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Medical Studies 2A > 5.6 Disorders of the Peripheral Nervous System > Flashcards

5.6 Disorders of the Peripheral Nervous System Flashcards

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USMLE® Step 1 flashcards
1
Q

A bundle of nerve fibres is called a…

A

Nerve fascicle/bundle

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2
Q

Outline the components of a peripheral nerve (be careful with the wording…)

A
  • Axon
  • Schwann cell
  • Endodeurium
  • Perineurium
  • Epineurium
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3
Q

What is the function of Schwann cells?

A
  • Myelinates axons & supports unmyelinated PNS axons
  • Central role in axon development/maintenance
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4
Q

Where is the endoneurium. What does it do?

A
  • Surrounds each axons and Schwann cell
  • Rich in components that promote axonal growth
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5
Q

What is the name of the CT sheath that surrounds a nerve fascicle?

A

Perineurium.

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6
Q

What is the name of the dense CT that surrounds all nerve fascicles in a peripheral nerve?

A

Epineurium.

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7
Q

What symptoms might we see with a loss of motor function of a peripheral nerve?

A
  • Weakness
  • Areflexia
  • Atrophy (if chronic)
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8
Q

What symptoms might we see with a loss of sensory function of a peripheral nerve?

A

Loss of somatosensation (e.g. pain, temp, numbness)

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9
Q

Describe some “+” symptoms of peripheral neuropathy

A

Hyperexcitability (burning, tingling/”pins and needles”)

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10
Q

Describe some “-“ symptoms of peripheral neuropathy

A
  • Weakness of muscle
  • Loss of somatosensation
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11
Q

What is the name of the category of peripheral nerve disorders that affect a single nerve?

A

Mononeuropathy

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12
Q

What is the name of the category of peripheral nerve disorders that affect multiple nerves, usually symmetrically? Are these deficits distal or proximal?

A

Polyneuropathy. Usually distal deficits.

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13
Q

Describe mononeuritis multiplex

A
  • Individual nerves affected
  • In a haphazard fashion (asymmetrical)
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14
Q

What is polyradiculopathy? Does it cause proximal or distal deficits? Are symptoms symmetric or asymmetric?

A
  • Peripheral neuropathy affecting multiple nerves and nerve roots
  • Proximal AND distal deficits (makes sense)
  • Usually symmetric symptoms
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15
Q

List the three targets of peripheral nerve disorders

A
  1. Cell body
  2. Axon
  3. Neuromuscular junction
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16
Q

Give an example of a peripheral axonopathy that can present as either demyelinating or axonal.

A

Guillian-barre syndrome

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17
Q

What components of an axon are damaged in a peripheral demyelinating axonopathy?

A
  • Schwann cells
  • Myelin sheath
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18
Q

Why might synchrony be lost within a nerve fibre as a result of demyelinating disease?

A
  • Saltatory conduction is no longer uniform
  • Impulses arrive at different times to the end of their respective axons
  • :(
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19
Q

List the two kinds of peripheral axonopathy

A
  • Demyelinating
  • Axonal
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20
Q

Give an example of a peripheral neuropathy that affects neuromuscular junctions

A

Myasthenia Gravis

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21
Q

Describe the proximal changes that occur during peripheral nerve degeneration

A
  • Cell body swells
  • Nucleus moves to periphery
  • Chromatolysis (Nissl bodies; less secretory)
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22
Q

Describe the distal changes that occur during peripheral nerve degeneration

A
  • Denervation (pulling away from effector cell)
  • Dying back phenomenon
  • Myelin breakdown
  • Macrophages clear
  • Effector cell atrophy
23
Q

In full, describe the damaging and regrowth of a peripheral nerve (successful)

A
  • Nerve is damaged
  • Denervation, dying back, chromatolysis
  • Eventually, neuron kicks itself back into gear:
  • Regrows Nissl bodies (Secretory function), and proximal axons begins sprouting in all directions
  • Wise Schwann cells guide young axon into endoneurium tube
  • Great success
24
Q

How long does it take for a peripheral nerve to regrow?

A

~3 months

25
Q

Describe two ways in which peripheral nerve regeneration can go wrong

A
  • New axon is not properly guided into endoneurium tube (partial recovery of sensory/motor function)
  • Neuroma (tangling), may lead to phantom pain
26
Q

What factors affect the peripheral nerve repair outcomes?

