Psychology of Pain Flashcards

1
Q

What are the definitions of pain?

A

‘Pain is a personal, subjective experience influenced by cultural learning, the meaning of the situation, attention, and other psychological variables’ (Melzack & Wall, 1996)

… an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage (IASP).

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2
Q

What is the difference between acute and chronic pain?

A

Acute: brief - lasts less than 6 months, usually after injury or infection, has genuine survival value

Chronic: lasting longer than 6 months; serves no useful purpose, is out of proportion to an injury or other pathology and may persist long after healing is complete, cause(s) often a mystery

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3
Q

What are the different types of pain?

A

Nociceptive – injury to body tissues (thearmal, mechanical, chemical); usually well localized (somatic), and is often described as sharp, aching, throbbing, or gnawing

  • This type of pain can either be somatic or visceral. Somatic pain results from injury to parts of the body such as bones, joints, and soft tissues. It is usually well localized, and is often described as sharp, dull, aching, throbbing, or gnawing.
  • Examples would include bone fractures, metastastatic cancer to the bone, tumours, and arthritis.
  • Visceral pain results from inflammation, distension, or stretching of the internal organs. It is not well localized and is often described as aching, cramping, deep pain, or pressure. Examples would include pain in the abdomen from a bowel obstruction and left arm/jaw pain from an acute myocardial infarction (heart attack).

Neuropathic – results from injury to nerves in either the central nervous system or the peripheral body; described as burning, tingling, shooting, stabbing, or shocking
- may be more difficult to treat than nociceptive

Nociplastic – arises from altered nociception despite no clear evidence of actual tissue damage or disease or lesion of the somatosensory system (IASP, 2017)

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4
Q

What did Fayaz et al find about pain in the UK?

A

Fayaz et al. (2017) meta-analysis of chronic pain in UK
Prevalence of chronic pain ranged from 35.0%-51.3%
Prevalence of moderate-severely disabling chronic pain ranged from 10.4%-14.3%.
Trend towards increasing prevalence with increasing age; from 14.3% in 18–25 years old to 62% in over 75 years group
Prevalence for chronic widespread pain 14.2%, chronic neuropathic pain 8.2% and fibromyalgia 5.4%
Chronic pain more common in females than males

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5
Q

What is the impact of pain on the NHS?

A

Patients in pain, especially chronic pain, are high consumers of healthcare resources

Primary care management of patients with chronic pain accounts for 4.6 million appointments per year

£584 million spent on prescriptions for pain annually

Chronic pain patients use the NHS 5x more frequently than patients who do not suffer

Cost to society enormous; annual UK cost for back pain is £12.3 billion; £1.6 billion in direct healthcare costs (Maniandakis & Gray, 2000)

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6
Q

Describe the early theories of pain.

A

Pre-cartesian: pain attributed to gods, based on assumption that pain related to punishment

Descartes (1664): Specificity theory - extent of pain directly proportional to degree of tissue damage - specific stimulus has specific receptor
- Focus on Nociceptors (receptors that respond preferentially to noxious stimuli) Nociceptors signal pain. Signals alert the organism to potential injury. Highly specialized sensory fibres which provide information to the CNS about the environment and the organism itself. Receptors respond preferentially to noxious stimuli – so are called nociceptors.

Biomedical & Freudian mind / body dualism: pain = damage OR ‘hysteria’

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7
Q

What are the limitations of the early theories of pain?

A

Don’t explain pain without damage

Don’t explain damage without pain

Don’t explain ‘normal’ variations in pain perception as related to individual differences in genetics AND environment

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8
Q

What new theory emerged for pain?

A

Away from the concept of a specific dedicated pain pathway…
…to brain mechanisms that integrate inputs from parallel sensory, emotional and cognitive systems

Emergence of gate control theory (Melzack & Wall, 1965) & pain ‘body-self neuromatrix’ (Melzack, 2001)

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9
Q

What did Harris (2013) say about the brain areas associated with pain?

