AIMS Lecture 4

PAIN
Detail the development of pain theories Highlight current thinking Describe current methods of treatment

Associated with trauma, procedures etc. Meaningful signal to inhibit more harm Adrenalin release often co-occurs Anxiety goes after diagnosis and treatment (tx) Tx typically medicines, activity, tractions Recovery time usually short

Acute Pain

Chronic Pain
Various opinions on time-lag 8 weeks (Jensen, 2004) 6 months (Hardin, 2004)

Essentially, sig. > expected recovery time Often not related to tissue damage Medical tx unsuccessful Anxiety does not decrease

Important?
LBP most common cause of absenteeism & disability in Europe (van Tulder et al, 1998) Lifetime prevalence LBP: 70% (Andersson et al, 1991) 1.7% GDP - Holland (van Tulder et al, 1998) 5-25% children report pain headaches, abdominal & limb pain (Campo et al, 2002) ~ 25% kids attending for JRA report mid-high levels of pain (Schanberg et al, 1997)

Chronic Pain Syndrome

Common, understandable pattern of behaviour seen in those with on-going pain Continual seeking of medical help without success Acute pain treatments seem to worsen matters eg bed rest leads to muscle atrophy Despair, hopelessness, dependency, clinical depression, worthlessness, anger, social withdrawal

Early Theories
Pain as a sensation Stimulus-response theory Von Frey (1895) specificity theory Specific receptors for specific sensations Pain Warmth Touch

Biomedical View
Reflects approach to sensory systems Led to similar research to identify:
Receptive organs / cells Pathways that conduct sensory info. Part of brain that processed pain info.

PAIN

Biomedical View - Assumptions

Tissue damage causes pain Psychological states are outcomes of pain Pain experience is an automatic response Pain is either organic or psychogenic

Pain Receptors
Attempt to explain variability across skin Led to id. of polymodal nociceptors / free nerve endings (in skin surface, around blood vessels etc.) for: Pain Touch

Warmth Relationship between pain & FNE unclear

Nociceptors in Skin
Epidermis

Pain Pathways
Lots of effort to id neural pathways Found distinct categories of nerve fibres
A : mylinated, carry rapidly sharp pains (2030 ms-1) C : unmylinated, carry slowly burning pain (0.52 ms-1)

Free Nerve Endings

Dermis

Hence, short sharp, then delayed slow pain

Associated Area of Brain

Fibres pass signals up spinal cord as electrical impulses then onto the thalamus Evidence for:

Summary
Pain receptors Pain pathways Associated areas of the brain (?) Consequently, unsurprising that surgery & medications are effective in many cases

Thalamus relays messages to cortex Proved difficult to id. specific area of the cortex that produce pain

Problems for the Biomedical View

Similar tissue damage dissimilar pain (Beecher, 1956) Medical tx not always helpful Disease severity explains only 1 10% of variance (Ilowite, 1992) Phantom limb pain: up to 60% have pain 7 years post-amputation (Krebs, 1984)

Gate Control Theory - Melzack & Hall (1965)

Pain Perception

Experience Emotion Behaviour Tissue damage

Gate amplifies or attenuates signal

Opening & Closing the Gate

Factor
Physical Emotional

Gate Control v Biomedical Theory

Pain as perception not sensation (active) Multiple factors influence pain perception Move away from mind-body dualism Tries integrating biological & psychological

Opens
injury agitation anxiety stress frustration depression tension rumination boredom

Closes
medication relaxation optimism happiness

Behavioural (Cognitive)

enjoyable activities complex tasks distraction social interaction

views Variability in people not inherent problem

Problems for Gate Control Theory

Evidence for propsed moderators, but no physical evidence of gate Still organic basis for pain (phantom limb?) Not truly integrative re: psyche & soma Still improvement on stimulus-response paradigm

Subsequent Pain Theories

Reflect trends in general psychology Fordyce (1976) - pain as behaviour Reinforcement contingencies +ve reinforcement (e.g. attention / affection for pain behaviours) -ve reinforcement (e.g. avoid unpleasant events such as work, school) Recently, growth in cognitive behaviour models

Fear-Avoidance Model - Vlaeyen et al, (1995)

Disuse Depression Disability Avoidance Hypervigilence Pain-Related Fear Pain Catastrophising

Fear-Avoidance Theory
(-ve) appraisals (catastrophising) fear of pain (illness cognitions) & re-injury Fear of pain avoidance of potentially painful events (illness behaviour) Little opportunity to disconfirm beliefs p

Injury Pain Experience -ve affect Threatening illness info

Recovery

Confrontation

Avoidance disuse syndrome & (mood problems)

No Fear

Disuse leads to

p (painful experience)

Treatments
Mirror pain theories Medical (especially acute pain) Non-anti-inflammatory non-steroid (paracetamol) Opioids (eg morphine) Behavioural initially

CBT for Chronic Pain

Education: offering another possible explanation for individual situation Meaning: linking illness cognitions & behaviour Individually designed graded exposure to dangerous situations Restructruring of illness cognitions & changing illness behaviour

Anti-inflammatory non-steroids (eg ibprofen)

Psychological

Mostly cognitive behavioural now

Vlaeyen et al 2001
Compared:
Graded Activity (Treatment B) Chronic pain for > 5 years CBT in-vivo graded exposure (Treatment A)

Treatments
CBT (Treatment A)
Pain as common, manageable experience Explanation of fear-avoidance model Hierarchy of fearful situations Practice outside therapy

Subjects

Substantial fear of movement / re-injury Spent most of their time lying down

Graded Activity (Treatment B)

Baseline activity measured Individual regime designed & implemented High fear situations excluded

Total N = 4

Measures
Pain catastrophising Fear of movement**
e.g. When I am in pain I wonder whether something serious might happen

Design
Group A N=2 Tx A CBT Tx B GA

Pain disability**

e.g. If I exercise I might be in danger of reinjuring myself

e.g. I only walk short distances because of my back pain

Group B N=2

Tx B GA

Tx A CBT

Baseline

Crossover

End

60 40 20 0 Base Start CBT Start GA

60
Subject 1 Subject 4

40

Subject 2 Subject 3

20

End

0 Base Start GA Start CBT End

Figure 1. Fear of movement: CBT then graded activity

Figure 2. Fear of movement: graded activity then CBT

25 20 15 10 5 0 Base Start CBT Start GA

Subject 1 Subject 4

25 20 15 10 5 0 Base Start GA Start CBT

Subject 2 Subject 3

End

End

Figure 3. Self-report disability: CBT then graded activity

Figure 4. Self-report disability: graded activity then CBT

Conclusions
Pain-related fear reduced by CBT not GA Exposure leads to disconfirmation of painrelated cognitions This leads to less self-report disability Chronic pain patients should be screened for pain-related fear

Issues
Small number of subjects Individual variation in effectiveness High fear activities excluded in graded exposure No assessment of pain perception

Summary
Acute & chronic pain are different Chronic pain impacts on society & individuals Theories of pain have changed over time Psychological models reflect general trends Treatment approaches reflect theories CBT is the current psych treatment of choice

The End