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Physiology Exam 6 > 67-68 - Physiology of Pain > Flashcards

67-68 - Physiology of Pain Flashcards

1
Q

Define and differentiate between pain and nociception.

A

Pain

  • The perception of nociceptive (noxious) sensory information
  • “The unpleasant sensory and emotional experience which we associate with actual or potential tissue damage and/or describe in terms of such damage.”

Nociception

  • The sensory response to a noxious stimulus
  • Unconscious activity induced by harmful stimulus
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2
Q

Components of pain

A

Pain is a multifactorial and multisystem phenomenon

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3
Q

Sensory-Discrimination

A

Perception of exteroceptive and enteroceptive noxious information and the localization of the site of the stimulus - primary and secondary somatosensory cortices

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4
Q

Motivation-Affective

A

Emotional and sympathetic responses and associated behaviors - frontal cortex, limbic system, brainstem areas

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5
Q

Exteroceptive pain

A

pain information coming from the outside the body (skin pain)

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6
Q

Enteroceptive pain

A

pain information coming from inside the body (visceral pain)

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7
Q

When a nociceptive stimuli is experienced, what does the sensory-discriminative component contribute?

A
  • Location
  • Intensity
  • Modality (hot/cold, stabbing/burning)
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8
Q

When a nociceptive stimuli is experienced, what does the emotional component contribute?

A
  • Negative impact on affect/mood

- Chronic pain accompanied by depression

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9
Q

What do both the sensory-discriminative and emotional components contribute to?

A

Conscious perception of pain

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10
Q

Describe physiologic pain

A
  • Acute pain
  • Critical for survival
  • Body’s own warning signal
  • Protects the body from potential or further damage and injury
  • Felt within ~0.1 sec after initiation of stimulus
  • Also known as “fast pain” because the sensation is felt so quickly
  • Very adaptive - As tissue injury heals, the pain lessens
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11
Q

Describe the fibers utilized in fast conduction

A

Fast conduction - Aδ fibers @ 6 - 30 m/sec

  • Elicited by either mechanical or thermal pain stimuli
  • Sharp, prickling, electric and cutting types of sensation
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12
Q

Describe pathologic pain

A
  • Chronic Pain
  • Begins after > 1 sec after the stimulus and then increases slowly
  • Usually associated with tissue injury
  • Can become maladaptive – T12 injury that should heal in 3 months, patient comes back in 3 months, the bone has health and there is no longer visible pathology on x-ray, but he is still in pain
  • Persists even if there is no more tissue damage and injury is healed
  • In that case, it does NOT have a physiological function!
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13
Q

Describe the fibers utilized by pathologic pain

A

Persistent and slow conducting - C-fibers @ 0.5 – 2 m/sec

  • Can be elicited by chemical, mechanical and thermal stimuli
  • Dull, throbbing, aching, nauseous sensation
  • Strong emotional component
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14
Q

4 types of pain

A

1 - Nociceptive pain
2 - Inflammatory pain
3 - Dysfunctional pain
4 - Neuropathic pain

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15
Q

Nociceptive pain

A
  • Physiologic (“normal”) pain
  • Transient, localized
  • No real or minimal tissue damage
  • Pathologic when chronic

*** Warning – protective function

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16
Q

Inflammatory pain

A
  • Acute and chronic
  • Tissue damage
  • Inflammatory process
  • Hypersensitivity

*** Protective, promotes healing

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17
Q

Dysfunctional pain

A
  • No understanding lesion found, disproportionate to tissue injury
  • IBS (irritable bowel syndrome), fibromyalgia
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18
Q

Neuropathic pain

A
  • Damage to the nervous system (CNS or PNS)
  • Disproportionate to intensity of nociceptor activation
  • Originates with damage to the nervous system
  • Pathologic pain, maladaptive

*** NO protective function

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19
Q

Describe the characteristics of somatic pain

A

Superficial

  • discreet localization
  • Initial (sharp; A delta fibers= 20 M/sec)
  • Delayed (dull, burning; C-fibers= 1 M/sec)

Deep

  • diffuse localization
  • Connective tissue, bones, joints, muscle; muscle cramps, headache
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20
Q

Describe the characteristics of visceral pain

A
  • Primarily mediated by C-fibers
  • Poorly localized, nauseating, frequently accompanied by sweating and changes in BP
  • You can localize it, just not very well, not as well as somatic pain
  • Often radiates or is referred to a other somatic site following a dermatome pattern

E.g., angina, colic, ulcer, appendicitis, renal stones

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21
Q

Describe the steps in the physiology of processing pain

A

1 - Transduction (At the location of the painful stimulus)
2 - Transmission (Travels via fibers to the dorsal horn of the spinal cord)
3 - Modulation (Arrives at spinal cord)
4 - Perception (Arrives at brain)

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22
Q

What is involved in pain transduction at the location of the painful stimulus?

