Pain Flashcards
Definition of Pain
- unpleasant sensory and emotional experience
- associated with tissue damage
- international association for the study of pain, 1994
Types of Pain
Acute
- 3 months
- tissue damage
- single or recurrent episodes
- anxiety provoking
Chronic
- persists beyond normal healing time (IASP, 1986)
- no adaptive function
- recurrent and progressive
- depression link
Assessment:
Verbal Rating Scale
- unidimensional measure
- 4 point scale (no pain, mild, moderate, severe)
- number associated with adjective
- combine to create pain intensity score
- critique : assumes equal intervals between ranks
Assessment:
Visual Analogue Scale
- unidimensional measure
- score marks across line to represent pain intensity
- distance measured from start to mark indicates pain intensity
Strength - has ratio qualities
- high number of response outcomes
Critique - scoring time consuming
- no account for psychological factors
Assessment:
Numerical Rating Scale
- unidimensional measure
- 0 = no pain, 10 = worst pain possible
Strength - good validity
- easy to administer to wide variety of patients
Critique - no ratio properties
- Jensen and Karoly, 2002
Assessment:
McGill Pain Questionnaire
(Melzack, 1975)
- multidimensional measure
- measures 20 classes of words
- sensory (gnawing)
- affective (punishing)
- evaluative (intense)
- choose word from each subclass
- measure number and word combo (0 = no pain, 5 = excruciating)
Strength - able to discriminate between conditions
Weakness - confusion about word meaning
Early Theories of Pain
Plato
- pain peripheral and emotional response in the soul
Galen
- established anatomy of cranial and spinal nerves, brain the centre for sensitivity
Aristotle
- brain has no direct function in sensory processes
Hippocrates
- pain due to deficiencies/excess in one of four humours or fluids
Main and Spanswick, 2000
Specificity Theory
Von Frey, 1895
- stimulus-response, direct relationship between pain and injury
- painful stimuli picked up by receptors in the skin and transmitted to the pain centre in the brain
- intensity proportional to damage
Specificity Theory Critique
- pain without injury (tension headache, some back pain)
- pain disproportionate to injury (gall stone, kidney stone)
- pain after injury heals
- episodic analgesia (Beecher’s soldiers, 1959)
- phantom limb pain (explains acute not chronic pain)
Pattern Theories
Skevington (1997)
- excessive stimulation of the nerves creates patterns of nerve impulses
- summated in dorsal horns of the spinal cord and cause pain
- pain due to excessive stimulation of peripheral non specific receptors which is interpreted centrally as pain
- can lead to pain after I just had healed (Livingstone, 1943)
Pattern Theories Critique
Strength
- can explain chronic pain mechanisms
Critique
- does not consider complex experience of pain
- requires that stimuli triggering pain must be intense
Gate Control Theory of Pain
Melzack and Wall, 1965
Pain signal ⬇️ C fibres (throbbing, chronic) or A delta fibres (quick, intense) ⬇️ Laminae ⬇️ A beta nerve fibres (inhibitory neurone not activated) ⬇️ Spinal cord ⬇️ Brain
Gate Control Theory
Continued
- pain is a pathophysiological process
1. Pain receptors in skin transmit damage info to “gates” in the dorsal horns in the spinal cord
2. Psychological factors (at brain level) can activate nerve fibres taking info from brain to spinal cord - worry/ catastrophising; reduce endorphins and open pain gate
- positive; increase endorphins and close pain gate
- level of pain felt results in differing activation of both systems (Morrison and Bennett, 2006, Main and Spaswick, 2000)
Types of Pain Receptors
Myelinated a-delta (types 1 and 2) - light touch, mechanical and thermal - short lasting pain Unmyelinated c-fibres - slow conducting - dull throbbing pain A-beta fibres -tactile info related to touch - if site of injury actions by a-delta, a-beta activates and supersedes a-delta at spinal cord
Pain Receptor Actions
- a-delta and c-fibres transmit info to substantia gelatinosa in dorsal horn
- SG contains executory and inhibitory cells
- nerve impulses trigger chemical release to SG that activates t-fibres
- a-beta inhibits t-fibre activity
- balance of activity influence gate being open or closed
- a-fibres; info to hypothalamus and cortex
- c-fibre; info to limbic system, hypothalamus, ANS
- reticulospinal fibres - results of neural activity to spinal gating mechanism may cause chemical release to SG
Gate Control Theory Critique
Strengths
- acknowledges multifaceted experience of pain
- provided testable model of psychological influences in pain experience
- stimulated research on the role of cognition
Critique
- debate about physiological mechanisms
