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AIM - The Brain > Peripheral Neuropathies > Flashcards

Peripheral Neuropathies Flashcards

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1
Q

what % of peripheral neuropathies are idiopathic?

A

10-30% are idiopathic

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2
Q

subtypes of neuropathy

A

1) axonal
2) demyelinating
3) wallerian degeneration

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3
Q

perineurium

A

surrounds each nerve fascicle

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4
Q

epineurium

A

binds all the fascicles in a nerve

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5
Q

blood supply of peripheral nerves

A

longitundinal, highly anastamosing vascular supply of arterial branches

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6
Q

size and myelination of touch, pressure, spindle afferents

A

Large, heavily myelinated

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7
Q

size and myelination of sharp pain, temperature

A

smaller, thinly myelinated

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8
Q

size and myelination of dull/burning/poorly localized pain

A

small, unmyelinated

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9
Q

type I PNS sensory fibers

A

myelinated
80-120 m/sec (fastest)

touch, pressure, spindle afferents

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10
Q

type II PNS sensory fibers

A

thinly myelinated
30-75 m/sec (medium speed)

sharp pain, temperature

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11
Q

type III PNS sensory fibers

A

unmyelinated
0.5-30 m/sec (slowest)

burning, dull, diffuse pain

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12
Q

PNS Motor: large myelinated fibers terminate on _____

A

PNS Motor: large myelinated fibers terminate on MUSCLE

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13
Q

PNS Motor: small unmyelinated fibers terminate on _____

A

PNS Motor: small unmyelinated fibers terminate on parasympathetic/sympathetic ganglia

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14
Q

alpha motor unit

A

80-120 m/sec (fast)
large, myelinated

main movers of skeletal muscle

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15
Q

gamma motor unit

A

4-25 m/sec (kinda slow)
large, myelinated

terminate on muscle spindles, maintain tension

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16
Q

preganglionic autonomic

A

3-15 m/sec (slow)

small, unmyelinated

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17
Q

postganglionic autonomic

A

.5-2 m/sec (super slow)

small, unmyelinated

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18
Q

axonal transport runs along __________

A

axonal transport runs along MICROTUBULES

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19
Q

anterograde transportation

A

away from cell body

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20
Q

retrograde transportation

A

towards cell body

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21
Q

T or F: axonal transport does not require energy

A

F.

Axonal transport requires energy – ox phos in mitochondria

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22
Q

effects of vincristin/vinblastine (chemotherapeutic drugs) on axons

A

Disrupt neurotubule organiation.

Results in neuropathy.

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23
Q

________ transport is necessary to maintain the axon itself

A

ANTEROGRADE transport is necessary to maintain the axon itself (and thus the muscle too since denervated muscles atrophy)

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24
Q

what happens to denervated muscle?

A

atrophy

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25
Q

what is transported with rapid axonal transport?

A

synaptic vesicles,

membrane bound proteins

26
Q

what is required to link proteins to microtubules in anterograde axonal transport?

A

kinesin

27
Q

what is transported with slow axonal transport?

A

soluble enzymes,
tubulin (used in making microtubules)

100x slower

28
Q

what determines the rate of recovery from nerve injury?

A

slow axonal transport

-bc it is needed to transport the structural components

29
Q

what is transported with retrograde transport?

A

Signal of nerve injury

-induces chromatolysis

30
Q

neurotropic viruses and axonal transport

A

Neurotropic viruses: polio, herpes, rabies.

  • enter peripheral nerve endings
  • use retrograde transport to ascend to nerve body
31
Q

what protein is required with retrograde axonal transport?

A

dynein (instead of kinesin)

32
Q

Wallerian degeneration

A

“dying forward”

  • axonal injury occurs
  • axon dies from site of injury to the end of the axon (peripherally)
  • chromatolysis
  • muscle atrophy
  • can regenerate if myelin sheath is still intact
33
Q

axonal degeneration

A

“dying back”

  • metabolic derangement
  • distal part dies first (due to lack of nutrients etc)
  • proximal direction
  • chromatolysis
  • muscle atrophy
34
Q

segmental demyelination

A
  • myelin is stripped off in some places
  • AP dies out
  • axon is still intact, just missing myelin
  • NO chromatolysis
  • NO muscle atrophy
35
Q

nerve conduction studies

A
  • used to diagnose peripheral neuropathies
  • measure nerve function
  • measure evoked action potentials (either motor or sensory)

does NOT look at overall nerve function
-just between cell body and end organ

-helps distinguish between types of lesions

36
Q

Peripheral nerve injury: appearance on nerve conduction studies

A

Motor: abnormal
Sensory: abnormal

  • lesion distal to dorsal root ganglion
  • both axons are cut between cell body and muscle
  • neither trigger an AP
37
Q