A

Pain neurons or nociceptors

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23
Q

Which free nerve endings are involved in the body and face?

A

Body - spinal ganglia

Face - trigeminal ganglia

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24
Q

What does high threshold mean in terms of nociceptors?

A
  • This is important so you are not responding to pain all the time
  • Need a low threshold for proprioception, for example
  • If these activated each time you touched something or sat down, we would have problems and a lot of pain
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25
Q

Are nociceptors fast or slow adaptors?

A

Slow

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26
Q

What types of stimuli do nociceptors respond to?

A

1 - Mechanical – only noxious stimulus

2 - Thermal - TRP receptor family
- CMR-1 (52⁰C, TRPV2) - Noxious heat
VR-1 (>42⁰C, TRPV2) - Noxious heat, capsaicin

3 - Chemical

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27
Q

Describe “inflammatory soup” in relation to peripheral nociceptive processing

A

There are three components

  • Nociceptor activation
  • Vasodilation
  • Inflammation

Inflammatory soup is the release of all the things that nociceptors respond to and that participate in the inflammatory process

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28
Q

Describe direct and indirect nociceptor activation

A

Direct activation

  • Opening of cation channels (e.g., Na+)
  • Membrane depolarization
  • Generation of action potentials

Indirect sensitization
- Lowered thresholds

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29
Q

What is hyperalgesia

A

Hyperalgesia is an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves.

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30
Q

What do we call hyperalgesia when it occurs in the periphery?

A

Primary hyperalgesia

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31
Q

Describe primary hyperalgesia

A
  • Spreading of action potentials over other areas where membrane is at resting state
  • Increased sensitivity occurs because the threshold is lowered
  • This leads to an increased ‘receptive field’ size
  • Inflammatory mediators and
    Substance P induced
  • Activation of “silent nociceptors”
    – Only signal in response to the molecules secreted by other activated nociceptors
    – Expand the receptive field for the pain stimulus
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32
Q

Where will we see secondary hyperalgesia?

A

In the CNS, not the periphery

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33
Q

Describe allodynia

A

Pain resulting from non-noxious stimulus

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34
Q

Describe hyperalgesia

A

An increased response to a stimulus that is normally painful (noxious stimulus)

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35
Q

What is the axon reflex?

A
  • When stimulation of the sympathetic nervous system occurs by pain processes
  • It is the coupling of sensory and autonomic systems
  • The sympathetic nerves get activated and actually contribute to the development of a flare response, leading to the triple response of Lewis
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36
Q

What causes a flare response?

A

Flare response due to activation of peripheral nerves (e.g. vasodilation)

There is a release of Substance P and movement of action potential along the primary afferents towards the spinal cord

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37
Q

What is the triple response of Lewis?

A
  • Redness
  • Edema
  • Wheal
38
Q

After transduction (at the site of the painful stimulus) is transmission (via the fibers of the dorsal horn). What are the two types of nociceptive fibers?

A

1 - A delta fibers (myelinated)

2 - C fibers (unmyelinated)

39
Q

A delta fibers

A
  • Responsible for localized, sharp “first pain”
  • Respond to intense mechanical (pinching) and thermal stimuli
  • Lightly myelinated, medium diameter
40
Q

C fibers

A
  • Mediate poorly localized, diffuse “second pain”
  • Polymodal as in it responds to mechanical, thermal and chemical stimuli
  • Unmyelinated, small diameter
41
Q

What are the four types of fibers associated with nociceptors?

A
  • Cutaneous
  • Articular (joint)
  • Muscle
  • Viscera
42
Q

Cutaneous fibers

A
  • A delta (mechanical)
  • A delta (mechanical + heat)
  • C fiber polymodal nociceptor
43
Q

Articular (joint) fibers

A
  • Approx. 2x as many unmyelinated fibers myelinated fibers
  • A delta (small myelinated)
  • C-fibers (unmyelinated)
  • Respond to mechanical stimulation, inflammation
44
Q

Muscle fibers

A
  • Similar to joint

- Respond to mechanical, thermal, chemical and ischemia

45
Q

Viscera fibers

A
  • Predominately C-fibers

- Respond to mechanical distention and chemical stimuli

46
Q

How does the spinal cord process fibers in the dorsal horn?