- pain is simultaneously physical and physiological
- doesn’t explain some chronic conditions (phantom limb pain)
Placebo Effect
- improvement of symptoms resulting in medical treatment with an inactive substance or stage procedure
- patient recovers without genuine medical intervention
- attributed to belief in the effectiveness of treatment
Placebo Research
- “sham” surgical treatment of angina improved pain over 6 month period (Diamond et al, 1958, Cobbs et al, 1959)
- saline injection post lung surgery reduced pain intensity 2.5 points over 1 hour (Benedetti et al, 1998)
- chronic low back pain sufferers injected with placebo reduced pain 15 mins - 1 hour after and up to several days (Roberts et al, 1994)
- “fake” ultrasound treatment of dental pain reduced swelling (Ho et al, 1988, Hashish et al, 1988)
Pain Hypothesis
Some pain sufferers have a style of interacting with the world that interferes with adjustment (Pincus, 2006)
Maladaptive Cognitions:
Catastrophising
- negative self statements and thoughts about the present and/or future
- dispositional or situational
- pain catastrophising scale (Sullivan et al, 1995):
1. Rumination (can’t forget about it)
2. Magnification (afraid it may get worse)
3. Helplessness (can’t stand it) - accounts for 7-13% of variance in pain and correlated robustly with disability independently of pain (Haythornwaite, 2009)
Catastrophising and Pain Research
- more negative pain related thoughts, emotional distress and pain intensity than non in experimental pain condition (Sullivan et al, 1995)
- associated with self reports pain intensity and disability and predicted independent from pain, depression and anxiety in clinical group of vehicle victims (Sullivan et al, 1998)
- higher pain related disability and psychological stress independent from intensity, age and gender in spinal pain group (Turner et al, 2003)
- communal coping model (Sullivan et al, 2001)
- interpersonal coping strategy to produce support, proximity and empathy
- observer infers more intense pain ( Sullivan et al, 2006)
Maladaptive Cognitions:
Fear Avoidance Model
(Vlaeyen et al, 1995)
- why acute may become chronic pain
- the way pain is interpreted can lead to one of two pathways:
1. Non threatening: engage in activity and recover
2. Threatening: fear and safety seeking (escape) that worsens pain
Increases pain through: - increased vigilance to pain
- contributes to depression (gate control theory)
- contribute to disability (through limiting activity)
Fear Avoidance Research
- high levels of disability and avoidance behaviour in sample of acute back pain sufferers (Swinkles-Meewise et al, 2003)
- heightened pain related fear and pain catastrophising during acute phase, increased risk of future chronic low back pain and disability (Picav et al, 2002)
Maladaptive Cognitions:
Perceived Injustice
- perceived injustice questionnaire (Sullivan et al, 2008)
- scale and sample item (e.g. blame and someone else’s negligence)
- 226 musculoskeletal injuries
- high perceived injustice = greater pain severity, depression, catastrophic thinking, fear of movement and predicted return to work status one year later
Perceived Injustice Research
- associated with protective pain behaviour in 85 whiplash sufferers (Sullivan et al, 2009)
- predicts post traumatic stress symptoms in 112 whiplash sufferers (Sullivan et al, 2009)
- moderated pain related depression in 107 musculoskeletal pain suffers (Scott and Sullivan, 2012)
- less acceptance of pain in 250 fibromyalgia sufferers (Rodero et al, 2012)
- predicts return to work status in 103 whiplash victims (Scott et al, 2013)
Possible Mechanisms of Action
Pain catastrophising
- perceive injustice may lead to rumination and increased pain (Sullivan et al, 2012)
Anger
- PI triggers anger and increased pain due to muscle tension/ reducing endogenous opioid analgesia (Scott et al, 2013)
Depression
- PI acts as cognitive vulnerability for depression through focus on loss and lock of validation increasing suffering (Scott and Sullivan, 2012)
Critique
- methodological problems
- psychological concepts not clearly defined
- overlap in psychological variables
Treating Negative Pain Cognitions:
Cognitive Behavioural Therapy (CBT)
Assumptions (Turk and Okifuii,2002):
- individuals active processors of info
- thoughts and behaviours have mutual influences on each other
- behaviour influenced by both individual and environmental factors
- can learn more adaptive ways of thinking, feeling and behaving
- individuals should be active, collaborative agents of changing their own maladaptive thoughts, feeling and behaviours
Dominant and most effective model for treating chronic pain (Morley, Eccleston and Williams, 1999)
