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Neuroscience > L48 PNS Disorders > Flashcards

L48 PNS Disorders Flashcards

1
Q

define paresthesias.

A

a morbid or abnormal sensation, as burning, prickling, pins and needles, numbness

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2
Q

define ephapse.

A

pathological contact between parallel nerve fiber where electrical nerve impulses can “leak” from one fiber to the other

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3
Q

What are negative manifestations?

A
  • muscle weakness (paresis)
  • loss of tendon reflexes
  • autonomic nerouvs deficits (eg. anhydrosis)
  • impaired sensations (eg. pain and temperature loss)

*lose your strength and become weak

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4
Q

what is the cause of negative manifestations?

A

conduction failure in efferent and/or afferents

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5
Q

what are positive manifestations?

A
  • Fasciculations - unpredictable activity in path motor units
  • paresthesias (tingling, numbness and pins and needles) - may reflect ephaptic transmission between adjacent damaged sensory nerve fibers that have become hyperexcitable
  • brief periods of pain (eg. trigeminal neuralgia, carpal tunnel syndrome) - prob causes by acute periods of compression of nerves that produce brief hyperexcitabiliy
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6
Q

what is the conduction of velocity formula?

A

conduction velocity = D/(T1-T2) for sensory and motor!

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7
Q

what is the mean conduction velocity for sensory and motor nerves?

A

55 m/s

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8
Q

What type of CV measurement do you see with a lesion at the motor neuron soma?

A

slight/no change in motor

no change in sensory

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9
Q

What type of CV measurement do you see with a lesion at peripheral nerve specifically with demyelination?

A

REDUCTION of motor + sensory

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10
Q

What type of CV measurement do you see with a lesion at peripheral nerve specifically with compression?

A

slowing of motor + sensory AT THE SITE

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11
Q

What type of CV measurement do you see with a lesion at peripheral nerve specifically with axonal degeneration?

A

no/slight reduction

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12
Q

What type of CV measurement do you see with a lesion at NMJ?

A

no change in motor + sensory

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13
Q

What type of CV measurement do you see with a lesion at muscle?

A

no change in motor + sensory

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14
Q

what are examples of mechanical trauma to nerves?

A
  • compression, stretching (carpal tunnel syndrome)
  • crush
  • axotomy

*note - the smaller the structure is, the more vulnerable it is to damage

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15
Q

what is CV measurement used to rule in or out?

A

can detect demyelinating diseases

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16
Q

what is the most vulnerable part of the peripheral nerve?

A

axon covered in endoneurium (within fascicles surrounding small clusters of axons)

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17
Q

what is the least vulnerable part of the peripheral nerve?

A

epineurium (outer covering of the entire nerve)

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18
Q

what does the perineurium cover?

A

covers each fascicle

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19
Q

Describe carpal tunnel syndrome

A

occurs spontaneously!

compression of the medial nerve passing from the forearm into the narrow carpal tunnel at the wrist

sometimes the tendon develops an irritations or swelling, causing the carpal tunnel to narrow even further, compressing the median nerve (maybe due to overuse or from soft tissue swelling due to edema)

weakness, pain and numbness affecting the hand and wrist will accompany pain that often radiates up the arm

causes difficulty handling small objects (maybe wasn’t got abductor brevis and opponents pollicis) and muscular atrophy of the thenar eminence

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20
Q

what are risk factors for carpal tunnel syndrome?

A

women (middle aged)
pregnancy
hypothyroidism
elderly

21
Q

what does the carpal tunnel contain?

A

tendon of FPL, long finger flexors and median nerve

22
Q

what happens in a crush injury?

A

there is extensive damage to musculature and nerve

you will see LOTS of edema!

23
Q

define axotomy?

A

nerve injury with ruptured or cut axons that yields many consequences

24
Q

what are some of the consequences of axotomy?

A

wallerian degeneration
anterograde transneural degeneration
retrograde transneural degeneration

25
Q

what is Wallerian degeneration?

A

degeneration of the axon distal to injury

26
Q

what is anterograde transneural degeneration?

A

degeneration of nerve cells distal to injury
retraction of synaptic terminals proximal to injury
chromatolysis seen

27
Q

What is chromatolysis

A

is the dissolution of the Nissl bodies in the cell body of a neuron. It is an induced response of the cell usually triggered by axotomy, ischemia, toxicity to the cell, cell exhaustion, virus infections, and hibernation in lower vertebrates.

