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Neuro Block 5 > Peripheral Nerve Pathology > Flashcards

Peripheral Nerve Pathology Flashcards

1
Q

Where does the PNS start

A

Intervertebral foramen

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2
Q

Loss of somatosensation or viscerosensation (numbness)

A

Anesthesia

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3
Q

Altered/abnormal somatosenation (tingling)

A

Pareathesia

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4
Q

Alternation in the type of sensation experience (painful reaction to normal non-painful stimuli )

A

Allodynia

Pain sensation that occurs spontaneously without actual pain stimulus present, typically described as ‘burning’, shock-like’ etc

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5
Q

Affects dorsal (posterior) or ventral (anterior) roots

A

Radiculopathy

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6
Q

Etiology of local pathology

A

Traumatic, compression (by disc herniation or osteophyte, spinal stenosis (narrowing of spinal canal), tumors, access, viruses including varicella-zoster (shingles), cytomegalovirus

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7
Q

Etiology of systemic pathology

A

Irritates roots to causes abnormal firing and/or loss of normal firing pattern, including diabetes, infection, inflammation, and auto-immune disease

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8
Q

Radicular pain

A

Spontaneous, radiating, shock like, cutaneous and muscle

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9
Q

Presentation of radiculopathy

A
  • radicular pain
  • anesthesia
  • paresis
  • distribution (focal and segmental)
  • temporal profile (acute, subacute, or insidious)
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10
Q

Distribution of radiculopathy

A

Focal and segmental, dermatomal, myotomal

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11
Q

Temporal profile of radiculopathy

A

Acute, subacute, or insidious depending on the cause

Highly variable

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12
Q

Posteriolateral herniation

A

Disc impinges on lateral portion of dorsal or ventral root or proximal spinal nerve

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13
Q

Far lateral herniation

A

Near the intervertebral foramen impinging on both dorsal and ventral root

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14
Q

Central herniations

A

Common in lumbar vertebrae, impinges on multiple roots (cauda equina)

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15
Q

Disc of herniation usually impinges on what

A

Root of adjacent level #

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16
Q

Local manipulation and radical are pain or paresthesia

A

Straight leg raises produces traction on roots. Unaffected leg with symptomatic leg down.

Induced pain is a sign of local mass compressing roots

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17
Q

Compression or irritation of descending roots. Same range of various causes as with radiculopathy at more rostral levels.

A

Cauda equina syndrome

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18
Q

Motor deficits of caudal equina syndrome

A

Depend on whihc root levels are affected (L1-S4)

Causes saddle anesthesia (S2-S5)

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19
Q

Infection via nerve terminals of DRG sensory neuron, retrograde transport to cell body

A

Herpes zoster

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20
Q

How does herpes zoster initiate pain

A

Viral proliferation irritates neuron, alters firing pattern, spontaneous pain

Cutaneous blisters in dermatome

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21
Q

What’s the difference between dermatome map and cutaneous nerve

A

Dermatome is related to the actual spinal nerve, cutaneous map is where the cutaneous sensory nerves innervate a certain area

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22
Q

Damage to cervical, brachial, or lumbosacral plexus

A

Plexopathy

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23
Q

Location of plexopathy

A

Damage to part of plexus- root, trunk, cords, major nerves near their proximal origins

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24
Q

Etiology of plexopathy

A
  • Anesthesia
  • Paresthesia
  • Wide spread pain over multiple dermatomes
  • paresis of a muscle group
  • fasciculations may or may not
  • Focal distribution and likely multi segmental
  • acute, fluctuations depending on case
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25
Q

Temporal profile of plexopathy

A

Acute, fluctant depedning on the cause

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26
Q

Location of mononeuropathy

A

Distal to plexus or not derived from a plexus (median or ulnar)

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27
Q

One nerve affected

A

Mononeuropathy

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28
Q

Presentation of mononeuropathy

A
  • anesthesia (cutaneous map)
  • paresthesis (cutaneous map)
  • wide spread cutaneous nerve territory
  • paresis of a muscle group, multi segmental
  • fasciculations may or may not present
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29
Q

Distribution of mononeuropathy

A

Territory of one nerve, isolated muscle paralysis

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30
Q

Temporal profile of mononeuropathy

A

Acute, fluctuatant depending on the cause

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31
Q

Multiple nerves affected in a region affected

A

Polyneuropathy

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32
Q

Location of polyneuropathy

A

May distal nerves, often selective impact on large diameter axons (fine/discriminative touch, motor function)

33
Q

Etiology of polyneuropathy

A

Auto-immune, mutation, toxins (lead)

34
Q

Presentation of polyneuropathy

A
  • sensory and motor

- paresis of several distal muscles, usually bilaterally

35
Q

Distribution of polyneiropathy

A

Symmetrical and diffuse, distal extremities

36
Q

Temporal profile of polyneuropathy

A

Acute, subacute, or insidious depending on the cause

37
Q

Examples of polyneuropathy

A

Guillaine-Barre (autoimmune), Charcot Marie tooth (hereidatary), diabetic polyneuropathy (DM)

