Lecture given to the West of Scotland Pain Group on Wednesday 28th November 2012 by Emma Mair, Specialist Physiotherapist in Pain Management about Complex Regional Pain Syndrome (CRPS) and its treatment with Graded Motor Imagery (GMI).
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CRPS and Graded Motor Imagery
1. CRPS and Graded
Motor Imagery
Programme
Emma J Mair
Emma.Mair@ggc.scot.nhs.uk
November 2012
2. Tonight- an overview
Aetiology
Pathophysiology
UK Guidelines
Diagnosis
Treatment
Graded Motor Imagery
programme
3. European Incidence rate of 26/100,000
person-years
Incidence with age till 70
60% in upper limb, 40% in lower limb
Approximately 15% of sufferers will have
unrelenting pain and physical impairment
2 years after CRPS onset
4. Cause Unknown
45% following fracture
18% following sprains
12% following surgery
<10% spontaneous
5. CRPS-1
Type 1: sympathetically maintained pain
can start for no apparent reason but most
commonly follows distal radial fracture.
Characterised by pain which is
disproportionate to inciting event, swelling,
autonomic and motor disturbances,
changes in skin blood flow
6. CRPS-2
Type 2: Onset develops after injury to a
major peripheral nerve. May occur
immediately or be delayed for several
months
Most commonly involved are the median
and sciatic nerves
Allodynia and hyperalgesia occur but not
limited to the territory of one single
peripheral nerve
8. Pathophysiology
Multi-factorial
Other factors: environmental, genetic,
psychological
The stereotyped stages are now obsolete
A definition of recovery has not yet been
agreed
CRPS is not associated with a history of
pain preceding psychological problems, or
with somatisation or malingering
9. Contralateral cortical changes
Ipsilateral cortical
Reorganisation of sensory
changes
maps in S1*
↓Inhibition and
Reorganisation of motor
↑excitation in M1
maps in M1†
↓Inhibition and ↑excitation
in M1 and SMA
↓Endogenous pain
control
Pain
Central sensitisation
Allodynia, hyperalgesia,
secondary
hyperalgesia, and wind-up
Sympathetic– ↓Sympathetic outflow
afferent
coupling
Vasodilation (early stage) •Sensory abnormalities
Pain
Endothelial dysfunction •Autonomic dysfunction
↓NO and ↑ET-1
Impaired circulation (chronic stage) •Neurogenic inflammation
•Motor abnormalities
•Sensitisation
• Swelling
• Glossy skin
•Central reorganisation
Peripheral sensitisation
• Increased nail and
↑IL-1β, IL-6, TNFα, NGF, CGRP,
hair growth
substance P, and bradykinin
• Hyperaemia‡
Pain, vasodilation of the
skin, and oedema
11. UK Guidelines
Published April 2012
Recommendations for assessment and management
Speciality Guidelines:
Primary Care
Physio & OT
Orthopaedic Practice
Rheumatology, neurology and neurosurgery
Dermatology
Pain Medicine
Rehabilitation Medicine
Long-Term support in CRPS
Available from: http://www.rcplondon.ac.uk/resources/complex-regional-
pain-syndrome-concise-guideline
12. Diagnosis
Physio’s probably best equipped to
identify a patient with CRPS
Confirmation of diagnosis based on
Budapest guidelines
Confirmation with GP/cons
Differential diagnosis
Diagnosis tool:
http://www.trendconsortium.nl/diagnosis/
13. A The patient has continuing pain which is disproportionate to any inciting event
All A-D must
B The patient has at least one sign in two or more of the categories apply
C The patient reports at least one symptom in three or more of the categories
D No other diagnosis can better explain the signs and symptoms
Category Sign (you can see or Symptom (the
feel a problem) patient reports a
problem)
1. SENSORY Allodynia (to light Hyperesthesia does
touch and/or temp also qualify as a
sensation and/or symptom
deep somatic
pressure and /or
joint movement)
and/or hyperalgesia
(to pinprick)
2. VASOMOTOR Temperature Temp asymmetry
asymmetry and/or must be >1°C
skin colour changes
and/or skin colour
asymmetry
3. SUDOMOTOR/ Oedema and/or
OEDEMA sweating changes
and/or sweating
asymmetry
4. MOTOR/ Decreased range f
TROPHIC motion and/or motor
dysfunction
(weakness, tremor,
dystonia) and/or
trophic changes
(hair/nail/skin)
14. Sensory
Alloydnia – pain due to a stimulus which does not
normally cause pain. E.g. touch and temperature
Hyperalgesia– increased response to stimulus that is
normally painful
Hyperesthesia– increased sensitivity to stimulation
Hyperpathia- a state of exaggerated and very painful
response to stimulation especially repetitive stimulus
Hypoesthesia- a reduced sense of touch or sensation,
or a partial loss of sensitivity to sensory stimuli sensory.
