Psychology of Pain Flashcards
(106 cards)
1
Q
What does the experience of pain serve as
A
A protective and adaptive role
2
Q
What does acute pain teach us
A
To recognise and avoid things with potential to produce injury.
3
Q
What does adversive quality of pain in the case of deep tissue injury, infection or bone fracture promote
A
Immobilization of affected limb and promotes healing
4
Q
What happens if you have a congenital insensitivty to pain
A
You have a reduced life expectancy
5
Q
What is the most common response when patients are asked what they fear most about illness and treatment
A
Pain
6
Q
What is a common reason for euthanasia requests
A
Inadequate pain relief
7
Q
What can pain lead to when experienced or anticipated
A
Distress
8
Q
What is pain according to the international association for the study of pain (IASP)
A
An unpleasant sensory or emotional experience associated with actual or potential tissue damage, or described in terms of tissue damage, or both
9
Q
What did Beecher find about the elusive nature of pain
A
No direct one-to-on correspondence between tissue injury and experience of pain
10
Q
How is pain classified by duration
A
Acute or chronic
11
Q
How is pain classified by nature
A
Nociceptive or non-nociceptive
12
Q
Describe acute pain
A
Acute pain is transient. Typically results from specific injury that produces tissue damage (broken limb, wound)
13
Q
What may inadequately treated acute pain evolve into
A
Chronic pain
14
Q
Describe chronic pain
A
It lasts much longer and is beyond the normal expected healing time for injury
15
Q
What are the types of nociceptive pain
A
Somantic or visceral
16
Q
What are the types on non-nociceptive pain
A
Neuropathic or sympathetic
17
Q
Describe nociceptive pain
A
Arises from any actual or threatened damage to non-neural tissue and is due to activation of nociceptors
18
Q
Describe neuropathic pain
A
Arises from a leison or disease of the somatosensory nervous system. Disease can be central (e.g. multiple sclerosis) or peripheral (e.g. diabetic neuropathy)
19
Q
What is more important in transitioning to chronic pain
A
Functional disability plays more of a role than pain intensity
20
Q
What can chronic patients experience which helps maintain pain behaviours
A
Secondary gains such as increased attention form family members or compensation
21
Q
What can be used to measure pain
A
The McGill pain questionnaire
22
Q
What does the verbal report of pain do
A
Draw on large, informal vocabulary people use to describe pain- throbbing pain; shooting pain, a constant dull ache
23
Q
What do pain questionnaires take into account
A
Nature of pain; intensity of pain; emotional components and functional impact of pain. “Gold standard” but subject to bias and cultural variation.
24
Q
What are two subjective measurements of pain
A
Verbal report and pain questionnaires
25
What is a non-verbal assessment of pain
IASP- inability to communicate verbally does not negate the possibility that an individual is experiencing pain and in need of appropriate pain-relieving treatment
26
How does pain serve its protective functions
By not only warning the sufferer but also by impelling expressive behaviours that warn and solicit help from others
27
How can we see pain experience of those who cannot communicate pain through language e.g. infants, dementia
Use facial behaviour as a window of pain
28
What is the process through which potentially damaging stimuli is detected
Nociception
29
What are examples of noxious stimuli
Thermal, chemical and mechanical stimuli capable of causing tissue damage
30
What are specialised sensory neurones that are activated by noxious stimuli called
Nociceptors
31
How are nonceptive signals transmitted to the CNS
Via glutamate
32
What is activation of nociceptors modulated by
Inflammatory influences in local extracellular environment
33
What are the four main phases of nociception
Transduction, transmission, perception and modulation
34
Describe transduction
Exposure to noxious stimuli produces action potential
35
Describe transmission
Travels along fibres from point of transduction to dorsal horn and subsequently to the brain
36
Describe perception
Experience of discomfort, pain. Concious, emotional and subjective
37
Describe modulation
Response to pain, facilitation or inhibition of nociceptive input
38
What are the 3 primary types of afferent nerve fibres
A-delta fibres, C fibres and A-beta fibres
39
Describe A-delta fibres
Fast, myelinated- respond to heat and pressure
40
Which type of fibre is responsible for the first sharp pain
A-delta fibres
41
Describe C fibres
Slow, unmyelinated- polymodal, respond to thermal, mechanical and chemical stimuli
42
Which type of fibre is responsible for the second 'throbbing' or 'burning' pain sensation
C-fibres
43
Describe A-Beta fibres
Respond to non-noxious stimuli, detect light, touch, vibrations
44
Describe ascending pain pathways
Nociceptive inputs enter CNS at spinal dorsal horn where primary afferent terminal synapse with second-order projection neurons. Substantia gelatinosa (SG) of the dorsal horn receives input from A𝛿 & C-fibres & also receive inputs from large-diameter myelinated A𝛽 fibres, which transmit innocuous sensory inputs. Beyond the peripheral nociceptor and dorsal horn, pain related information ascends in the contralateral spinothalamic tract. Also direct connections to medulla and brain stem via spinoreticular and spinomesencephalic tracts, and to hypothalamus via spinohypothalamic tract.
