PAIN

Dr Akhavan akbari

Fellowship of pain

Ardebil university of medical science

AIMS

Detail the development of pain theories

Highlight current thinking

Describe current methods of treatment

Acute PainAssociated 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

Chronic PainVarious 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

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.

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

Dermis

Free Nerve Endings

Pain PathwaysLots 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

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

Summary

Evidence for:

Pain receptors

Pain pathways

Associated areas of the brain (?)

Consequently, unsurprising that surgery & medications are effective in many cases

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)

Experience

Behaviour

Tissue damage

Gate – amplifies or attenuates signal

Pain Perception

Emotion

Opening & Closing the GateFactor Opens Closes

Physical injuryagitation

medication

Emotional anxietystress

frustrationdepression

tension

relaxationoptimismhappiness

Behavioural

(Cognitive)

ruminationboredom

enjoyable activitiescomplex tasks

distractionsocial interaction

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

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)

Injury

Pain Experience

Pain Catastrophising

No Fear

Confrontation

Recovery

Pain-Related Fear

Avoidance Hypervigilence

Disuse Depression Disability

-ve affect

Threatening illness info

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)

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

CBT for Chronic PainEducation: 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

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

TreatmentsCBT (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

MeasuresPain 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

Design

Baseline

Tx B GA

Tx B GA

Tx A CBT

Group B N=2

Group A N=2

Tx A CBT

Crossover End

0

20

40

60

Base Start CBT Start GA End

Subject 1

Subject 4

Figure 1. Fear of movement: CBT then graded activity

0

20

40

60

Base Start GA Start CBT End

Subject 2

Subject 3

Figure 2. Fear of movement: graded activity then CBT

0

5

10

15

20

25

Base StartCBT

StartGA

End

Subject 1

Subject 4

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

0

5

10

15

20

25

Base StartGA

StartCBT

End

Subject 2

Subject 3

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

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

Issues

Small number of subjects

Individual variation in effectiveness

High fear activities excluded in graded exposure

No assessment of pain perception

SummaryAcute & 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