20. The Environment
Therapy environment – breezes, open windows,
fans
Lighting
Invasion of personal space
Therapist movement and language (“your” vs
“it”)
Other people nearby
Noise
Privacy
21. Treatment
Prompt diagnosis and early
treatment are considered best
practice
Aims of treatment:
Reduce pain
Preserve or restore function
Enable patients to manage their
condition
Improve quality of life
23. Best practice recommendations
Be aware of CRPS and identify the clinical signs
Be aware of the Budapest criteria for diagnosing
CRPS
Initiate treatment as early as possible
Provide patient education about the condition
Know of the nearest MDT pain service or CRPS
centre
Recognising non-resolving or moderate
symptoms for onward referral
24. Rehabilitation Algorithm
Identify CRPS
signs and symptoms
Consider Meet Budapest Confirm Diagnosis
Differential Diagnosis criteria Via GP or consultant
Consider
Mild/Moderate yellow flags Moderate/ severe
symptoms symptoms
Educate, commence Educate, refer via GP
treatments To specialist pain clinic
Failing to respond Pain Management
to treatment in 4 weeks programme
Noticeable response to
Treatment within 4 weeks
And ongoing improvement
26. Four Pillars of Treatment
Physical and
vocational
rehabilitation
Pain relief Psychological
(medication and interventions
procedures)
Patient information
and education to
support self-
management
27. Engagement: education and
information for the patient &
family
Understanding pain and CRPS
Learning self management principles
Self efficacy- the patient remains
responsible and involved
Empowering the patient and the family
28. Medical Management
Investigation and confirmation of
diagnosis
Pharmacological intervention to provide a
window of pain relief
Reassurance that PT and OT are safe and
appropriate
Provide medical follow up
Support any litigation/ compensation claim
29. Pain Medicine Guideline
Recommendations
No drugs are licensed to treat CRPS in the UK
Neuropathic drugs should be used in according to NICE
& IASP guidelines
Pamidronate (single 60mg intravenous dose) should be
considered in suitable patients with less than 6mths
duration as a one off treatment
Intravenous regional sympathetic blocks with
guanethidine should not be routinely used
Other additional drugs demonstrate efficacy but a lot of
the evidence is still preliminary
Spinal Cord Stimulators
30. Psychosocial and behavioural
management
Psychological intervention is based on individualised
assessment, to identify and proactively manage any
factors which may perpetuate pain or disability/
dependency including:
Mood evaluation- management of anxiety and
depression
Internal factors, eg counter productive behaviour
patterns
Any external influences or perverse incentives
It usually follows principles of CBT delivering:
Coping skills and positive thought patterns
Support for family/carers
31. Physical Management
Emphasis should be on restoration of normal function
and activities through acquisition of self management
skills, with the patients actively engaged in goal setting
The programme may include elements of chronic pain
management including:
General body re-conditioning through graded
exercise, gait re-education, postural control
Restoration of normal activities, including self care,
recreational physical exercise and social/ leisure
activities
Pacing and relaxation strategies
Vocational support
32. It may also include specialised techniques
to address altered perception and
awareness of the limb, for example:
