8/30 Neuropathy - Glendinning Flashcards

1
Q

peripheral neuropathy

A

lesions affecting peripheral nervous system

  • cranial nerves
  • spinal nerves
  • peripheral nerves
  • nerve plexuses
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2
Q

symptoms of neuropathy vary depending on…

potential symptoms

A
  • whether myelin or axons are affected
  • which axons are affected
  • where the axons are affected

symptoms can include:

  • weakness, muscle atrophy
  • loss of reflexes
  • loss of sensation (numbness)
  • abnormal sensation (tingling, burning) - paresthesia
  • pain
  • autonomic changes (sweating, HR, vascular)
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3
Q

neurotpathic pain

A

different from nociceptive pain (tissue might be damaged, but nerves/nervous system intact)

  • arises from lesions in peripheral and central nervous system
  • can include burning, shooting, stinging pain mixed with areas of numbness
  • can include changes in pin threshold, quality of pain, and spontaneous pain

DEPRESSION is a common feature of chronic pain

ex. herpes zoster, trigeminal neuralgia
* antidepressants and anti-epileptics are primary drugs used to treat neuropathic pain

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4
Q

radiculopathy

vs

mononeuropathy

vs

plexopathy

vs

polyneuropathy

A

all FOCAL LESIONS

radiculopathy: sx follow a nerve root pattern (dermatome or myotome)

  • often caused by compression of nerve roots from protruding discs

mononeuropathy: sx follow a peripheral nerve

  • often caused by injuries

plexopathy: sx follow a nerve plexus

polyneuropathy: generalized process affects peripheral nerves → distal and symmetrical sensorimotor (poss autonomic) distribution

  • “glove and stocking” pattern
  • common causes: diabetes, alcohol, hypothyroidism, vitB12 def; also pts in intensive care
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5
Q

“Wallerian degeneration”

A

peripheral neuropathy results from damage/injury to cell bodies, axons, or myelin sheaths → leads to “Wallerian degeneration” aka “dying forward”

  1. distal axonal degeneration
  2. “chromatolysis” of cell body
    * nucleolus expands and moves to cell wall, Nissel substance disintegrates
  3. recruitment of macrophages

proximal stump can recover at rate of 1-2mm/day

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6
Q

“dying back” of axons

A

conditions that affect the health of the neuron (ex. metabolic diseases) → “dying back”

  • can be accompanied by loss of myelin

longer axons most susceptible and are affected first → distal extremities are affected first

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7
Q

“segmental demyelination”

A

occurs when myelin sheaths are damaged by trauma or disease

  • myelin may be affected secondarily to axonal death

sx of demyelination detected by Nerve Conduction tests, revealing:

  • conduction block
  • slowed conduction velocity

myelin and conduction can return in days to weeks

trauma affecting myelin : metaphorical “nerve concussion” - rapid effect, slow recovery

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8
Q

non-traumatic peripheral neuropathies

nutritional/metabolid

A
  • diabetes mellitus
  • vitamin def
  • uremia
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9
Q

non-traumatic peripheral neuropathies

toxic drugs

other toxins

A
  • drugs
    • vinblastine, vincristine (affect microtubule formation)
    • paclitaxel, cochicine, INH
  • toxins
    • alcohol, lead, aluminum, arsenic, mercury, acrylamide
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10
Q

non-traumatic peripheral neuropathies

vasculopathic

inflammatory

infection

A
  • vasculitis, amyloidosis
  • autoimmune: systemic lupus erythematosus, rheumatoid arthritis, sarcoidosis, Sjogren syndrome, Guillain Barre syndrome
  • chronic infl demyelinating polyneuropathy
  • herpes zoster
  • leprosy
  • HIV
  • Lyme disease
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11
Q

non-traumatic peripheral neuropathies

inherited

A
  • Charcot-Marie-Tooth neuropathy
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12
Q

