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
Your patient comes in with LMN disease. What types of sensory deficits might you see in her?
- sensory loss (including proprioception) in same areas of motor weakness - hypersensitivity of neurons (hyperalgesias, pins/needles)
26
T/F: autonomic dysfunction is present in those with LMN issue.
true (edema from poor vasomotor tone, orthostatic hypotension)
27
Your patient comes in with a diagnosis of postpolio syndrome. What are some symptoms you might expect?
myalgias since it's an inflammatory myopathy
28
What diagnostic tests can be done to confirm peripheral nerve disorders?
NCV testing (measuring time of conduction from place to place) EMG (needle in muscle looking at motor unit potentials)
29
T/F: Cranial nerves are part of the CNS.
false, they're peripheral
30
What are some causes of trigeminal neuralgia?
compression on basilar artery or cerebellopontine tumor - or degeneration, unknown etiology
31
Exacerbations of trigeminal neuralgia?
stress, cold -> causes spasms of pain along trigeminal nerve distribution, restricted to one side of face - relieved by relaxation
32
T/F: those with trigeminal neuralgia have good motor control of facial muscles.
true, motor control is normal | - just a neurogenic pain issue
33
What mode of relief can you give these patients?
TENS
34
Bell's palsy involves what cranial nerve?
CN VII -> unilateral facial paralysis
35
What is recovery time for Bell's palsy?
several weeks/months
36
T/F: Full sensation is present in Bell's palsy
true (that's from trigeminal)
37
Etiology of Bells palsy?
acute inflammatory process causing compression of CN VII
38
What should you assess for with Bell's palsy?
1) drooping of mouth, eyelids that don't close 2) taste to ant. 2/3rds of tongue 3) facial expression muscles
39
PT treatment of bells palsy includes what?
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
What is Bulbar palsy, and what are typical deficits?
bulbar palsy = weakness/paralysis of motor nuclei (face, tongue, larynx, pharynx) - difficulties with swallowing, phonation, coughing
41
What does your pharynx do?
promotes swallowing
42
What type of disease is GBS?
LMN disease, characterized by acute demyelination of both cranial and peripheral nerves - often occurs after recovery from infectious illness (respiratory/gastrointestinal)
43
In GBS, is it more sensory or motor involvement?
motor more, but also sensory
44
What is the prognosis with GBS?
85% make full recovery, rarely any die | - recovery slow though, 6mo - 2 years
45
In what direction do symptoms occur with GBS?
distal to proximal
46
What are especially important to check in your assessment of a patient with GBS?
``` MMT Cranial nerve function Sensory Skin integrity (d/t prolonged hospitalization) Vitals and reflexes Respiratory function ```
47
What should you avoid with exercise prescription for patients with GBS?
over fatiguing exercise, as that can delay recovery
48
Is ALS a disorder of UMN or LMN?
BOTH | - degeneration of anterior horn cells and descending corticobulbar/corticospinal tracts
49
Prognosis of ALS?
death in 2-5 years
50
You have an evaluation of a patient with ALS. What symptoms might you expect?
LMN issues: muscle weakness/atrophy, fasciculations UMN issues: spasticity, hyperreflexia bulbar issues (dysphagia, dysphonia) near end autonomic dysfunction pain
51
You have an evaluation of a patient with ALS. What symptoms might you expect?
LMN issues: muscle weakness/atrophy, fasciculations UMN issues: spasticity, hyperreflexia bulbar issues (dysphagia, dysphonia) near end autonomic dysfunction pain
52
What is PTs role in ALS?
1) maintain respiratory function (cough production, breathing technqiues, chest stretching) 2) prevent indirect impairments for as long as possible 3) energy conservation
53
T/F: overwork damage can occur in ALS
true, so only give mild resistance exercises to muscles with 3/5 or above
54
What is postpolio syndrome?
new, slowly PROGRESSIVE muscle weakness in people that had polio before and were functioning for awhile
55
What is the reticular formation and what does it do?
in brainstem and responsible for wakefullness/alertness, sexual functioning
56
What are some symptoms that characterize postpolio syndrome?
myalgia weakness/atrophy in asymmetrical distribution abnormal fatigue with poor recovery with rest cold intolerance concentration/memory difficulty
57
For which PNS diseases should you really be focusing on energy conservation teaching as well as respiratory function focus and limiting high intensity training?
post polio GBS ALS
58
When is exercise contraindicated for those with post polio?
severe atrophic polio