nerve root injury: appearance on nerve conduction studies

A

Motor: abnormal
Sensory: normal

  • axon bringing sensory info to cell body is still intact; still transmits AP
  • motor axon is cut between anterior horn cells and muscle; degenerates; no AP
38
Q

patterns involved in diagnosis of peripheral neuropathies

A
  • Focal v. Systemic
  • Motor v. Sensory v. Autonomic v. Mixed
  • Chronic v. Acute
  • Axonal v. Demyelinating
  • weakness: myotomal or peripheral nerve pattern
  • atrophy?
  • distal weakness (axonal) or proximal weakness (demyelinating)?
39
Q

patellar reflex tests

A

L4

40
Q

achilles reflex tests

A

S1

41
Q

how to measure conduction velocity

A

Stimulate nerve at two spots
Subtract the time between the two

slower in demyelinated nerve

42
Q

pattern of root damage v. peripheral n damage

A

ROOT

  • dermatomes overlap
  • difficult to pinpoint

PERIPHERAL N

  • do not overlap
  • easier to pin point
43
Q

muscles atrophy suggests

A

axonal damage

44
Q

no atrophy suggests

A

demyelinating damage

45
Q

distal weakness suggests

A

axonal damage

46
Q

proximal weakness suggests

A

demyelinating damage

OR myopathy

47
Q

symptoms of axonal neuropathy

A
  • slow, chronic
  • stocking glove distribution
  • loss of reflexes distally
  • muscle wasting distally
  • low amplitude CMAPs (muscle AP)
  • absent SNAPs (sensory AP)
48
Q

causes of axonal neuropathy

A
  • metabolic: diabetes, uremia, endocrine, porphyria
  • toxic: environmental or pharmalogical agents
  • deficiency: thiamine, pyridoxine, vit E
  • genetic: HSMN II
  • paraneoplastic: tumors make antibodies that injure nerves
49
Q

Guillian-Barre Syndrome

A
  • acute demyelinating polyneuropathy
  • segmental demyelination
  • primarily motor (some sensory)
  • cause: autoimmune: Abs cause inflammation, destroy myelin
  • rapidly progressive
  • no reflexes (afferent pathology)
  • ataxia (afferent pathology)
  • conduction block
  • treatment: immune modulating therapy (IVIg)
50
Q

if reflexes are lost, it is most likely due to a ______ injury

A

sensory/afferent

51
Q

what part of the nerve is most susceptible to injury?

A

myelin

  • may degenerate as part of primary disease process
  • or as secondary effect of axonal disruption
52
Q

causes of demylinating polyneuropathy

A
  • autoimmune: Guillain-Barre, CIDP (chronic inflammatory demyelinating neuropathy), certain antibodies
  • genetic: Charcot-Marie-Tooth I, metachromatic leukodystrophy
53
Q

causes of chronic demyelinating neuropathy

A
  • hereditary: Charcot-Marie-Tooth I

- chronic inflammatory demyelinating neuropathy (CIDP)

54
Q

histological sign of chronic demyelinating neuropathy

A

onion bulb sign

-myelin grows, dies, grows, dies…

55
Q

ischemic mononeuritis multiplex

A
  • commonly seen in polyarteritis nodosa (vasculitis)
  • fascicular injury –> individual fascicles are injured by interruption of microcirculation of nerve
  • confluent mononeuritis makes it look like generalized neuropathy
  • biopsy: arteritis, fascicular injury

-tx: steroids (vasculitis), cyclophosphamide (immune modulating drug)

56
Q

fascicular injury

A
  • Individual fascicles are injured, not the whole nerve.

- Due to interruption of the microcirculation of the nerve.

57
Q

types of focal neuropathies

A
  • Compressive/traumatic
  • Ischemic: diabetic or vasculitic – fascicular injury
  • autoimmune; brachial plexopathy

-Injury: wallerian degeneration

58
Q

injury associated with focal neuropathies

A

wallerian degeneration

  • disruption of anterograde transport so axon dies forward
  • retrograde transport starts chromatolysis, increases metabolic activity for axonal regeneration
  • axonal sprouting occurs
  • regeneration depends on if schwann cell sheaths are disrupted or not
59
Q

traumatic nerve injury classification

A

CLASS 1: Neurapraxia

  • compression with focal demyelination
  • no denervation (no atrophy)
  • quick recovery

CLASS 2: Axonotmesis

  • axonal damage
  • intact nerve sheath for sprouting to occur through
  • slower recovery (sometimes incomplete)

CLASS 3: Neurotmesis

  • scarred/disrupted nerve sheath
  • no recovery
60
Q

neurotmesis

A
  • scarred/disrupted nerve sheath

- no recovery

61
Q

Axonotmesis

A
  • axonal damage
  • intact nerve sheath for sprouting to occur through
  • slower recovery (sometimes incomplete)
62
Q

Neurapraxia

A
  • compression with focal demyelination
  • no denervation (no atrophy)
  • quick recovery

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