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Peripheral and Central Sensitization Flashcards

1
Q

How many people does chronic pain effect in the USA

A

100 million

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2
Q

What is the annual cost for management of chronic pain in the USA

A

$560-635 billion

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3
Q

True or False:

Chronic pain has significant biological, psychological, and emotional implications

A

True

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4
Q

What is the most common location for chronic pain

A

Lower back

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5
Q

What percent of individuals with acute lower back pain will go on to develop chronic LBP

A

10-15%

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6
Q

What is the direct and indirect cost associated with the management of chronic LBP in the USA

A

$100-200 billion

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7
Q

What 2 mechanisms lead to pain becoming chronic

A
  1. Nociceptive

2. Non-nociceptive

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8
Q

How does the nociceptive mechanism contribute to chronic pain

A

Increased input from the periphery

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9
Q

What is increased input from the periphery considered

A

Central and peripheral sensitization

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10
Q

How does the non-nociceptive mechanism contribute to chronic pain

A

Cognitive processing of information

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11
Q

What are non-nociceptive mechanisms

A

Things that may amplify pain and make the pain last longer than it should

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12
Q

True or False:

Chronic pain occurs due to neural plasticity

A

True

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13
Q

True or False:

Peripheral sensitization has a cognitive aspect to it as well as signals sent to the brain

A

True

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14
Q

What is peripheral sensitization

A

Increase responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields

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15
Q

True or False:

peripheral sensitization can be due to alterations in ion channels

A

True

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16
Q

What can be altered about the ion channels (2)

A
  1. The number of channels

2. How long the channels are open

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17
Q

What is the most common alteration to the ion channels for peripheral sensitization

A

How long the channels are open

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18
Q

True or False:

There is a growing body of literature supporting the targeting of peripheral mediators to treat chronic pain states

A

True

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19
Q

What are the peripheral mediators that are targeted (3)

A
  1. Tumour necrosis factor alpha
  2. Cytokines
  3. Pro-inflammatory prostaglandins
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20
Q

What conditions are the peripheral mediators seen in (3)

A
  1. Tumour necrosis factor alpha: RA
  2. Cytokines: RA
  3. Pro-inflammatory prostaglandins: OA
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21
Q

True or False:

There are a wide range of receptors on the outside of cells

A

True

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22
Q

What do the receptors on the outside of the cell lead to

A

Pain, swelling, warmth, and redness

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23
Q

True or False:

Hyperalgesia has both peripheral and central mechanisms

A

True

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24
Q

What is hyperalgesia

A

Increased sensitivity to pain

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25
Q

What is the flare of a wound

A

The area where there is no direct injury but the pain spreads thre

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26
Q

What are the characteristics of hyperalgesia (3)

A
  1. Decreased pain threshold
  2. Increased pain in response to suprathreshold stimuli
  3. Spontaneous pain
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27
Q

What are the characteristics of sensitization (3)

A
  1. Decreased threshold for response
  2. Increased response to suprathreshold stimuli
  3. Spontaneous activity
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28
Q

Will you see hyperalgesia in the clinic

A

Yes’m

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29
Q

Where does sensitization occur

A

In the spinal cord itself

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30
Q

What do neuromodulators do

A

Make it easier for receptors in the periphery to respond

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31
Q

During the neurogenic inflammation process what occurs after tissue injury

A

Prostaglandins and bradykinin are released sensitizing nociceptors in the periphery

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32
Q

During the neurogenic inflammation process what happens when nociceptors are sensitized in the periphery

A

Substance P and calcitonin gene related protein (CGRP) are released

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33
Q

During the neurogenic inflammation process what does substance P do

A

Acts on mast cells releasing histamine further exciting nociceptors

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34
Q

During the neurogenic inflammation process what does substance P and CGRP cause the release of

A

Bradykinin

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35
Q

During the neurogenic inflammation process what does bradykinin do

A

Causes extravasation and blood vessel dilation

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36
Q

What is plasma extravasation

A

Fluid leaking out of blood vessels

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37
Q

How are TRP channels effected during the process of neurogenic inflammation

A

They are increased due to the increased osmolarity, pressure, and stretch

38
Q

Are CGRP, substance P, histamine, and nerve growth factor (NGF) taken up by the terminal

A

No they stay in the tissue until they degrade or bind to something

39
Q

What happens to the neuromodulators that because they aren’t taken up by the terminal

A

They spread to other sites in the tissue

40
Q

What does the neuromodulators traveling to other sites in the tissue lead to

A

The wide spread effect seen during injury where there is a focal point but the tissue around the wound still hurts

41
Q

What is the response to peripheral exposure of NGF (3)

A
  1. Retrograde transport of signaling endosomes
  2. Increased transcription of BDNF
  3. Central release of BNDF
42
Q

