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Neuroscience > Peripheral Neuropathies. > Flashcards

Peripheral Neuropathies. Flashcards

1
Q

Describe: Paranodal/Segmental Demyelinization

A
  • Axon is spared, myelin covering is attacked.
  • Slowed conduction velocity without denervation.
  • Mild symptoms include impairment of vibratory sense, loss of reflexed, decreased proprioception or weakness.
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2
Q

Describe: Axonal degeneration

A
  • Intrinsic axonal disease or motor neuron disease
  • Distal dying back process
  • Normal conduction is maintained in intact neurons, absent in affected axons/nerves.
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3
Q

Describe: Wallerian degeneration

A
  • Damage to a local aspect of the axon, death back to proximal node of ranvier.
  • Muscle is no longer innervated
  • Growth of axon 1-3mm per day, but may not recover.
  • ROM must be maintained during repair via electric stimulation.
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4
Q

What is the distribution of polyneuropathies?

A
  • Symmetrical
  • LONGEST NEUROPATHY
  • STOCKING GLOVE DISTRIBUTION
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5
Q

What are the four classifications of polyneuropathies?

A
  • Inherited
  • Metabolic/Nutritional
  • Toxic
  • Immune/Inflammatory
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6
Q

Give the examples of inherited polyneuropathy

A
  • Charcot-Marie Tooth

- Friedrichs-Ataxia

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7
Q

Give the examples of metabolic/nutritional polyneuropathy

A
  • Diabetic
  • Alcoholism
  • Vit. B12 deficiency
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8
Q

Give the examples of toxic polyneuropathy

A
  • Heavy Metals

- Drugs

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9
Q

Give the examples of immune polyneuropathy

A
  • Guillain-Bare

- Chronic Inflammatory Demyelinating Polyneuropathy

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10
Q

What are the symptoms of polyneuropathies?

A

STOCKING GLOVE DISTRIBUTION

  • Weakness or flaccid paralysis
  • Sensory loss or paresthesias
  • DTRs decreased or gone
  • Pain
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11
Q

What is Charcot-Marie-Tooth?

A
  • AKA Peroneal muscle atrophy.
  • Only non-rare polyneuropathy.
  • Typically effects myelin, but there are different forms
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12
Q

How is Charcot-Marie-Tooth passed on?

A

-autosomal dominant

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13
Q

What are the sings and symptoms of Charcot-Marie-Tooth

A
  • Distal LE muscle atrophy: startingwith peroneals, foot intrinsics, and anterior tib.
  • UE affected later in diseases, hand then forearm
  • Rarely goes above thigh or elbow
  • Decreased DTR, sometimes sensory loss.
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14
Q

When does CMT occur?

A

End of 1st decade to second decade

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15
Q

How is CMT diagnosed?

A

-EMG, NCV, nerve biopsy, genetic test

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16
Q

What is fredriechs ataxia?

A
  • Mixed peripheral neuropathy and CNS degeneration, beginning with dorsal root ganglion, impact sensory fibers
  • Develop degenerative changes of lateral column of spinal cord and clarkes nucleus.
  • CN involvement and dysarthric speech
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17
Q

What are the signs and symptoms of friedrichs ataxia?

A
  • Initially clumsiness of hands, ataxic gait, and decreased DTRs.
  • Later: spasticity, severe ataxia, weakness, hyper-reflexia to areflexia
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18
Q

When is the onset of friedrichs ataxia?

A

-Early teens

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19
Q

What is the clinical course of friedrichs ataxia?

A

-Death in 10-20 years, usually due to cardiac and/or pulmonary complications (usually by age 35)

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20
Q

What is the clinical course for CMT?

A

-Slow progression that may self stabilize for long periods.

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21
Q

What is the most common complication of Diabetes?

A

-Neuropathy

22
Q

What is the most common cause of neuropathy?

A

-Diabetes

23
Q

What happens to nerves during a diabetic neuropathy?

A
  • Combo of axonal degeneration and demyelinization

- Leads to decreased connection velocity.

24
Q

What are the specific factors that cause diabetic neuropathy?

A
  • Metabolic abnormalities in neurons
  • Small blood vessel damage
  • Mechanical injury related to entrapments
  • smoking/alcohol use
25
Q

Describe polyneuropathy in the context of diabetes?

A
  • Most common form of diabetic neuropathy (75%)
  • Symptoms may be worse at night
  • Commonly: distal to proximal loss of sensation starting at the feet, decreased DTRs, not so much pain
  • Sometimes: pain and burning in feet, deep aching in legs, loss of temperature sense and normal DTRs.
26
Q

Describe multiple mononeuropathy in the context of diabetes?