A

Through different lamina (layers) found within the dorsal horn

You need to know

  • Lamina I
  • Lamina II and III
  • Lamina V
47
Q

Role of lamina I of dorsal horn

A

A delta fibers

- Fast, acute pain

48
Q

Role of lamina II and III of dorsal horn

A

C fibers

- Slow, chronic pain

49
Q

Role of lamina V of dorsal horn

A 
WDR neurons (wide dynamic range)
- Noxious and non-noxious signals
50
Q

Describe the “wind up” phenomenon of central sensitization

A

This is a process of increased sensitivity that includes three components

  • Secondary hyperalgesia (CNS and PNS)
  • Recruitment of adjacent neurons in the spinal cord
  • Changing pharmacology
51
Q

Describe secondary hyperalgesia

A

“Secondary Hyperalgesia” = PNS and CNS events

Prolonged and increased activation of nociceptors in the periphery and projection
pathways at the spinal cord

Recall that primary hyperalgesia was due to PERIPHERAL sensitization

52
Q

Describe the changing pharmacology in the “wind up” phenomenon

A
  • Release of neurotransmitters occurs (glutamate, Substance P, BDNF, etc.)
  • NMDA (n-methyl-d-aspartic acid) does not get activated right away, but once it is activated, the flood gates are opened…
  • Influx of calcium into the post-synaptic cell, depolarization occurs
  • Overall the post-synaptic cell with have increased activation and firing
  • We call this “wind up” phenomenon
53
Q

What other components are there of the “wind up” phenomenon?

A
  • Neuronal plasticity

- Memories of pain and pathophysiology

54
Q

Neuronal plasticity

A

Modulation of intracellular signaling (cAMP, etc.) and changes in gene expression (c-fos, jun)

55
Q

Memories of pain or pathophysiology

A

Lasting effects –> Chronic pain

56
Q

Need to remember the different function of acute sensitization and chronic sensitization

A

REMEMBER:

1) Acute sensitization
Protective

2) Chronic sensitization
Maladaptive
No function

57
Q

What is the last step in pain processing?

A

Supraspinal perception

58
Q

What are the two ascending somatosensory pathways?

A
  • Dorsal column (medial lemniscus - DC-ML)

- Anterolateral system (AL)

59
Q

What does the DC-ML carry?

A

Discriminative Touch

Proprioception

60
Q

What does the anterolateral system carry?

A

Temperature
Pain
“Crude touch”

61
Q

Two components of the spinothalamic tract

A

Neospinothalamic

Paleospinothalamic

62
Q

Describe the neospinothalamic tract

A
  • Fast type A delta fibers for mechanical and acute thermal pain
  • Projections form Lamina I, IV and V
  • Anterolateral Columns to the Thalamus (Ventral Posterolateral (VPL))
  • Contributes to primary sensory cortex ***
63
Q

What is the role of the primary sensory cortex?

A 
Primary sensory cortex
Lateral system
- Sensory-discriminative component
- ***PRIMARY FUNCTION***
This tract will tell you “I have a sharp pain on my left arm and the level of pain is 5/10
- Location, intensity and modality 
- “First” pain – sharp, well-localized
- Sharp pain in my left arm
64
Q

Describe the paleospinothalamic tract

A
  • Slow type C-fibers
  • Lamina II, III + V
  • Anterolateral Columns
  • Thalamus
  • Dorsomedial nucleus (DM)
  • Limbic system
65
Q

Describe the contribution to the limbic system

A

Limbic system
- Medial system: Affective-motivation pathways
- Emotional and visceral responses to pain
** PRIMARY FUNCITON **
- The emotional reaction to pain
- The pain that really “gets to you”
- “Second” pain – dull, throbbing, poorly localized
Release of stress hormones, attention, etc.
- You really start focusing and stressing about your pain!!!
- Ouch!! That hurts – I don’t like it

66
Q

What are two other ascending tracts?

A

Spinoreticular tract

Spinomesencephalic tract

67
Q

Spinoreticular tract

A

Reticular Formation
Motor response to pain
Descending pain control

68
Q

Spinomesencephalic tract

A

Midbrain – PAG
Regulation and modulation of pain experience
Descending pain control
Superior colliculus - eye movements and regulation of gaze to the site of injury

69
Q

Describe the role of the brain in pain perception and the specific role of the amygdala and pre-frontal cortex

A

Once the pain signal reaches the brain, there are a number of brain areas that are being activated…
This is where the perception of pain is really happening
You need your brain to interpret where you’re hurting
Initially they are just nociceptive signals and physiological responses

Amygdala – major center for fear, plays a role in pain perception

Prefrontal cortex – center for cognitive function and the cognitive perception of pain

70
Q

Some of the most activated areas in the pain state are the…

A

Anterior cingulate cortex and the insula

71
Q

Anterior cingulate cortex (ACC)

A

Active during 1) perception of pain, 2) imagining pain and 3) observation of pain in others
Attention to pain
Initiation of behavioral reactions to pain

72
Q

Insula

A

relay station to the limbic system (learning and pain memory) and to the hypothallmus

73
Q

Gate control theory example

A

When you’re in pain, you kiss it, shake your hand, put it in your mouth, rub it, etc.