What does local production of cytokines promote

A

Synthesis and release of NGF

43
Q

What does NGF due

A

Binds to TrKA triggering increased excitability

44
Q

What does increased excitability due to TrKA do

A

Promotes increased BDNF production

45
Q

What does increased production of BDNF cause

A

Increased release from sensory terminal in CNS causing increased excitability

46
Q

What is NGF good for

A

Neural development

47
Q

What can NGF cause

A

Increased pain after development

48
Q

NGF resulting in the release of BDNF in the CNS is an example of what type of mechanism

A

Central mechanism

49
Q

What are the 2 mechanisms that lead enhanced excitability in the dorsal horn neurons

A
  1. Windup

2. Elevated Ca++

50
Q

What causes windup

A

Repetitive stimulation of C-fibers

51
Q

How does the response of A-delta fibers change after repetitive stimulation

A

The response doesn’t change it remains the same

52
Q

How does the response of the C-fibers change after repetitive stimulation

A

There is a summation effect after each time the C-fiber is stimulated

53
Q

What is the summation effect after each stimulation of the C-fiber called

A

Windup

54
Q

What does windup lead to

A

Central sensitization

55
Q

What does elevated Ca++ lead to

A

Increase glutamate release which stimulates AMPA and NMDA receptors

56
Q

What does stimulating NMDA and AMPA receptors lead to

A

Longer depolarization of neurons

57
Q

What do NK1 receptors do

A

Enhance the action of NMDA via second messengers

58
Q

What activates NK1

A

Substance P

59
Q

True or False:

A-delta fibers have fast membrane depolarization that is transient

A

True

60
Q

True or False:

C-fibers have long lasting depolarization that is cumulative

A

True

61
Q

What 2 lamina send long projections up to the thalamus

A

Lamina 1 and 5

62
Q

True or False:

Lamina 5 sends projections back up to lamina 2

A

True

63
Q

What does central sensitization refer to

A

The neurons in the dorsal horn

64
Q

Is central sensitization a good or bad thing

A

It is somewhat of a bad thing

65
Q

What does peripheral sensitization refer to

A

Free nerve endings in the periphery

66
Q

What can nociceptor input trigger in central nociceptive pathways

A

A reversible yet prolonged increase in the excitability of neurons

67
Q

What is central sensitization

A

Increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input

68
Q

What are the symptoms associated with changes in excitability (3)

A
  1. Hypersensitivity
  2. Hyperalgesia
  3. Allodynia
69
Q

What is allodynia

A

Increased sensitivty to non noxious stimuli

70
Q

What is central sensitization maintained by (4)

A
  1. Activity dependent synaptic plasticity
  2. Physiologic changes in support structures
  3. Membrane excitability
  4. Gene transcription
71
Q

What causes hyperalgesia in central sensitization

A

Alterations in nociceptors

72
Q

What causes allodynia in central sensitization

A

Alterations in low threshold mechanoreceptors

73
Q

What do people with central sensitization have hypersensitivity towards (7)

A
  1. Bright light
  2. Touch
  3. Noise
  4. Pesticides
  5. Mechanical pressure
  6. Medication
  7. Temperature (high and low)
74
Q

What is causing central sensitization broad terms

A

Plastic changes occur in the dorsal horn due to second messengers changing the permeability and receptors on the cell membrane

75
Q

What are the 3 steps of pain becoming chronic

A
  1. Activation
  2. Modulation
  3. Modification
76
Q

What does the activation step lead to (2)

A
  1. Windup

2. Auto-sensitization

77
Q

What causes the activation step to occur

A

Ion channel excitability

78
Q

What does the modulation step lead to (2)

A
  1. Peripheral sensitization

2. Central sensitization

79
Q

What causes the peripheral and central sensitization during the modulation step

A

Second messengers

80
Q

How do the second messengers cause peripheral and central sensitization

A

They send signals back to the lamina causing an upregulation of membrane specific proteins which leads to more receptors embedded in the cell membrane

81
Q

What happens during the modification step (3)

A
  1. Altered gene regulation
  2. Altered connectivity
  3. Cell death
82
Q

What happens during the modulation step (1)

A
  1. Phosphorylation of receptor/ion channels
83
Q

What happens during the activation step (3)

A
  1. Transduction
  2. Transmission
  3. Use-dependent augmentation
84
Q

What is use-dependent augmentation

A

Responding with more umf

85
Q

When does the modification step occur

A

After the tissue has healed

86
Q

What does the modification step lead to

A

Chronic pain

87
Q

How does the modification step lead to chronic pain

A

The inhibitory neuron cell dies and a new excitatory synapse is formed where the inhibitory neuron cell was

88
Q

What sprouts from the dead inhibitory interneuron

A

A-beta fiber

89
Q

What does the newly sprouted A-beta fiber cause

A

Altered cell excitation

90
Q

Talk to Dr. Brown about this

A

Perfect

Neuro (15 decks)

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