Selfadministered desensitisation with tactile
and thermal stimuli
Functional movement to improve motor
control and limb position awareness
Graded motor imagery, mirror visual
feedback, mental visualisation
Management of CRPS- dystonia
33. Activities of ADL and societal
participation
Support graded return to independence in ADLs
and clear functional goals
Assessment and provision of appropriate
specialist equipment to support independence
Adaptation of environment
Extend social and recreational activities in and
outside the home
Workplace assessment/ vocational re-training
36. Treatment- what are the options?
Based on evidence based practise, guidelines
and innovative clinicians
Good quality evidence for graded motor
imagery(GMI) combined with pharmacological
management is the most effective
37. Educate, educate, educate
We do not know why some
people get CRPS and
About CRPS others don’t
About Pain
We DO know that it is not
because of psychological
frailty or abnormality
Several important changes
in the brain seem to
accompany CRPS
To normalise these
changes, we have to
identify ALL combinations
to perceived threat and
train the brain
38. Movement versus Pain
Remember pain science and
pathophysiology
Sensitisation of CNS
More harm than good?!
39. Desensitisation
Activities of daily living
Washing and
dressing
Sensory
Discrimination
Two-point
discrimination
Electrical Stimulation
42. Sequential activation
of cortical pre-motor
and motor networks
Laterality and
Imagery = pre motor
Mirror Therapy =
Primary Motor Cortex
and S1 cortices
?reversal of cortical
reorganisation
47. Laterality Recognition
Make a quick decision
about the laterality
then you mentally
rotate mental
representation of the
limb into the position
viewed to confirm
initial selection!
48. Limb Laterality Recognition
Pain affects the brains ability to recognise
laterality of images of limbs
Information processing bias
Working body Schema
49. “Normal Scores”
Accuracy of 80% and above
Speed of hands and feet ~ 2 seconds
Accuracies and RT should be equal
50. Differences in Speed
Identifies problems with
Information processing
… but what does that
mean?
51. Mentally Mentally
move move RT
LEFT RIGHT R>L
hand hand
Difficult decision,
Acute LEFT hand safest to presume
X
injury looking at its LEFT hand
correct
because my LEFT Wrong
RIGHT hand hand is injured, choice,
chose LEFT hand. start
Accuracy
again
L=R
Mentally
Difficult decision, move
safest to presume LEFT
Acute LEFT hand its LEFT hand hand
injury looking at because my LEFT
hand is injured,
LEFT hand chose LEFT hand. correct
Acute Pain
52. Mentally Mentally
move move RT
RIGHT LEFT L>R
hand
Difficult decision, hand
Chronic LEFT safest to presume
its RIGHT hand X
hand injury because my LEFT correct
Wrong
looking at RIGHT hand is in trouble
choice,
and I’m protecting it
hand by not focusing on it.
start
Accuracy
again
L=R
Mentally
Difficult decision, move
Chronic LEFT safest to presume RIGHT
its RIGHT hand hand
hand injury because my LEFT
looking at RIGHT hand is in trouble
correct
and I’m protecting it
hand by not focusing on it.
Chronic Pain
53. Why?
Incorrect selection leads to longer
reaction time as need to repeat
mental rotation of limb to confirm
laterality choice
Pain & information processing,
patients wrongly select
59. Motor Imagery
Sports Performance
Neuro-Rehabilitation
Cognitive Psychology
Graded Motor Imagery
60. Motor Imagery
Observing and
Imagining movements
Imagining yourself
doing the movement
not imagining
observing themselves
doing the movement
61. The Why?
If you can’t feel it, how can
you use it?
62. The What?
Patient Explanation
Food
Back pain & bending
63. The How?
Prompts:
Shape
Skin
Colour
Digits
Movement
64. Motor Imagery
Awareness of body
part
Imagining movements
Imagining functional
activities
Flash cards and online
images can be used
as prompts
67. The How?
Observation
De-sensitisation
Movement
Context- emotional, threat
Weight bearing
Functional rehab
68. Mirror Therapy
Practical:
Try bilateral movements with the mirror
Try asynchronous movements whilst watching
your limb in the mirror
Get someone to tap or stroke the unaffected
limb whilst looking at the reflected limb
69. Mirror therapy for the 21st century?
Prism Glasses
www.prismglasses.co.uk
73. Questions from you and from
me?