45
What does chronic noxious stimulation result in
Hyperalgesia and allodynia
46
Where may chronic noxious stimulation sensation occur
Peripherally or locally
47
What does localised inflammation lead to
Hyperexcitability of peripheral nociceptors
48
What is hyperalgesia
Hyperexcitability of peripheral nociceptors- exaggerated responsed to noxious stimuli (hyperalgesia)
49
What does central sensitization result in
Sensitisation may occur centrally (dorsal horn) enabling non-nociceptive A-beta fibres to evoke pain sensations
50
What is allodynia
Non-nociceptive A-beta fibres evoking pain sensations
51
What describes the blocking of pain sensation
Gate control theory
52
What does the gating mechanism within SG allow/ prevent
Passage of nociceptive signals from periphery to brain. Influences by relative degree of excitatory activity in spinal cord transmission cells
53
What opens the gate
Excitation along the A-delta and C-fibres
54
What closes the gate and what is this known as
A-beta fibres, known as counterstimulation
55
What influences gating mechanism
Descending input from brain regarding current cognitive/ affective state
56
What occurs beyond the gate
Neuromatrix theory and the multidimensional nature of pain
57
In the neuromatrix theory and the multidimensional nature of pain where does pain arise from
A neural network with sensory, affective and cognitive components
58
What is the role of the sensory component of pain
Transmits basic sensory information e.g. location of pain in body, pain;s sensory qualities (burning, piercing)
59
What is the role of the affective component of pain
Emotional and motivational (fight or flight) reactions to pain
60
What is the role of the cognitive-evaluative component of pain
Meaning of sensory experience
61
What is the cortical processing of pain and what does it consist of
The pain neuromatrix conceptualised of consisting of a medial and lateral pain system originating from medial and lateral thalamic nuclei.
62
What does the medial pain system consist of
Medial thalamic nuclei, anterior cortex (ACC) and insula
63
What does the medial pain system do
Mediates affective-cognitive-evaluative aspects of pain
64
What does the lateral pain system consist of
Primary (SI) and secondary (SII) somatosensory cortices and lateral thalamic nuclei
65
What does the lateral pain system do
Mediates sensory/ discriminative aspects of pain
66
How can you have an affective response in SI and SII without pain sensation
When the sematonsensory discrimination was absent due to stroke, the unpleasantness associated with noxious stimuli remained
67
What did PET scans reveal activated when healthy volunteers received noxious thermal stimuli
Activation of S1. S2, insula and ACC
68
Where is the affective component coded
In the ACC but not S1.
69
Describe the descending endogenous pain modulatory system
Brain does not passively receive pain info from body but actively regulates sensory transmission via descending influences on spinal dorsal horn. Pain inhibition. Contributes to environmental and opiate analgesia. Some descending pathways can facilitate pain and may contribute to chronic pain. Variety of high cortical brain systems contribute to descending pain modulatory patwhay
70
What forms a key part of the pain-inhibition system
Periaqueductal gray (PAG)
71
What is the role of the periaqueductal gray
Integration of ascending pain stimuli and descending influences from high cortical regions
72
Describe the psychological modulation of pain
Attentional orienting to painful sensation and its course. Cognitive appraisal of the meaning of sensation. Subsequent emotional, psychopathological and behavioural reactions. Which in turn feedback to influence pain and perception
73
What receive preferential neural processing and are likely to govern behaviour
Attended stimuli
74
How does pain automatically and involuntarily capture attention
By virtue of its significance.