A
  • Proximity to soma (closer = worse)
  • Restoring contact with effector
  • Type of injury
27
Q

Describe the different kinds of traumatic peripheral nerve injuries

A
  • Neuropraxia (transiently blocked nerve conduction; honeymooners’, ischaemia, cold). All components remain intact.
  • Axonotmesis (Axon & myelin locally damaged but nerve sheath is partially/fully intact)
  • Neurotmesis (axon & myelin & nerve sheath all damaged)
28
Q

True or false: axonotmesis has a longer term recovery than neuropraxia

A
  • True
  • Axon and myelin must regenerate, so takes longer (but, of course, peri and epineurium are retained)
29
Q

Axonotmesis, neurotmesis and neuropraxia are three types of nerve injury. Rank them from mildest to most severe.

A

Neuropraxia (mild)
Axonotmesis (mild-moderate)
Neurotmesis (severe)

30
Q

What is the prognosis of axonotmesis?

A
  • Neurotransmission interrupted until target innervation is restored
  • Longer term
31
Q

What is the prognosis of neurotmesis?

A

Long term partial/complete loss of motor/sensory functions.

32
Q

Give some examples of injuries that can cause axonotmesis

A

Nerve crush, stretch injury

33
Q

Give some examples of injuries that can cause neurotmesis

A

Nerve transection (sharp injuries, neurotoxins)

34
Q

What IS motor neuron disease? What ISN’T it?

A
  • Gradually progressing degeneration of motor neurons
  • Minimal or no cognitive dysfunction
  • Minimal or no sensory dysfunction
35
Q

What are typically the first and last symptoms of motor neuron disease?

A
  • First: weakness in hands or legs
  • Last: failure of respiratory muscles
36
Q

What is the typical age range of MND diagnosis?

A

50-60 years old

37
Q

Death typically occurs within _ years of diagnosis of MND

A

2 years

38
Q

Describe two clinical findings/features of motor neuron disease

A
  • Amyotrophy (muscle wasting due to lack of LMN input)
  • Lateral sclerosis (loss of lateral corticospinal tract)
39
Q

Which groups of motor neurons are spared of MND?

A
  • Autonomic nerves (fully motor, e.g. sphincter control)
  • Extraocular muscles
40
Q

What are the two main types of MND, and their relative proportion of all cases?

A
  • Genetic (10%)
  • Sporadic (90%)
41
Q

Which of sporadic/genetic MND affects older/younger people? At what age is genetic MND typically diagnosed.

A

Sporadic: typically late-age
Genetic: younger (20-80); avg 45 years old

42
Q

What occurs in spinal muscular atrophy? What is the result of this?

A
  • Recessive mutation: improper RNA movement and splicing
  • Progressive loss of LMNs:
  • Weakness, flaccid paralysis, atrophy, areflexia, hypotonia
43
Q

Name some different hypotheses for the cause of MND

A
  • Genetic cause
  • Excitotoxicity
  • Free radicals (SOD-1)
  • Impaired axonal transport
  • Lack of neurotrophic support
44
Q

List some argument for and against the genetic theory of MND

A
  • Mutations have been linked to various forms of MND (such as SMA)
  • Only a minority (10%) of MND cases have a genetic/familial cause
45
Q

Describe the theory of SOD-1 specific MND

A
  • SOD-1 is an enzyme
  • The theory was that, if SOD-1 (pacman) is dysfunctional, he cannot gobble the free radicals (ghosts)
46
Q

Outline the excitotoxicity hypothesis of MND

A
  • Glial glutamate transporters (e.g. astrocytes) lost
  • More glutamate remains in synapse
  • Nerve cells may die from glutamate poisoning
47
Q

How do we categorise the clinical features of MND? What are they?

A

Diminished function:
- Weakness
- Atrophy
Flaccid paralysis
- Hyporreflexia
- Hypotonia
Excessive function:
- Pathological fasciculations
- Hyperreflexia
- Hypertonia
- Spastic paralysis

48
Q

LMN lesions cause “diminished function” symptoms. What is the exception?

A

Pathological fasciculations: spontaneous, grossly visible, contractions of small muscle groups

49
Q

DO we see weakness in UMN lesions, LMN lesions, or both?

A

Both

50
Q

Do we see fasciculations in UMN lesions, LMN lesions, or both?

A

LMN

51
Q

Do we see atrophy in UMN lesions, LMN lesions, or both?

A

Both (although typically more prominent in LMN due to denervation)

52
Q

Effect of UMN vs LMN lesions on reflexes

A

UMN: hyperreflexia
LMN: Hyporeflexia

53
Q

Effect of UMN vs LMN lesions on tone

A

UMN: Hypertonia
LMN: Hypotonia

Medical Studies 2A (110 decks)

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