How do we support
our primary &
secondary care
clinicians treating this
condition?
Specialised Pathways
and Clinics required?
Notas del editor
So for those who do not know me my name is Emma Mair. I am a clinical specialist physio here at the New Victoria Hospital and I have a specialist interest in CRPS and that’s why its me here speaking to you tonight.
Its going to be a bit of a whistle-stop-tour as those who know me I can talk and I could talk for crps and do for hours on end so I’ll just crack on and hopefully we can cover some of the newer information coming out of the guidelines and also explain a bit more about graded motor imagery and why I’m often seen wandering over the hospital with a big mirror as you can see its clearly not that I’m completely vain.
I had old information which quoted 1 in 50 of us got CRPS, with a 1 in 32 for women and 1 in 119 in men but that seemed an awful high rate so I’ve never been able to find my source so I’m secretly glad as my odds in 26 in 1 hundred thousands sounds so much better. Increases with age, More in the upper limb but I wonder at times if that is just more reported and researched 15% will continue to have symptoms 2 years on, I maybe a bit skewed by that data as obviously I see a lot of chronic CRPS patients and not always the early ones but I would have thought that would be a bit higher.
So the cause is unknown but the majority of patients are after injuries such as sprains and strains and those spontaneous onset unfortunately also have a much worse prognostic factor.
Typically we always reported CRPS in Types. One for crps after injuries and
Two for after definate nerve injury.
To be honest there was a lot of discussion regarding dropping these terms but it was decided to keep them but other than in nerve injuries which may require surgery crps 1 and 2 equal crps when it comes to diagnosis and treatment.
We know that the actual cause of CRPS is unknown but there is multifactorial pathophysiology including both the Peripheral and Central nervous system. Current thoughts are on an inflammatory overload which doesn’t switch off and theres a lot of studies re genetic predisposition and other factors. There is no current definition of recovery so it makes it defficult in research and I think it’s a term that sticks even when a patient no longer has alloydnia and hyperalgesia they sometimes report their pain as CRPS which it no longer would be diagnosed as such, but we can come on to that later. The guidelines say these patients should still be termed ‘CRPS-NOS’ (not otherwise specified). We absolutely know that crps is not a result of psychological problems although that doesn’t mean there is a host of psychological distress that goes along with crps.
Figure 4: Clinical features and proposed pathophysiological mechanisms of CRPS Although these pathophysiological mechanisms have all been identified in CRPS, they might occur independently of each other. The absence of such fixed relations explains the clinical heterogeneity that is often encountered in this condition. *Reorganisation of contralateral primary somatosensory cortex is associated with spontaneous CRPS pain and mechanical hyperalgesia. This reorganisation might also explain altered sensations (eg, perceptual disturbances and referred sensations). Reorganisation of contralateral Primary motor cortex is associated with motor dysfunction (ie, tapping). However, these changes might be secondary to the symptoms rather than being a cause of the symptoms. Perception of threat- smashed window, flight/fright reaction different systems working causing causes not only in physical sensations but thoughts and feelings… this ongoing changes the nervous system not exactly technically correct but it starts to highlight to the patient the multi systems involved and then ongoing to further pain explanations.
ACE inhibitors inhibit the breakdown of substance P obviously involved within sensitisation Coexisting medical conditions –osteoporosis, recent h/o menstrual cycle related problems and pre-existing neuropathies The association with asthma and migraine favours existing ideas of neurogenic inflammation involvement with CRPS (de Mos et al. 2008 ) Studies on immobilisation, people even without fractures who were immobilised high percentage started to show signs of CRPS so it should be something that people who are casted are given advice to monitor for changes etc. the guidelines gives a handout template for use in ortho clinics.
So most of the information about the diagnosis is from the new UK guidelines which were published earlier this year, although like anything its knowing they are there. There is a concise guideline then a more detailed guideline which is categories into different areas.