A

Harris (2013):
There is no single region in the brain dedicated to nociceptive processing; rather a complex network of brain regions are appear to be associated with pain experience

  • some of which are also involved in other sensory, motor, and cognitive functions where information is often processed in parallel In experiments on animals, various sub-cortical structures have been found to respond to painful stimuli (including the amygdala, hypothalamus, and peri-aqueductal gray).
  • One issue is whether this activity reflects the pain itself, or some secondary effect of the pain, such as emotional arousal or fear.
  • More controversial has been the role of the cortex in pain, since, for example, stimulation of human S1 only infrequently leads to painful sensations.
  • Understanding of the role of the cortex in pain perception has been greatly advanced by brain imaging. Analysis of neuroimaging studies shows the areas of the brain that consistently respond to (experimentally-induced) acute pain are the primary and secondary somatosensory cortices (SI and SII), the insular cortex (IC), the anterior cingulate cortex (ACC), and the prefrontal cortex (PFC) as well as several subcortical structures (see Figure 8.10) (Apkarian et al, 2005).
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10
Q

What is the role of pain expectancy and capability?

A

Experimental studies suggest that predictability and controllability of pain are major determinants of perceived pain intensity (Muller, 2012; Oka et al, 2010)

Objectively uncontrollable noxious stimuli are perceived as more intense, harmful, and unpleasant than are controllable and predictable stimuli (Carlsson et al, 2006)
Most compelling evidence for role of cognitive top-down processes in the perception of and response to painful stimuli come from studies examining placebo analgesia (Kaptchuk et al., 2020)

Expectation-induced placebo analgesia appears to be mediated by prefrontal function

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11
Q

What did Enck et al find about pain?

A

Open-hidden paradigm (Enck et al., 2013):

Post-op patients needed much higher dose than usual to reduce pain by 50% when in hidden group

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12
Q

What is central sensitisation?

A

Clear that majority of chronic musculoskeletal pain cases reflect alterations in central nervous system (CNS) processes (Nijs et al., 2011)

Central sensitisation:
defined operationally as an amplification of neural signaling within the CNS that elicits pain hypersensitivity (Woolf, 2010)
encompasses impaired functioning of brain-orchestrated descending anti-nociceptive (inhibitory) mechanisms
leads to (over)activation of descending and ascending pain facilitatory pathways
causes decreased pain thresholds (hyperalgesia), and may apply to touch (allodynia) as well as to movement of trunk or limbs
in people suffering from chronic pain, sensitization remains present after nociception has resolved

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13
Q

Expand on the psychosocial influences of pain.

A

Cognitive-emotional dimensions are capable of modulating pain signals—in both positive and negative ways
Emotional stress, mood, and anxiety can impact the reporting of pain symptoms, disability levels, and response to treatment (Turk & Okifuji, 2002)
Brain imaging studies indicate that anxiety, depression, dissatisfaction, and catastrophising are psychological factors leading to greater experience of pain through altered activation of limbic structures (van Wilgen et al., 2012)
Levels of social support modulate pain (Jensen et al, 2002

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14
Q

What is the effect of chronic pain on the brain?

A

Persistent pain ages the brain reducing gray matter twice as much as what normal aging would (Apkarian et al. 2004)

Persistent pain can change brain structure and re-wire patients so that how they think and what they pay attention to is biased

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15
Q

What is the biopsychosocial model and what are its key considerations?

A

The Biopsychosocial model is the most widely accpeted model (Adams & Turk, 2018)

  • it says the perception of pain and the response to pain is dependent on 3 aspects:
    1. Biological factors
    2. Psychological factors
    3. Social factors

Its Key considerations are:

  • Pain is a dynamic process
  • Pain experiences are unique to each individual
  • There is a difference between contributing factors and causes of pain
    • Psychological factors can influence ways people experience chronic pain
    • Little empirical evidence that psychological or social factors directly cause central sensitisation
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16
Q

What affects your risk of chronic pain?

A

Can exist where and when there is no obvious cause
Can affect any part of the body and any age group

Higher risk ?

Severe and long-lasting nociception
Genetically sensitive to noxious stimulation
Depression/anxiety
Certain vocations (e.g., truck driving)
Trauma survivors (early life stress)
Lower socioeconomic status + low job satisfaction

17
Q

What are the yellow flags of chronic pain?

A

Low mood/depression
Attention & vigilance (vigilance to pain is a predictor of disability)
Catastrophizing & worry (extreme form of a normal process of worrying about pain)
Avoidance (fear of pain is more disabling than pain itself)

look at ppt for more

18
Q

What impact can chronic pain have on an individual?