These things actually work

74
Q

Describe the gate control theory

A

Gating mechanism within the spinal cord that closes in response to normal stimulation of the fast conductivity large nerve fibers (Aβ - touch, proprioception)

However, it opens when the slow conduction pain fibers (Aδ and C) transmit a high volume and intensity of sensory signals

The gate can be closed again if these pain signals were countered by renewed stimulation of the large fibers

75
Q

There are three sites of action in descending pain control. What are they?

A

1 - Periaqueductal gray - midbrain
2 - Rostral ventral medulla - brainstem
3 - Locus coeruleus - pons in brainstem

76
Q

What do you need to understand about descending pain control?

A
  • It is a regulatory mechanism used to control the descending pain pathways (occurs in the spinal cord)
  • It is complex, but you just need to know that this is an endogenous system that our bodies use to control pain
77
Q

What types of medications utilize the descending pain control pathway?

A

Opioids

78
Q

Describe the periaqueductal gray matter (midbrain)

A

Activates enkephalin-releasing neurons that project to the raphe nuclei in the brainstem

79
Q

Describe the rostral ventral medulla (brainstem)

A

Nucleus raphe magnus

5HT projections to the dorsal horn of the spinal cord

80
Q

Describe the locus coeruleus (pons and midbrain)

A

NE projections to the dorsal horn of the spinal cord

81
Q

Describe pain modulation that occurs in the ventrolateral periaqueductal gray matter (PAG)

A
  • Analgesia (inability to feel pain) blocked by naloxone
  • Inhibit A and C fibers
  • Decreased BP
  • Decreased HR
  • Vasodilation
  • Immobility
  • Inhibition of sympathetics (time to recover)
82
Q

Describe pain modulation that occurs in the dorsal periaqueductal gray matter (PAG)

A
  • Analgesia (inability to feel pain) is not blocked by naloxones
  • Selective inhibition of nociceptive input
  • Defense reaction so BP and HR go up
  • Vasoconstriction of skin and viscer
  • Vasodilation of skeletal muscles
  • Pupillary dilation
  • Piloerection
  • Fight/flight behavior
  • Muscle tone increase
  • Aversive behavior
  • Sympathetics are excited in preparation of fight or flight
83
Q

How can you therapeutically modulate pain?

A 
Typical Pharmacologic Approaches:
Opioid analgesics
NSAIDs
Glucocorticoids
DMARDS

Can either relieve pain or delay or arrest a disease process

Occurs primarily at the site of injury and in the dorsal horn

84
Q

What are the common pain types?

A

Chronic pain
Referred pain (visceral – cutaneous)
Projected pain
Neuropathic Pain

85
Q

What are all the different types of neuropathic pain?

A 
Thalamic
Phantom limb pain (amputation)
Sympathetic mediated pain (SMP)
- Complex Regional Pain Syndrome (CRPS) **
- Reflex sympathetic dystrophy **
- Causalgia **
Fibromyalgia
Diabetic neuropathy
86
Q

Referred (reflective) pain and convergence

A

Reflective pain - perceived at a location other than the site of the painful stimulus

Convergence -
of somatic and visceral pain fibers on secondary afferents in the dorsal horn (dermatomes)
You will have convergence at the spinal cord – this is why it follows dermatomes

87
Q

Projected pain

A

Provides evidence in support of the labeled line theory of sensory processing

Example would be hitting your ‘funny bone’ at the elbow and perceiving the pins and needles sensation (paresthesias) localized to the hand and fingers

88
Q

Phantom pain and reorganization

A

Imaginary pain
When you have amputation, but you still feel pain when the limb is no longer there
This is because of some of the reorganizations that occur

89
Q

Sympathetic mediated pain (SMP)

A

Two types:

  • Complex Regional Pain Syndrome - CRPS (can result in neuroplasticity following recovery)
  • Reflex Sympathetic Dystrophy (RSD); Causalgia
90
Q

Reflex Sympathetic Dystrophy (RSD); Causalgia

A
  • Continuous burning pain long after seemingly trivial injuries
  • May develop following a traumatic peripheral injury
    hyperpathia
  • Dystrophic changes
    skin, nails, hair, muscles and/or bone
  • Sympathetic hyperactivity (variable)
    temp. changes and hyperhidrosis
  • Pain enhanced by:
    allodynia
    sympathetic activation
91
Q

Treatment

A

Treatment
sympathectomy or a sympathetic nerve block
other interventions

Physiology Exam 6 (16 decks)

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