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TMD > 2. Pain Models > Flashcards

2. Pain Models Flashcards

1
Q

Describe the bidirectional processing of pain

A 
Bottom up (Periphery --> brain)
- Facilitation, inhibition and interneurons
Top down (Brain --> SC)
-Person, beliefs, affect behavior
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2
Q

What are the networks with potential to affect the risk for chronic pain in the brain

A
  • Reward network
  • Descending pain modulatory system (DPMS)
  • Areas also relevant to pain percept but that may not affect risk (Descending inhibitory and facilitatory influences)
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3
Q

What are the different pain receptors

A

A-delta (mechanical noxious stimuli

C-fibers= thermal and chemical noxious stimuli

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4
Q

Role of A-beta fibers

A

Detect non-noxious mechanical stimuli

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5
Q

Describe the biobehavioral model of pain

A

Many circles (from inside to out

  • Tissue damage and nociception
  • Perception
  • Appraisal
  • Pain behavior
  • Social and external environment
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6
Q

What are the three methods of pain transmission in the nervous system

A
  • Peripheral transmission
  • Synaptic transmission
  • Central transmission
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7
Q

What are the three fundemental concepts of pain

A
  • nociception is not equal to pain
  • acute pain is not equal to chronic pain
  • pain=meaning
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8
Q

Define pain

A

Unpleasant sensory and emotional experience associated with actual tissue damage, or percieved tissue damage, or described in terms of such damage

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9
Q

Describe the common phenomenology associted with pain

A

Unpleasant sensory and emotional experience

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10
Q

What are the three different subtypes of pain

A
  • Actual tissue damage
  • Potential tissue damage
  • Description (from patient) involving reference to tissue damage
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11
Q

T/F Activity induced in the nociceptor and nociceptive pathways by a noxious stimulus is not pain

A

t- it is always a psychological state even though pain is often associated with a physical cause

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12
Q

Describe the difference between nociceptive and neuropathic pain

A

Nociceptive pain

  • Results from tissue damage that stimulates nociceptors
  • Associated with acute tissue injury, dentistry, etc.

Neuropathic pain

  • Disease state caused by damage to the nervous system
  • Chronic pain conditions often the result of neuropathic pain
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13
Q

Be familiar with all the pain measurement scales

A 
101- point numeric rating scale (NRS-101)
11-point Numeric rating scale (NRS-11) 
11-point box scale (BS-11)
6-point behavioral rating scale (BRS-6) 
4-point verbal rating scale (VRS-4)
4-point verbal rating scale-alt 
5-point verbal rating scale
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14
Q

Look at the graph on slide 25 and understand the difference between someone who is more tolerant to stimuli and who is more tolerant to pain

A

ok

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15
Q

Which is more accurate- recording pain ratings throughout the day or end of the day

A

throughout the day

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16
Q

Define hyperalgesia and allodynia

A

Hyperalgesia
-Increased pain response to a noxious stimuli

Allodynia
-Pain from a non-noxious stimulus

17
Q

Define Hyperesthesia and Dysesthesia

A

Hyperesthesia

  • Increased sensitivity to stimulation
  • (Like blowing on a sunburn)

Dysesthesia

  • Evoked or spontaneous altered sensation
  • I.e discomfort rather than pain
18
Q

Describe the mechanism and characteristics of inflammatory pain

A

Mechanism

  • Activation (caused by tissue damage and action of immune cells)
  • Modification (structural changes)
  • Modulation (peripheral and central sensitization)

Clinical manifestations
-Localized pain hypersensitivity (i.e heat hyperalgesia or allodynia + spontaneous pain)

19
Q

Describe the mechanism and clinical manifestations of functional pain

A

Mechanism

  • Central amplification
  • Normal peripheral nerves and tissues

Clinical manifestation
-Generalized hypervigilence (Pain that is spontaneous and hypersensitive)

20
Q

Describe the mechanism and clinical manifestations of nociceptive pain

A

Mechanism
-Activation (nociceptors) by chemical, mechanical, or thermal stimuli

Clinical Manifestations

  • Pain linked to stimulus
  • Autonomic response= withdrawl
21
Q

Describe the mecahnism and clinical manifestations of neuropathic pain

A

Mechanism

  • Activation
  • Modification (structural changes– peripheral n. damage)
  • Modulation (peripheral and central sensitization)

Clinical

  • Localized pain hypersensitivity (i.e allodynia or hyperalgensia, sensory loss and paroxysms)
  • Same as inflammatory pain
22
Q

What are the two different kinds of neuropathic pain

A

central and peripheral

23
Q

Central sensitization moves in what direction

A

SC –> brain

24
Q

What analgesics are taken for

  • Central sensitization
  • Descending modulation
  • Peripheral transduction
A

Central sensitization

  • Anticonvulsants
  • Opiods
  • Ketamine
  • Cannabinoids

Descending modulation

  • Antidepressant (amitryptilline)
  • Opiods
  • Muscle relaxants

Peripheral transduction

  • Topical agents
  • Anti-inflammatory agents
  • LA
25
Q

Describe the process of modulation

A

Peripheral nociception –> Spinal cord integration –> Central processing –> Pain experience

26
Q

What can be used to block peripheral nociception to spinal integration

A

local anesthetic

27
Q

What types of drugs block movement of painful signals from the SC to the brain

A
  • NSAIDs
  • Opiods
  • etc.
28
Q

What are the clinical models of pain

A

Biomedical

  • Pain is always a sign of tissue damage
  • Linear relationship between tissue damage and pain

Psychoiatric model

  • Pain without observable pathology is psychogenic
  • Certain personality types are more prone

Biobehaviroal model

  • Pain is multi-dimensional
  • Not possible to separate the “physical” elements of pain from the “psychological” elements
29
Q

what are the two different sub-therories of the transmission system based pain model

A

Specificity theory and pattern theory

30
Q

The foundation of pattern theory is

A

summation theory

31
Q

What is the gate control theory of pain

A

-Non-painful stimuli or cognitive activity can dampen or block painful sensations from reaching the brain

32
Q

What is the significance of the gate control theory of pain

A

This is the physiological mechanism that explains how psychologic factors influence pain

33
Q

The gate control theory of pain involves a gate that opens and closes to modulate pain, where is this gate located

A

spinal cord

34
Q

Describe the path noxious signals take in traveling from the SC to the brain

A

SC

  • C fibers and A-delta fibers and dorsal root ganglion
  • Trigeminal subnucleus caudalis

Medulla
-Nucleus raphe magnus

Midbrain
-Periaqueductal grey matter

Forebrain

  • Cerebral cortex
  • Thalamus
35
Q

What are the four models of brain processing

A
  • Melzack: neuromatric theory
  • Leknes and Tracey: Pain and pleasure
  • Price: Sensory-affective dimensions
  • Craig: homeostasis
36
Q

All four models of pain processing agree with _ but differ on _

A

All agree with
-Inclusion of both sensory and affective dimensions

All differ
-Importance of peripheral and central mechanisms

TMD (13 decks)

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