diabetic neuropathy

A
  • most common compliation of diabetes
    • 30% of diabetic patients
    • 75-80% have subclinical neuropathy
    • 16% have chronic neuropathic pain
  • greatest source of M&M
    • 50-75% of all amputations
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13
Q

length-dependent diabetic polyneuropathy

A
  • accounts for 80+% of patients with diabetic neuropathy

sx start in feet → more to more proximal legs and and distal upper limbs

  • “glove and stocking” pattern of sensory loss
  • paresthesias, dysesthesias, numbness/tingling/burning
  • motor weakness of distal limbs
  • can lead to trophic changes : calluses and plantar ulcers
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14
Q

pathophys of diabetic neuropathy

A

axonal degen, dying back, and demyelination occur

  • includes effects related to ischemia, oxidative stress, infl processes

sensory neurons more affected than motor, but both may be affected

  • sensory often involves just small unmyelinated and myelinated fibers : small fiber polyneuropathy
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15
Q

vitamin B12 deficiency

A
  • most common metabolic neuropathy
    • 3-16% prevalence in US; 21% in geriatric pop
  • may affect peripheral nerves, optic nerves, spinal cord, brain
  • most common feature: loss of vibration sense
  • sx affect distal limbs, but begin more commonly in upper limb
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16
Q

subacute combined degeneration

A

primary or secondary effect of B12 definiciency in which lateral and dorsal columns of spinal cord affected

  • can lead to sx of ataxia and spasticity occuring together with sx of peripheral neuropathy
17
Q

causes of B12 deficiency

A

B12 ingested through animal protein → deficiency often seen in vegans/vegetarians or people with gluten sensitivity/malabsorption

may also see pernicious anemia also bc B12 needed to produce red blood

18
Q

pathophys of B12 deficiency neuropathy

A

without B12, myelin production is abnormal → decreased nerve conduction velocity

need to differentiate from MS, but once you do, treat with B12 therapy

19
Q

Guillan Barré

aka

A

acute inflammatory demyelinating polyneuropathy (AIDP)

most common cause of acute paralysis seen in clinical practice

  • incidence 1/100k
  • all countries, all ages, all seasons

most rapidly progressing and potentially fatal form of neuropathy

20
Q

major features of Guillain Barré

A

primarily motor symptoms

  • ascending symmetric paralysis → acute cases? can affect breathing and require resp support

may begin with parasthesias in toes/fingers, aching in thighs/back

2 sx used to make diagnosis

  • decreased nerve conduction velocity (with conduction blocks)
  • increased protein in CSF with normal cell count (albuminocytologic dissociation)
21
Q

cause of GBS

A

60% of time, GB begins 1-3 weeks after infection or vaccination

ex. Campylobacter jejuni or Herpesvirus infection (NOT a definitive link!)

infection causes an autoimmune/infl attack on peripheral myelin

22
Q

GBS inflammatory process

A

widespread infl process affecting myelin sheaths

  • lymphocytes attach to vessel wall → migrate through wall and enlarge
  • lymphocytes attack myelin (segmental demyelination); axons may also be affected
  • severe cases → nerve cell body may die

see presence of polymorphonuclear leukocytes

23
Q

dx of GB

A

usually follows inf or vaccination

2 more important diagnostic tests are:

  • CSF analysis → increased protein
  • nerve conduction test → decreased cond velocity
24
Q

Charcot-Marie-Tooth Disease

A

“hereditary motor and sensory neuropathy”

  • group of several hereditary diseases that directly affect either myelin (CMT1) or axons (CMT2)
25
Q

CMT1

A

most common: CMT1 (myelin) → combined motor/sensory neuropathy

  • primarily affects distal muscle, esp affecting peroneal nerve
  • bc of demyelination, small fiber types carrying pain and temp are not affected
  • frequently occurs with pes cabus and hammertoes (true for all CMT)

prevalence: 1/2500

typical onset: late childhood

ID: slow progressive nature, decr cond velocity in all nerves

  • can see fewer numbers of myelinated axons in peripheral nerves