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BOARDS: Neuromuscular > Cranial and Peripheral Nerve Disorders > Flashcards

Cranial and Peripheral Nerve Disorders Flashcards

1
Q

What are the 3 pathological processes behind peripheral nerve disease/injury?

A

1) wallerian degeneration
2) segmental demyelination
3) axonal degeneration

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2
Q

What is destroyed with wallerian degeneration?

A

axons and myelin distal to injury degenerate d/t transection of nerve

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3
Q

Can wallerian degeneration improve?

A

endoneurium (nerve sheath) doesn’t regenerate but forms a tube direction regeneration

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4
Q

What type of cells do the myelinating in the PNS?

A

schwann cells = myelinate the peripheral nerves

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5
Q

Describe the layers of protections for a neuron.

A 
epineureum = surrounds entire spinal nerve
perineureum = surrounds a fascicle in the spinal nerve
endoneureum = surrounds a myelinated/unmyelinated neuron
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6
Q

T/F: Neurons in the PNS typically don’t regenerate.

A

false, they can

- it’s in the CNS that neurons typically don’t regenerate d/t oligodendrocytes, the enviro, etc

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7
Q

What helps clean up neuronal cell damage in the PNS?

A

macrophages, schwann cells

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8
Q

How fast does an axon regenerate?

A

1mm/day

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9
Q

What are the three types of traumatic nerve injury, least issue to most issue?

A

1) neuropraxia (transient loss of function; conduction block ischemia)
2) axonotomesis (injury to nerve interrupting axon causing wallerian degeneration distal to lesion; regeneration possible
3) neurotomesis: cutting of nerve with severance of all structures; reinnervation typically requires surgery

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10
Q

What remains intact in neuropraxia?

A

everything: axon and endoneurium are all good, just myeline is squished/compressed
- think about radial nerve compression at night, causes wrist drop when you wake up
- this is a rapid reversal case cause it goes away when you move

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11
Q

What remains intact in axonotmesis? What issues occur?

A

endoneurium still intact!!

  • only myelin/axon interrupted
  • so since everything still contained, regeneration is possible

BUT distal end: terminal bulbs die off since no complete connection; wallerian degeneration occurs

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12
Q

Crush injuries and displaced bone injuries often have what kind of nerve damage?

A

axonotmesis (endoneurium intact, axon disrupted)

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13
Q

Wallerian degeneration occurs in which of the three nerve injury types?

A

axonotmesis

neurotmesis

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14
Q

What is intact with neurotmesis?

A

nothing: endoneurium is damaged, no pathway for axon to regrow and find its terminal bulbs (wallerian degeneration occurs)

  • worse case: epineurium is damaged, indicating NO growth potential
  • if perineurium is split, poor growth may occur
  • fair growth with only endoneurium involved
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15
Q

What is polyneuropathy?

A

bilateral, symmetrical involvement of peripheral nerves

  • degeneration usually occurring more in legs, distal to proximal
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16
Q

In segmental demyelination, does wallerian degeneration occur? In what disease do we see this occur?

A

no

See this is GBS

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17
Q

What is the pathological process behind peripheral neuropathy?

A

axonal degeneration: degeneration of axon/myelin, progressing proximal to distal

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18
Q

A disease with involvement of nerve roots is indicated by what term?

A

radiculopathy

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19
Q

The nerve roots coming off the spinal cord exit to form peripheral nerves through what foramen?

A

intervertebral foramen

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20
Q

A dorsal ramus carries what kind of information?

A

both sensory and motor
- it’s the dorsal branch off of the spinal nerve (which was the joining of the ventral/dorsal root)

ventral root + dorsal root = spinal nerve -> dorsal and ventral rami

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21
Q

Are axons damaged in segmental demyelination?

A

NO just demyelinated (like in GBS)

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22
Q

What does the term neuropathy mean?

A

any disease of the nerves characterized by deterioration of nerve function

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23
Q

What is the pathologic process for peripheral neuropathy?

A

axonal degeneration -> degernation of axon/myelin from distal to proximal

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24
Q

Do people with LMN disorders have muscle weakness? What kind?

A

yes, rapid and atrophy and fatigue

- in a root-innervated pattern

25
Q

Your patient comes in with LMN disease. What types of sensory deficits might you see in her?

A
  • sensory loss (including proprioception) in same areas of motor weakness
  • hypersensitivity of neurons (hyperalgesias, pins/needles)
26
Q

T/F: autonomic dysfunction is present in those with LMN issue.

A

true (edema from poor vasomotor tone, orthostatic hypotension)

27
Q

Your patient comes in with a diagnosis of postpolio syndrome. What are some symptoms you might expect?