75
What can pain experience vary according to and why
Locus of attention: when attention is focused on pain it is perceived as more intense, whereas when attention is distracted from pain it is perceived as less intense
76
Where does attentional distraction reduce pain related brain activity
In S1, S2 and thalamus
77
Where does distraction increase activity
Prefrontal cortex, ACC and PAG
78
What happened to spinal cord activity under high working memory load
Neuronal responses to painful stimulation in the dorsal horn were reduced
79
What does attentional distraction related to spinal process involve
Endogenous opioid neurotransmission and possibly top-down modulation involved in cognitive control of pain
80
What does the fact that pain involves a degree of cognitive appraisal mean
Individual (consciously or unconsciously) evaluated meaning of sensory signals emanating from bosy
81
What does the manner in which bodily sensation is appraised influence
Whether it is experienced as unpleasant or not
82
When is pain intensity reduced in relation to cognitive appraisal
When pain is perceived to be controllable e.g. re-interpret pain as harmless sensation of warmth
83
What predicts the development of chronic pain problems in relation to cognitive appraisal of pain
Pain catastrophising is associated with greater pain intensity and predicts development of chronic pain problems
84
How can activity in the brain pain matrix be changed
By changing the meaning of pain
85
How may acute fight or flight response dampen pain
Via release of noradrenaline and activation of PAG and endogenous opiods
86
What effect can chronic stress and negative emotional states (e.g. anxiety) have on pain
Intensify pain intensity, pain unpleasantness and reduce sense of perceived control over pain
87
What do pain affect and negative emotions activate
Overlapping brain circuits e.g. ACC- heightened activity related to negative emotione (e.g. sustained anxiety) may 'prime' subsequent perception of pain
88
What is fear of pain in chronic patients associated with
Hyper-vigilance for and sustained attention pain-related stimuli
89
What effect does emotion influences on pain have in young depressed adults
Increased pain sensitivity
90
What is a placebo
Any medical procedure that produces an effect in a patient because of its therapeutic intent and not its specific nature, whether chemical or physical
91
What can the expectation of pain relief exert
A powerful analgesic effect even when pain is severe
92
Where do mechanisms for placebo analgesia operate within
The neural circuit for the descending control of pain, including the PAG and opioids
93
What prefrontal areas of related to cognitive modulation of pain
DLPDC. VLPF. ACC
94
What cortical regions are associated with modulation activation of pain
ACC, SI, SII, insula, thalamus, brainstem and dorsal horn (e.g. PAG)
95
Explain the effect of treatment expectation on drug effiacy
Positive expectation activated descending pain inhibition systems (including PAG), whilst negative expectation activates regions involved in negative emotion
96
What are changed in the descending pain modulatory network implicated in
Chronic pain and functional pain disorders. Brain imaging reveals altered structure, function and neurochemistry within descending pain modulation circuitry in chronic pain patients
97
Alterations in which higher level brain systems are implicated in generation and maintenance of central sensitisation states and hyperalgesia/ allodynia
Prefrontal cortex, ACC, PAG and dorsal horn
98
How are changes in the brain defined in patients with chronic pain
Either a dysfunctional descending inhibitory system or an activated/ enhances descending faciliatory system
99
What changes in grey matter density were observed in chronic back pain patients
Neocortical grey matter volume reduced by 5-11% compared with controls, equivalent to loss in 10-20 years of normal ageing
100
What is chronic pain accompanied by in the brain
Brain atrophy
101
Pain is not a hard wired system, instead it is
A system in which noxious input is passively transmitted along sensory channels to the brain
102
What components does pain comprise
Sensory, affective and cognitive components
103
Explain how pain is complex
It is a subjective experience nor linearly related to nociceptive input
104
What is nociceptive information processing and consequent pain perception subject to
Multiple modulating influences
105
What necessary survival function do psychological modulations of pain provide
They allows pain experience to be tailored to situations
106
What is chronic pain associated with
Alterations in multidimensional pain systems
