the time frame in the Fibroplasia/Repair Stage of Tissue Healing?
(For Neurotmesis and Axonotmesis)

A

Axons regenerate 1mm per day; can take months or longer

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13
Q

For Nerve (Axon), what is the time frame in the Remodeling/Maturation Sate of Tissue Healing?
(For Neurotmesis and Axonotmesis)

A

If Axon not regenerated by 18 months, the muscle it innervates is likely not viable

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14
Q

What happens after there is a complete Axonal Transection?

A

The Neuron undergoes a degenerative process called, Wallerian Degeneration. (This takes time and requires monitoring)

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15
Q

What is Wallerian Degeneration?

A

Wallerian degeneration is an active process of anterograde degeneration of the distal end of an axon that is a result of a nerve lesion.

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16
Q

What happens with New Axonal Growth?
What does success depend on?

A
  • Cell increases in metabolic activity, protein synthesis, and mitochondrial activity
  • New Terminal sprouts project from proximal segment

(Success depends on location, type of injury, inflammatory response, and scar tissue formation)

17
Q

What would be the prognosis for Neurotmesis?

A
  • Recovery after neurotmesis depends on whether the nerve was repaired and the length of the nerve that nerve must be regenerated
  • After transection, muscle atrophy rapidly, and after 2 years, they have undergone irreversible changes and have become fibrotic
  • If re-innervation occurs after 1 year, function is poor; with a delay of 18-24 months, there is no hope for return of function
18
Q

What is Neuropraxia?

A

Injury or inflammation the peripheral nerve. Can lead to Axonotmesis if left untreated

19
Q

In neuropraxia, there is reduction in nerve conduction at the site of injury due to?

A
  • Compression, traction, repetitive movements (Friction)
  • Causes ischemia or Schwann cell damage
  • Functional recovery in minutes, weeks, or a couple months
20
Q

In Neuropraxia, what is a conduction block?

A
  • The least sever injury
  • Conduction across the zone of nerve injury in inhibited, HOWEVER, conduction within the nerve both proximal and distal to the lesion remain intact
  • Continuity of all structures is preserved
  • Wallerian Degeneration DOES NOT occur (No axonal loss)
21
Q

Which peripheral nerves are at risk for compression, tension, and friction neuropathy?

A
  • Spinal nerve roots (Cervical and Lumbar)
  • Brachial Plexus
  • Median, Radial, Ulnar nerve
  • Fibular, Tibial, Sural nerve
22
Q

If compression, traction, friction, tensile, or shear forces become excessive, the nervous tissue has a biological response to injury, these responses include? (6)

A
  • Tissue anoxia (absence of O2)
  • Local Ischemia
  • Nerve fiber deformation
  • Vascular Permeability
  • Intraneural Edema
  • Fibroblastic proliferation
23
Q

How can Neurogenic Inflammation occur?

A

Its sympathetically mediated inflammation. From excessive mechanical loading of the nerve

24
Q

What are some neurogenic inflammatory reactions?

A
  • Vasodilation
  • Edema
  • Sensitization of nerve endings
  • Waking of sleeping or ineffective nociceptors
    etc.
25
Q

How does Intraneural edema increase?

A
  • Intraneural edema increases following nerve injury
    (Plays a major role in acute and chronic nerve lesions, even a moderate pressure increases can interface with endoneural capillary flow, causing hypoxia and electrolyte imbalance)
26
Q

What are the results of Intraneural edema?

A
  • Mechanical constriction and inflammatory biproducts further decrease blood flow and perpetuates congestion within the nerves.
  • Poor edema resolution, which can lead to nerve death.
  • Disrupts axoplasmic flow
27
Q

What are the classifications of Neuropraxia?

A
  • Neuropraxia involves segmental demyelination, which slows or blocks conduction of the action potential at the point of demyelination in a myelinated nerve
  • Neuropraxia often occurs after nerve compression that induces mild ischemia in nerve fibers
  • Conduction of the action potential is normal above and below the point of compression; because the axon remains intact, muscle does not atrophy
    (May identify myotomal weakness or specific muscle weakness due to decreased conductivity)
28
Q

What is the mechanism of Burner-Stinger Syndrome?

A
  • Tensile load on brachial plexus
  • Head and neck are rotated and laterally bent away from depressed shoulder.
  • Shoulder is hyper-abducting
  • Scapular depression
29
Q

What is Axonotmesis? How can it occur?

A

Damage/Injury to the axons, due to sever compression, friction/shear or traction.
- Epineurium/Perineurium/Endoneurium remain intact

  • Due to prolonged low loads or short duration high loads
30
Q

In order to regenerate, can Axonotmesis undergo Wallerian Degeneration like Neurotmesis?

A

Yes it will under go Wallerian’s, and will undergo the same process for “New Axonal Growth”.

Question 15 and 16 for review

31
Q

Is surgery needed for Axonotmesis?

A

Yes, surgery is often required to achieve functional recovery