A
Depressive symptoms / depressed mood
Psychological processing
Role of stress 
Quality of life
Psychosocial impact
19
Q

What did the Annual Report find in 2008 regarding chronic pain?

A

Donaldson Sir L. (2008)
Chief Medical Offer Annual Report

Each year over 5 million people in the UK develop chronic pain, but only ²/3 will recover
49% of chronic pain patients experience depression
25% of sufferers lose their jobs
16% of sufferers feel their chronic pain is so bad that they sometimes want to die
1 pain specialist for 32,000 people in pain

20
Q

Describe depression in chronic pain

A
  • Depressive disorder is a common sequelae to the psychological experience of living with chronic pain; has additive effect on disability (Cocksedge et al 2016)
  • One of the most commonly reported comorbid conditions in patients with chronic pain (30-54%)
  • Pain is strongly associated with depressive disorders; odds ratio (OR) in range 1.9–7.3 (Beesdo et al 2010)
  • Depressive symptoms / depressed mood
21
Q

What are the specific psychological factors relating to chronic pain?

A
  • Heightened attention & vigilance to pain and threat of pain
  • Pain catastrophizing & worry (extreme form of a normal process of worrying about pain)
  • Avoidance of potentially pain inducing activities (fear of pain is more disabling than pain itself)
  • Perceived (lack of) control of pain condition
  • Neurocognitive slowing and/or difficulties
22
Q

What is the role of stress in chronic pain disability?

A

Stress = ‘any experience, physiological, or psychological that disrupts homeostasis’

Persistent pain can lead to dysregulation of the neuroendocrine response (stress response) in HPA axis

Leads to chronic over/under production of cortisol – damaging

Altered downstream signalling from HPA axis may lead to sensitization of nearby nociceptive afferents (Eller-Smith et al, 2018)

Symptoms mimic sickness: fatigue, dysphoria with muscular aches and pains, hyper-vigilance, impaired physical functioning and impaired cognition

23
Q

What is the chronic pain cycle?

A

Psychologists use a version of this diagram to explain the phenomenon to patients, including how psychology might help.

see ppt for diagram

24
Q

What are the biopsychosocial interventions for pain management?

A

Psychological: CBT, counselling, ACT, mindfulness (MBSR)

Biological pain management: medications for pain/sleep/ depression/anxiety etc…

Somatic: TENS, injection therapy, acupuncture, manipulation, massage

Relaxation techniques: biofeedback, visualisation

Body alignment / strengthening: physiotherapy, yoga, tai chi, alexander technique

All of these can be used alone or with other (usually multidisciplinary) treatments

25
Q

What are the psychological interventions for chronic pain?

A

Cognitive behavioural therapy (CBT) - Goal is not to reduce pain, rather to improve quality of life and management of pain through, education, coping strategies, stress management and increasing perceived control and self-efficacy.

ACT / Mindfulness approaches - mindfulness-based stress reduction (MBSR) and ACT focuses on observing and being aware of thoughts, feelings, physical sensations in the moment and changing individual’s relationship
to pain and other psychological
experiences so as to modulate the
pain experience overall.

26
Q

Describe the persistent pain management programme (gold standard).

A

Differs from a chronic pain clinic (biomedical focus, e.g., medication, injections)

Usually reserved for those with severe impact on life (anxiety, depression) but no active, severe, psychiatric co-morbidity

Focuses on psychological education and support – CBT, ACT, mindfulness

Within a group setting – to focus on social aspects

Includes physiotherapy and occupational therapy

27
Q

Do the psychological interventions work?

A

2020 Cochrane Review of 59 trials involving >5000 participants: CBT has small but reliable beneficial effects for reducing pain, disability and distress in chronic pain; changes maintained at 6 months (Williams et al., 2020)

Between 1 in 2 and 1 in 5 chronic pain patients (depends on outcome measure) achieve clinically significant gains (Smith et al., 2015)

Evidence that positive effects of CBT are due to structural changes in the grey matter in sensory, motor, and affective brain areas and/or in the functional connectivity of these regions (Seminowicz et al.,2013; Shpaner et al., 2014)

ACT/Mindfulness - no evidence of superiority to standard CBT interventions