The main thing with diagnosis is that usually it is the physios who are seeing these patients early on so they really are at the best place to recognise and identify CRPS, as long standing some areas of medicine will still require a medical practitioner to “signoff” that diagnosis especially within medico-legal claims so it is always beneficial to discuss with the cons/GP. The guidelines have now all been compressed into what is known as the Budapest criteria which is still based on signs and symptoms. Obviously differential diagnosis needs to be considered but they is little confirmatory investigations for CRPS other than thermography but we don’t have them lying around and later stages MRI and x-ray changes.
So the budapest criteria is based on signs and symptoms in 4 areas: Sensory Vasomotor Sudomotor/ oedema Motor/ trophic changes Which I will go through quickly. To confirm a diagnosis the patient has to have a continuing pain which is disproportionate to any injury, They must have at least one sign( you can see it) in two or more of the categories And the patient reports at least one symptom in 3 or more of the categories. For research, diagnostic decision rule should be at least one symptom in all four symptom categories and at least one sign (observed at evaluation) in two or more sign categories.
Sensory Reports of hyperesthesia and/or allodynia Sensory: Evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or temperature sensation and/or deep somatic pressure and/or joint movement
Reports of temperature asymmetry and/or skin color changes and/or skin color asymmetry Usually hot crps initially and develops to “cold” crps Vasomotor: Evidence of temperature asymmetry (>1°C) and/or skin color changes and/or asymmetry
Reports of edema and/or sweating changes and/or sweating asymmetry Evidence of edema and/or sweating changes and/or sweating asymmetry
Motor / Trophic: Reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin) Motor / Trophic: Evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
The 4 D’s 54.4-84% report disturbances in body perception. Thoughts about the painful limb: Hate it Refer to it in the 3 rd person Foreign / alien to them Don’t want to think about it Feeling of amputation (early onset) Lack of attention to the limb (think, look, touch) Poor limb/digit position awareness and performance Perceptual changes in limb size and shape Perceptual mismatch in temp, pressure and weight Perceptual distortions in mental representation of the limb
Targeted screening to the patient about how the limb feels to them, does it feel apart of them and does it feel bigger, smaller to what they know it to be. Often pateints with body perception dysfunction will position the limb differently, round the back of a chair or give the area much more space. We now use the Bath body perception scale as an outcoem measure as I think this is also a way for us to report changes in these patients with treatment.
Because of Body perception dysfunction you need to be mindful of the treatment environment. It will be my CRPS patients who will tell me how drafty the new department feels whereas I had never noticed it or they often give me into trouble about speaking with my hands as I would be creating a change in pressure and at times the feeling of coming to close to them. It is worth noting as it can make a huge different to the patient
The guidelines suggests the main aims of treatment are: Reduce pain Preserve or restore function Enable the pateint to manage the condition and Improve quality of life… If it was so simple as that these patients wouldn’t be coming to pain clinics and you all certainly wouldn’t be giving up your time to talk about it. Luckily there is a bit more guidance
I’ve split this into the primary care physio and OT as in the guidelines
All the expectation is that you are aware of crps, the diagnosis and early input. If things aren't improving knowing where to get advice and/ or referral on.
Are suggesting 4 weeks of no change the patients should be referred on to MDT specialist services.
Some of the guidelines are based also on PMPs which I think is based on the Bath CRPS service model but early patients wouldn't go to the PMP here in Glasgow.
Just like in any complex and pain condition understanding is key. Explaining pain and crps is really a bit of a soap box theme for me. This isn't exclusive to crps either!
Intravenous regional sympathetic blocks with guanethidine should not be routinely used as 4 RCTs have not demonstrated any benefit. Immunoglobulin trials SCS- evidence shows that scs benefit generally declines over time. Baclofen- within input from specialised centres and when side effects out weigh within dystonia crps.