A

myalgias since it’s an inflammatory myopathy

28
Q

What diagnostic tests can be done to confirm peripheral nerve disorders?

A

NCV testing (measuring time of conduction from place to place)

EMG (needle in muscle looking at motor unit potentials)

29
Q

T/F: Cranial nerves are part of the CNS.

A

false, they’re peripheral

30
Q

What are some causes of trigeminal neuralgia?

A

compression on basilar artery or cerebellopontine tumor

  • or degeneration, unknown etiology
31
Q

Exacerbations of trigeminal neuralgia?

A

stress, cold -> causes spasms of pain along trigeminal nerve distribution, restricted to one side of face
- relieved by relaxation

32
Q

T/F: those with trigeminal neuralgia have good motor control of facial muscles.

A

true, motor control is normal

- just a neurogenic pain issue

33
Q

What mode of relief can you give these patients?

A

TENS

34
Q

Bell’s palsy involves what cranial nerve?

A

CN VII -> unilateral facial paralysis

35
Q

What is recovery time for Bell’s palsy?

A

several weeks/months

36
Q

T/F: Full sensation is present in Bell’s palsy

A

true (that’s from trigeminal)

37
Q

Etiology of Bells palsy?

A

acute inflammatory process causing compression of CN VII

38
Q

What should you assess for with Bell’s palsy?

A

1) drooping of mouth, eyelids that don’t close
2) taste to ant. 2/3rds of tongue
3) facial expression muscles

39
Q

PT treatment of bells palsy includes what?

A

1) providing active facial muscle exercises
2) e- stim to maintain tone/support facial muscle fxn
3) protect cornea with eye patching; decrease droop stretching with facial sling (no lacrimal gland right now)
4) functional retraining; easier foods to eat, one sided chewing, etc

40
Q

What is Bulbar palsy, and what are typical deficits?

A

bulbar palsy = weakness/paralysis of motor nuclei (face, tongue, larynx, pharynx)

  • difficulties with swallowing, phonation, coughing
41
Q

What does your pharynx do?

A

promotes swallowing

42
Q

What type of disease is GBS?

A

LMN disease, characterized by acute demyelination of both cranial and peripheral nerves

  • often occurs after recovery from infectious illness (respiratory/gastrointestinal)
43
Q

In GBS, is it more sensory or motor involvement?

A

motor more, but also sensory

44
Q

What is the prognosis with GBS?

A

85% make full recovery, rarely any die

- recovery slow though, 6mo - 2 years

45
Q

In what direction do symptoms occur with GBS?

A

distal to proximal

46
Q

What are especially important to check in your assessment of a patient with GBS?

A 
MMT
Cranial nerve function
Sensory
Skin integrity (d/t prolonged hospitalization)
Vitals and reflexes
Respiratory function
47
Q

What should you avoid with exercise prescription for patients with GBS?

A

over fatiguing exercise, as that can delay recovery

48
Q

Is ALS a disorder of UMN or LMN?

A

BOTH

- degeneration of anterior horn cells and descending corticobulbar/corticospinal tracts

49
Q

Prognosis of ALS?

A

death in 2-5 years

50
Q

You have an evaluation of a patient with ALS. What symptoms might you expect?

A

LMN issues: muscle weakness/atrophy, fasciculations

UMN issues: spasticity, hyperreflexia

bulbar issues (dysphagia, dysphonia) near end

autonomic dysfunction

pain

51
Q

You have an evaluation of a patient with ALS. What symptoms might you expect?

A

LMN issues: muscle weakness/atrophy, fasciculations

UMN issues: spasticity, hyperreflexia

bulbar issues (dysphagia, dysphonia) near end

autonomic dysfunction

pain

52
Q

What is PTs role in ALS?

A

1) maintain respiratory function (cough production, breathing technqiues, chest stretching)
2) prevent indirect impairments for as long as possible
3) energy conservation

53
Q

T/F: overwork damage can occur in ALS

A

true, so only give mild resistance exercises to muscles with 3/5 or above

54
Q

What is postpolio syndrome?

A

new, slowly PROGRESSIVE muscle weakness in people that had polio before and were functioning for awhile

55
Q

What is the reticular formation and what does it do?

A

in brainstem and responsible for wakefullness/alertness, sexual functioning

56
Q

What are some symptoms that characterize postpolio syndrome?

A

myalgia
weakness/atrophy in asymmetrical distribution
abnormal fatigue with poor recovery with rest
cold intolerance
concentration/memory difficulty

57
Q

For which PNS diseases should you really be focusing on energy conservation teaching as well as respiratory function focus and limiting high intensity training?

A

post polio
GBS
ALS

58
Q

When is exercise contraindicated for those with post polio?

A

severe atrophic polio

BOARDS: Neuromuscular (16 decks)

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