28
Q

what is retrograde transneural degeneration

A

degeneration of nerve cells proximal to the injury
chromatolysis seen

*this is seen in ALS (Lou Gehrig’s disease)

29
Q

axonal sprouts may use lingering ______ of the degenerated axons as guide tubes for regrowth

A

Schwann cells

30
Q

when does of the probability of successful regrowth increase?

A

when the site of injury is nearer to the original target

31
Q

in Bell’s palsy, there is sometimes regeneration error seen in peripheral nerves. What is an example of this?

A

some nerves regenerate and travel to buccal area
some nerve regenerate and accidentally travel to eye
so if you tell that pt a joke, they will attempt to smile but they may wink at you instead!

32
Q

what facilitates axonal regrowth?

A

nerve growth factor

33
Q

what releases nerve growth factor

A

Schwann cells, laminins and adhesion molecules

34
Q

the axonal sprout may grow at a rate of _____

A

1 mm per day!
slow process
if you have a lesion 30cm away, it will take a year for nerve to heal

after regeneration, Schwann cells redevelop and CV may increase!

35
Q

why don’t axons in the CNS regenerate?

A
  • oligodendrocytes do not release growth factor nor guide regenerating axonal sprouts
  • GLIOSIS occurs - astrocyte multiply in regions of trauma and form a scar that mechanically impedes sprouting axons
  • chemical signaling may also oppose axonal regeneration in the adult
36
Q

following nerve damage, motor axons may regenerate and form new ____

A

NMJ

37
Q

the regenerating axons differentiate into _____ when they contact the basal lamina

A

nerve terminals

38
Q

components of the _____ facilitate rein nervation of the synaptic sites and trigger differentiation of axonal growth cones into presynaptic nerve terminals

A

basal lamina

39
Q

what is necessary in the formation of functional NMJ

A

basal lamina

40
Q

what are the different laminins that exist in the basal lamina

A

laminin 11 - synaptic + extrasynaptic basal lamina

laminin 2 - extrasynaptic basal lamina

41
Q

Describe Guillain-Barre syndrome (acute idiopathic polyneuritis, infectious polyneuritis, acute inflammatory polyneuropathy)

A

rapidly ascending motor and sensory loss 2-3 weeks after respiratory or GI illness - demyelination of peripheral nerves

autoimmunity implicated!

good recovery following, remyelination occurs in PNS

incidence: 2/100,000

more common in men than women

42
Q

how is Guillain-Barre syndrome diagnosed?

A

lumbar puncture - find elevated protein in CSF (100-300 mg/dl)

NCV (nerve conduction velocity) - sensitive to demyelination
EMG - lack of nervous stimulation

43
Q

what is the treatment for Guillain-Barre syndrome?

A 
immune globulin (IV) 0.4 g/kg
plasmapheresis (plasma exchange)
ventilatory support
44
Q

what is the cause of Guillain-Barre syndrome?

A

acute nerve inflammation damages the myelin sheath
conduction and impulses through the nerve is slow/blocked
= muscle weakness, paralysis and sensory loss result

45
Q

what are the complications associated with Guillain-Barre syndrome

A

respiratory failure
aspiration
pneumonia
DVT

46
Q

describe Leprosy (Hansen disease)

A
  • commonest treatable neuropathy
  • infection of skin and peripheral nerves with mycobacterium leprae
  • LONG incubation period!
  • bacterial entry through skin lesions often following contact with nasal secretions from infected persons
  • enters unmyelinated areas (somatosensory - loss of pain sensation?)
  • bacterial multiplication causes compression and ischemia of all peripheral axons
  • profound sensory losses (pain and temp)
  • multidrug antibiotic tx usually successful
47
Q

describe lead poisoning

A 
motor neuropathy in adult
encephalopathy in infants
attacks the brain in children
NO sensory symptoms
bilateral focal weakness and wasting of EXTENSOR muscle of fingers, wrist and arms
48
Q

describe alcoholic peripheral neuropathy

A

sensory + motor losses = symmetrical
starts with sensory neuropathy (foot… leg)
later motor losses starting at lower leg
NCV in most cases NORMAL
more than 80-100 g alcohol/day
vitamin B1 (thiamin) deficiency related to malnutrition

49
Q

describe polyneuropathy in DM

A

sensory - symmetric
motor - asymmetric
autonomic (culminating in dry skin)
sensory symptoms begin in both legs as ‘stocking distribution’
vulnerable to hyperglycemia - sensory endings and axons of small unmyelinated DRG cells
problem may originate in the failure of the cell body to supply its distal parts with nutrients and essential proteins for its cytoskeleton
cases often complicated by diabetic vasculopathies

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