Suffering Fear Anxiety Anger Depression Failure to cope Behavioural illness
Individualised management - clinical reasoning +++ Little and often All hands on deck (MDT approach) Believe patient’s pain Gain trust It will hurt but not harm Function, function, function (valued) Emphasis on self management Be creative and compassionate Liaise and Refer to specialised MDT services
But can you be an official GMI practitioner? I don’t think so. It’s a constantly developing umbrella concept encompassing the neuromatrix paradigm, mindfulness, problem solving and most importantly is an individually tailored part of treating pain. Reduces threat of the movement as well as graded activation of different neuronal populations and cortical networks
GMI reduces pain intensity by a clinically relevant amount and this is maintained for up to 6 months (Daly and Bialocerkoswski 2009) Physiotherapy treatment for CRPS is not underpinned by any research
Pain physiology ed alters brain activity during task performance. We do not know why some people get CRPS and others don’t We DO know that
is a sequential process of rehabilitation where the therapeutic targets are synapses in the brain Laterality reconstruction Motor Imagery Mirror Therapy
These pictures above you all would have looked at them and made a decision about what you thought you saw and then perhaps knowing they are illusions investigated further to decide what else lies within the picture and these basic principles of visual perception. Not exactly the same as recognising laterality of an image but similar as, as I said when one looks at an image we initially make a guess and then mental rotate this image to confirm and reject our initial decision, best way to explain this is to give you a go. I’m going to show you an image and I want you to tell me if it is right or left sided. Just shout out right or left.
Quite often, people with painful limb problems lose the ability to recognise left or right images which can obstruct a successful recovery. The good news is the brain is plastic, and changeable, if given the right stimuli for long enough. So with a little bit of work, patience and persistence it is possible to reconstruct the brain’s feature of laterality, which would have existed prior to the limb problem. Laterality is the ability to select whether a presented image is right or left sided. A response requires initial selection of a right or left side then mental spatial transformation to confirm the choice i.e. we mentally rotate our own limb in our mid to confirm the choice. As such this requires an intact body schema. Body schemas are representations of the body within the spinal cord, thalamic and cortical structures which have a role in the guidance of imagined and actual movements. Melzack’s neuromatrix describes the self distinct identity from others and the world. This may be a genetic basis sculptured by life experiences, i.e. nature versus nurture. Modified by observation of others and modified by tool use- increases influence of body, modified by experience- skill acquisition such as musical instruments and using braille increases the representation of the hand. Nociceptive barrage also alters the representation in S1 and S2. The body schema can be fooled- rubber hand illusion Cognitive psychologists used laterality to investigate body schema Studies have shown that reaction times for recognition in laterality recognition can be reduced in CRPS and in phantom limb pain, however in acute experimental pain and expectation of pain there is delayed recognition in the opposite limb with no change to the affected limb. Researchers such as Moseley have shown that this change in reaction time in chronic pain are therefore unlikely to be due to nociceptive input, and in acute experimental pain there is unlikely to be a disruption to body schema. It also does not evoke protective premotor processes likely to be present with a problem which is perceived as threatening, i.e. volunteers know the pain will go away. Laterality tasks activates premotor cortices, not primary motor cortex, whereas imagined movements activate both allowing a basis for the GMI progression.
Motor imagery- the result of conscious access to the neurosignatures representing intention, preparation, carrying out and evaluation of a movement. There is a high degree of overlap in brain regions involved in actual movements or imagined movements. Essentially imagining movements and postures. This is kinaesthetic activation not a visual activation meaning the patient must imagine themselves doing the movement, not as an observer watching themselves do the movement.
Motor imagery- the result of conscious access to the neurosignatures representing intention, preparation, carrying out and evaluation of a movement. There is a high degree of overlap in brain regions involved in actual movements or imagined movements. Essentially imagining movements and postures. This is kinaesthetic activation not a visual activation meaning the patient must imagine themselves doing the movement, not as an observer watching themselves do the movement.
The use of the mirror to present the reversed image of a limb to the brain, illusion. Graded contextural activities
The Prism Glasses are a medical device created to help treat patients suffering from phantom limb pain and help rehabilitation of patients following a stroke. The Prism Glasses also have applications in the treatment of visual neglect syndrome and other chronic pain conditions such complex regional pain syndrome.
Based Phantom Limb Pain Research Moseley and Butler Daly & Bialocerkowski (2009) systematic review Clinical Evaluation- Bath / Liverpool experience Clinical site not clinician? CRPS conference