Transcript A different Paradigm to Approach Chronic Pain

A Different Paradigm to
Approach Chronic Pain
Stephan A. Schug
Anaesthesiology & Pain Medicine
University of Western Australia &
Royal Perth Hospital
Definition of Pain
“Pain is an unpleasant sensory and
emotional experience associated with
actual or potential tissue damage …”
IASP 1979
The Model of
Pain by
Descartes
“like pulling a rope would
ring a bell in the brain”
Pain
Nociception
The Gate Control Theory
1965
Melzack&Wall
Pain mechanisms: a new theory
Science 1965:150:971
The Gate Control Theory
1965
Melzack&Wall
Pain mechanisms: a new theory
Science 1965:150:971
Descending
Inhibition
Example: Stress Induced Analgesia
Pain
X
X
CNS
Inhibition
Excitation
Nociception Without Pain
Nociception
1983
The History of
Central Sensitisation
Example: Phantom Pain
Pain
Pain without Nociception
CNS
X
Nociception
Inhibition
Excitation
X
mismatch between stimulus and response
(homosynaptic sensitization)
disruption of the normal specialisation of the
somatosensory system
aberrant convergence (heterosynaptic sensitization)
Wind-Up
progressive increase
in response of second
order neurons to
repetitive C-fiber input
Glia and
Central Sensitisation
Even Peripheral Changes of CRPS
are Result of Central Sensitization!
Antidromic
Stimulation
Leads To
Neurogenic
Inflammation
Recruitment
of Medial
System
Projection
Cortical Reorganisation in
Phantom Limb Pain
Flor
Lancet Neurology
2002: 1: 182–89
Cortical Reorganisation in CRPS
At admission
Cortical Reorganisation in CRPS
At admission
After 12 weeks functional treatment
‘Persistent pain should be considered as
a disease state of the nervous system,
not merely a symptom of some other
disease conditions.’
Basbaum AI Reg Anesth 1999; 24: 59
Definition of Pain
“Pain is an unpleasant sensory and emotional
experience associated with actual or potential tissue
damage,
or described in terms of such damage.
Many people report pain in the absence of tissue
damage or any likely pathopysiological cause. …
If they regard their experience as pain and if they report
it in the same way as pain caused by tissue damage, it
should be accepted as pain.”
IASP 1979
‘We all experience pain as arising from “out
there”, and, in consequence imagine that it is
actually triggered by noxious stimuli where we
feel the pain.
Central sensitization reveals, however, that
this in many cases is a sensory illusion; specific
alterations in the CNS can result in painful
sensations occurring in the absence of either
peripheral pathology or noxious stimuli.’
Latremoliere & Woolf 2009
Woolf C, Pain 2010
Physiological Pain
The Journal of Clinical Investigation http://www.jci.org Volume 120 Number 11 November 2010
CNS
“Nociplastic pain”
“Nocipathic pain”
The Journal of Clinical Investigation http://www.jci.org
Volume 120 Number 11 November 2010
The Biopsychosocial Model of Chronic Pain
Time to Flip the Pain
Curriculum?
‘In other words, we propose to reframe the pain
curriculum from its current standard formulation as a
bottom-up “biopsychosocial” phenomenon to a topdown “sociopsychobiological” one.’
Carr et al. Anaesthesiology 2014; 120(1):12-14
'sociopsychobiomedical' philosophy of the revised
pain medicine curriculum
FPMANZCA
Faculty of Pain Medicine, Australian & New Zealand College of Anaesthetists
Chronic Pain – a Complex Issue!
There Cannot Be a Drug For All This!
BIOLOGICAL CHANGES
PSYCHOLOGICAL STATUS
SOCIOCULTURAL CONTEXT
• Injury/trauma to tissue or
nerves
• Previous pain experiences
• Activities of daily living
• Health/pain beliefs
• Relationships
• Nociceptive input
• Coping skills
• Family environment
• Inflammatory changes
• Fears/concerns
• Social support
• Neuropathic input
• Emotions
• Social expectations
• Mood disorders
• Cultural factors
• Thought patterns associated
with pain
• Financial concerns
• Central sensitisation
• Previous pain
experiences
• Genetic predisposition
• Work and employment
• Sleep
• Psychological symptoms
• Genetic predisposition
Gatchel RJ et al. Psychol Bull 2007; 133(4):581–624.
Analgesic Expert Group. Therapeutic guidelines: analgesic. Version 6. Melbourne: Therapeutic Guidelines Limited; 2012.
How to Manage Chronic Pain?
Management plans should be designed around specific
functional goals
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Function can be preserved/improved despite persistent pain
(‘hurt is not harm’)
Encourage self-management – do not focus on diagnostic details
and do not reinforce searching for a ‘cure’
Incorporate appropriate psychological interventions – be vigilant for
catastrophic thinking, which is a marker of poor treatment
outcomes
Patient centred – consider differences in pain beliefs and
attitudes3
Expectations need to be realistic – frank and encouraging
without being overly reassuring
Multidisciplinary
Treatment
Chronic pain needs a team approach:
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There is no single thing that will stop the pain!
It requires a range of different treatments and a team
of people to help!
The pain probably won’t go away, but you can change the
way your brain perceives pain so you can get on with
daily living!
We will work together to find the best way forward for you!
How Does Pharmacology
Fit Here?
Reduce central sensitisation!
Decrease function of excitatory systems:
 Based on excitatory amino acids (glutamate) binding
to NMDA receptor
 Reduce glutamate release: pregabalin, gabapentin
 Block NMDA receptor for glutamate: ketamine
Increase function of inhibitory systems:
 Based on noradrenergic mechanisms
 Increase synaptic noradrenaline concentration:
– Tricyclic antidepressants: amitriptyline, nortriptyline
– SNRI antidepressants: duloxetine, venlafaxine
– Atypical opioids: tramadol, tapentadol
What is the Role of Opioids
Here?
Limited role in chronic pain
Opioids rarely beneficial in patients with chronic pain
At best, pain intensity is reduced by 30% to 50%
Much less benefit in relation to improving function and quality
of life
Very limited long-term data on key treatment outcomes
 No improvement in pain relief, quality of life and functional
capacit
 No improvement in physical function and disability
Trial after reasonable attempts at multidisciplinary pain
management have failed – not as monotherapy
Adverse events are the rule rather than the exception
What are the Problems with
Opioid Use in Chronic Pain?
Risks and complications include:
 ventilatory impairment (death in overdose!)
 nausea and/or vomiting
 constipation
 opioid-induced hyperalgesia
 abuse
 risk of diversion
 testosterone and immune suppression
 failure to achieve treatment goals or
promote self-efficacy
Schug SA, Sekandarzad MW. Med Today 2015; 16(Suppl. 6):2–5.
Conclusions
 Central Sensitisation challenges the traditional
specificity theory of pain perception; pain is not
always the result of and directly proportional to
peripheral nociception.
 Central Sensitisation explains the remarkable
changes of the somatosensory nervous system to
activity, inflammation and injury.
 Central sensitisation is responsible for many of
the temporal, spatial and threshold changes in
acute and chronic pain states.
Conclusions
 Central sensitisation is the major contributor to many
chronic pain conditions (‘CNS dysfunctional’ or
‘pathological’ pain, ‘maldynia’).
 These chronic pain states are therefore not
symptoms of an underlying peripheral pathology, but the
result of an ongoing dysfunction of the CNS long after
healing of peripheral pathology.
 Attempts to treat such chronic pain states by
searching for and ‘repairing’ of peripheral pathology are
doomed for failure.