1. PAIN Dr Akhavan akbari Fellowship of pain Ardebil university of medical science

2. AIMS  Detail the development of pain theories  Highlight current thinking  Describe current methods of treatment

3. Acute Pain  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

4. 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

5. 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)

6. 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

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

8. 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.

9. 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

10. 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

11. Nociceptors in Skin Epidermis Dermis Free Nerve Endings

12. Pain Pathways  Lots of effort to id neural pathways  Found distinct categories of nerve fibres  A δ : mylinated, carry rapidly sharp pains (20- 30 ms -1 )  C : unmylinated, carry slowly burning pain (0.5- 2 ms -1 )  Hence, short sharp, then delayed slow pain

13. Associated Area of Brain Fibres pass signals up spinal cord as electrical impulses then onto the thalamus Thalamus relays messages to cortex Proved difficult to id. specific area of the cortex that produce pain

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

15. 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)

16. Gate Control Theory - Melzack & Hall (1965) Experience Behaviour Tissue damage Gate – amplifies or attenuates signal Pain Perception Emotion

17. Opening & Closing the Gate FactorOpensCloses Physicalinjury agitation medication Emotionalanxiety stress frustration depression tension relaxation optimism happiness Behavioural (Cognitive) rumination boredom enjoyable activities complex tasks distraction social interaction

18. 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 views  Variability in people not inherent problem

19. 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

20. 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

21. Fear-Avoidance Model - Vlaeyen et al, (1995) Injury Pain Experience Pain Catastrophising No Fear Confrontation Recovery Pain-Related Fear Avoidance Hypervigilence Disuse Depression Disability -ve affect Threatening illness info

22. 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  Avoidance → disuse syndrome & ↑ p (mood problems)  Disuse leads to ↑ p (painful experience)

23. Treatments  Mirror pain theories  Medical (especially acute pain)  Non-anti-inflammatory non-steroid (paracetamol)  Anti-inflammatory non-steroids (eg ibprofen)  Opioids (eg morphine)  Psychological  Behavioural initially  Mostly cognitive behavioural now

24. 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

25. Vlaeyen et al 2001…  Compared:  CBT in-vivo graded exposure (Treatment A)  Graded Activity (Treatment B)  Subjects  Chronic pain for > 5 years  Substantial fear of movement / re-injury  Spent most of their time lying down  Total N = 4

26. Treatments CBT (Treatment A) Pain as common, manageable experience Explanation of fear-avoidance model Hierarchy of fearful situations Practice outside therapy Graded Activity (Treatment B) Baseline activity measured Individual regime designed & implemented High fear situations excluded

27. Measures  Pain catastrophising  e.g. When I am in pain I wonder whether something serious might happen  Fear of movement**  e.g. If I exercise I might be in danger of re- injuring myself  Pain disability**  e.g. I only walk short distances because of my back pain

28. Design Baseline Tx B GA Tx A CBT Group B N=2 Group A N=2 Tx A CBT Crossover End

29. Figure 1. Fear of movement: CBT then graded activity

30. Figure 2. Fear of movement: graded activity then CBT

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

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

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

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

35. 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

36. The End