38
Q

Autoimmune attack myelin sheath or oligodendrocyte. Detected as slowing of nerve conduction velocity

A

Demyelinating

39
Q

Neurogenerative, genetic mutation? Detected as reduction in amplitude of nerve conduction

A

Axonopathy

40
Q

Neuronopathy (axonopathy): sensory

A

Degenerative of neuronal cell bodies of sensory neurons in DRG

41
Q

Neuronopathy (axonopathy): motor

A

Motorneurons of spinal cord

42
Q

Location of diabetic polyneuropathy (DM)

A

Damage large diameter axons innervating distal extremities

43
Q

Distribution of diabetic polyneuropathy

A

Diffuse and symmetrical due to glucose fluctuation

44
Q

Presentation of diabetic polyneuropathy (DM)

A

Stocking and glove pattern (lower leg, hands, feet)

45
Q

Temporal profile of diabetic polyneuropathy (DM)

A

Insidious/chronic

46
Q

Guillaine-Barre syndrome (polyneuropathy)

A

Acute inflammatory demyelinating polyneuropathy (AIDP)

47
Q

Etiology of Guillane-Barre syndrome

A

Often emerges after an infection resolves

48
Q

Location of Guillane-Barre syndrome

A

Motorneuron function in distal legs, than arms, then facial (lower motorneurons)

49
Q

Distribution of Gulliane-Barre

A

Symmetrical and diffuse

Lower motor neurons

50
Q

Presentation of guillane-barre

A

Motor weakness is more evident than sensory deficits

51
Q

What is Charcot-Marie-tooth disease (polyneuropathy, axonopathy)

A

Genetic mutation causing degeneration of sensory and lower motor neurons

52
Q

Distribution of Charcot Marie tooth disease

A

Diffuse and symmetrical

53
Q

Presentation of Charcot Marie tooth disease

A

Flaccid weakness, impaired fine/discriminative touch and proprioceptive (sensory ataxia, lower motor neurons), normal pain and temperature

54
Q

Location of Charcot Marie tooth disease

A

Preferentially impacts large diameter axons/fibers

55
Q

Temporal profile of Charcot Marie tooth disease

A

Insidious/chronic, progressive

56
Q

What kind of signs for neuropathies

A

Lower motor neuron signs

57
Q

Distribution of deficits of neuropathies

A

Fits with nerve distribution territory

58
Q

What is there an absence of in neuropathies

A
  • spastic weakness and hyperreflexia
  • spinal cord signs (long tract signs or level down signs)
  • brainstem signs (CN signs )
  • supratentorial signs (mental status, visual deficits)
59
Q

Is stocking and glove level down

A

No

60
Q

Neurological exam for peripheral nerve pathology and other disorders

A

Can narrow the localization of the problem; what general level of the CNS or PNS, what levels can be ruled out as the source of the problem?

61
Q

Nerve conduction studies

A

Can measure nerve conduction velocity (testing for demyelinated nerves) or amplitude (testing for axonopathy).

62
Q

What do you do to test for demyelinated nerves such as in MS?

A

Nerve conduction velocity

63
Q

What do you do to test for axonopoathy

A

Nerve conduction amplitude

64
Q

Stimulation electrode in muscle and recording of muscle response (motor unit potentials), measuring amplitude and whether firing pattern is continuous (normal recruitment of fibers) or intermittent (impaired muscle fiber recruitment)

A

Electromyopathy

65
Q

Shows firing is continuous (normal) or increased (compensatory) but amplitude is reduced

A

Myopathic disease

66
Q

Shows intermittent firing (impaired recruitment) but normal amplitude

A

Neuropathic disease

67
Q

To detec auto immune forms of neuropathy

A

Antibody testing

68
Q

To detect nerve or muscle disease

A

Genetic testing

69
Q

To assess tissue and cellular signs of myopathy

A

Muscle biopsy

70
Q

Nerve conduction studies

A

Measure distance and latency to compound motor action potential recorded from muscle, then calculate velocity (should be the same at all locations) also measure amplitude

71
Q

Different amps

A

Axonopathy

72
Q

Different velocity

A

Demyelination

73
Q

How is the pattern different in NMJ than in neuropathy

A

NMJ disorders can:

  1. No sensory loss (rare in neuropathies)
  2. Some show fatiguable weakenss
  3. Some may improve with sustained motor effort
  4. DX techniques for NMJ vs neuropathies: electromyography
74
Q

Myopathies vs neuropathies

A
  1. No sensroy loss in myopathies
  2. Diffuse weakness in myopathies vs focal/multifocal/diffuse neuropathies
  3. Diagnostic techniques techniques for myopathies: EMG, muscle biopsy, genetic testing
  4. Diagnostic techniques for neuropathies: nerve conduction, genetics, blood
75
Q

What is there none of in neuropathies?

A

Sensory loss

76
Q

What kind of weakness in neuropathies?

A

Diffuse weakness

77
Q

Diagnostic techniques for myopathies

A

EMG, muscle biopsy, genetic testing

78
Q

Diagnostic techniques for neuripathies

A

Nerve conduction, genetics, blood

Neuro Block 5 (11 decks)

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