A
  • Asymmetrical: Femoral nerve usually hit, pain and proximal weakness. Resolves over many months and most recover to walking.
  • Autonomic: postural hypotension, impaired thermoregulation, sweating, GI symptoms, vaginal dryness, increased heart rate.
27
Q

Describe mononeuropathies in the context of diabetes?

A
  • sudden focal neuropathy, usually improves over weeks or months.
  • high rate of entrapments.
28
Q

How is diabetic neuropathy treated?

A

Meds such as:

  • tricyclic antidepressants and other antidepressants
  • anticonvulsants
  • opioids
  • topicals such as capsaicin cream

Possibly acupuncture, biofeedback, TENS, magnetic therapy.

29
Q

What neuropathy arises from alcoholism and Vit B12 deficiency? Describe it?

A
  • Polyneuropathy
  • Mixture of sensory and motor
  • Aching in calves and soles of feet
  • Distal muscle weakness greater in LE than UE
30
Q

What is the treatment for alcoholic or Vit B12 neuropathy?

A

-Improved diet.

31
Q

What occurs during toxic neuropath?

A

-Axonal degeneration leading to sensory and motor loss

32
Q

What is the cause of Guillain Barre?

A
  • 50% occur post viral infection (mono or flu)

- Flu vaccine may cause it

33
Q

Who gets GB?

A

Very rare, but may occur in anyone.

34
Q

What happens in GB?

A

-Rapid inflammatory response of peripheral nerves causing:
1) Diffuse segmental demyelinization ventrally
OR
2) Axonal degeneration with peripheral demyelinization which slows nerve conduction.

35
Q

What is the pathology of GB?

A

-Lymphocytes infiltrate nerve roots and damage schwann cells and myelin, may destroy axons.

36
Q

How is GB diagnosed?

A

Lumbar puncture, EMG and NCV showing decreased speed of conduction

37
Q

What is the clinical course of GB?

A
  • Bilateral weakness and paresthesias
  • Progressing flaccid paralysis from the LE to the UE
  • May be minor motor involvement or major (respiratory muscles)
  • Back pain
  • Max weakness in 2-3 weeks
38
Q

What does recovery look like for GB?

A
  • Symptoms recover in reverse order of symptom onset.

- May be fatal (5%) but 85% regain ambulatory status in 6 months.

39
Q

How is GB treated?

A
  • Respiration is constantly monitored
  • IV Immunoglobulin is the preferred treatment but is expensive
  • Plasmapheresis is dangerous but used
  • PT is used as recovery has already progressed significantly, overworking muscles for strengthening may damage the nerves
40
Q

What does chronic inflammatory demyelinating neuropathy look like? How is it treated?

A
  • Severe for of GB
  • VERY RARE
  • Treated via IV immunoglobulin, chronic plasmapheresis, corticosteroids
41
Q

What are three causes of multiple mononeuropathies ?

A
  • Diabetes
  • Ischemic neuropathy secondary to peripheral vascular disease
  • Radiation damage
42
Q

What may cause mononeuropathies?

A
  • Trauma to a nerve
  • Pressure to a nerve
  • Radiation
  • Infections
  • Tumors
43
Q

What may add pressure to a nerve?

A

-Edema, positioning, tumors, compartment syndrome, entrapment.

44
Q

What are the three classes of trauma/pressure?

A
  • Neuropraxia
  • Axonotmesis
  • Neurotmesis
45
Q

Describe Neuropraxia

A
  • Nerve contusion leading to compression or slight stretching
  • Localized demyelinization WITHOUT DAMAGE TO AXON
  • Recovery in
46
Q

Describe Axonotmesis

A
  • Nerve sheath intact but damage to axon leading to wallerian degeneration in a distal direction
  • good prognosis
  • Time for recovery is related to distance
47
Q

Describe neurotmesis:

A

Complete disruption of nerve fibers and connective tissue due to complete severing leading to wallerian degeneration

-Poor prognosis
-May produce spiral or bulbous tips
-

48
Q

What happens in herpes zoster (shingles)?

A
  • Sensory root ganglion damaged, sometimes ventral damage due to recurrence off chicken pox virus
  • Follows unilateral dermatome pattern, sometimes bilateral
49
Q

What happens in bells pallsy? What causes it?

A
  • Viral infection leading to inflammation of CN 7
  • Facial symptoms show up as asymmetries
  • 85% recover spontaneously
50
Q

What is a radiculopathy?

A
  • Disease or compassion of spinal root.

- Leads to segmental demyelinization or axonal atrophy, or both

51
Q

Why are spinal roots vulnerable to damage?

A

-Thin covering, less blood supply, and less of a blood brain barrier.

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