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Brains In Pain

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Title: Brains In Pain


1
Brains In Pain
  • Dr.Helen Cohen
  • Honorary Consultant / Arc Clinical Research
    Fellow
  • RNHRD

2
Overview
  • CRPS Current views
  • My research investigating allodynia
  • CRPS What does the patient tell us?
  • Symptoms/signs as organic phenomena
  • Referred sensations
  • Visual disturbances
  • Parietal lobe

3
Complex Regional Pain Syndrome
Pseudonyms
  • Reflex Sympathetic Dystrophy RSD
  • Algodystrophy
  • Sudecks Atrophy
  • Causalgia
  • Shoulder-Hand syndrome

4
Types
  • Type 1 No nerve injury
  • Type 2 Nerve injury
  • No difference in presentation

5
Bruehl
6
CRPS
Swelling Sweating Colour Temperature Allodynia
7
Thermography
8
Definition
  • IASP definition of CRPS
  • Condition initiated by an injury (NOT always)
  • Not limited to distribution of single
    peripheral nerve
  • Pain disproportionate to inciting event
  • Associated at some point with
  • oedema
  • changes in skin, blood flow
  • abnormal sweating
  • or allodynia
  • or hyperalgesia
  • Site usually distal extremity

9
Diagnostic Criteria
IASP 2003
  • Continuing (spontaneous and/or evoked) regional
    pain that is seemingly disproportionate in time
    or degree to the usual course of any known trauma
    or other lesion
  • At least one symptom in 3 or more of the
    following categories
  • At least one sign in 2 or more of the following
    categories
  • Positive Sensory
  • allodynia, hyperalgesia, deep somatic allodynia
  • Vascular
  • colour or temperature changes/asymmetry
  • Sweating abnormalities or oedema
  • Motor/Trophic
  • weakness, ? ROM, skin/nail/hair changes, tremor,
    dystonia
  • Research criteria at least one symptom in each
    category, and one sign in 2 or more catagories

10
Typical CRPS literature
  • Sympathetic dependent / independent pain
  • Stages Hot / hot cold / cold
  • Rare
  • Cured by sympathetic blocks, sympathectomies,
    local guanethidine infusions etc

11
Possible mechanisms
  • Sensitised pain nerves CNS
  • Neurogenic inflammation
  • Autonomic sympathetic nerve involvement
  • Abnormal nerve firing
  • Motor system changes due to abnormalities in
    discharge patterns of a and ? motor neurons
  • Genetic predisposition
  • Other mechanisms such as exaggerated inflammatory
    response or protective disuse or myofascial
    dysfunctions

12
Epidemiology
  • Incidence of CRPS type 1 2 1 to 15.(1)
  • Incidence of CRPS type 1 is 1-2 after various
    fractures.
  • In prospective studies of Colles fracture the
    incidence is 7-35.
  • Approx. 5 of these patients have lasting
    problems.
  • Chronic, severe CRPS was rarer (lt2).
  • 2-5 may develop CRPS type 2 after peripheral
    nerve injury.
  • Ratio of female male is 31.(2)
  • The affected age group is between 18 and 71 years
    with a mean age of 41.8 years.(3)
  • CRPS can also occur in children. Children with
    diabetes have a higher incidence of CRPS as
    compared to non-diabetic children.(4)

(1) Purdy CA and Miller SJ. Reflex sympathetic
dystrophy syndrome. Comprehensive textbook of
foot surgery. (2nd ed), 1124-1134. 1992.
Williams and Wilkins. (2) Veldman PHJM, Reynen
HM, Arntz IE, and Goris RJA. Signs and symptoms
of reflex sympathetic dystrophy. Lancet 342,
1012-1016. 1993. (3) Allen G, Galer BS, and
Schwartz L. Epidemiology of complex regional pain
syndrome a retrospective chart review of 134
patients. Pain 80(3), 539-544. 1999. (4)
Schiller JE. Reflex sympathetic dystrophy of the
foot and ankle in children and adolescents.
Journal of the American Podiatry Medical
Association 79(11), 545-550. 1989.
13
Presentation
  • Severe, unremitting pain non-dermatomal
  • Vasomotor / sudomotor disturbance
  • Cast too tight
  • Oedema trophic changes
  • Allodynia
  • Guarding
  • Neuropathic quality to pain
  • Lack of effect of analgesics inc. opiates

14
Investigations
  • Often not very helpful
  • Xray osteoporosis
  • Isotope bone scan Classic findings include
    increased periarticular uptake throughout the 3
    phases (blood pool, blood phase, scan phase)
  • However, in some patients a reverse or mixed
    pattern is seen

15
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16
Investigations
  • MRI A variety of MRI features have been reported
    including skin thickening, oedema, synovial
    hypertrophy, joint effusions and bone marrow
    oedema
  • Thermography
  • Sympathetic function
  • EXCLUDE any other causes

17
Pharmacological Management of CRPS
  • OR
  • Why dont drugs seem to work?

18
CRPS Treatments
  • Whats the evidence ?
  • Very little
  • 2 Reviews
  • Local anesthetic sympathetic blockade for complex
    regional pain syndrome MS Cepeda, DB Carr, J Lau
    2005
  • 2 randomised clinical trials, 23 pts
  • Sympathectomy for neuropathic pain
    A Mailis-Gagnon and A Furlan 2002
  • 4 studies

19
Why dont drugs seem to work?
  • Causes of CRPS largely unknown
  • It is suggested that
  • Multiple mechanisms involving various regions
    of entire neuraxis underlie the development of
    CRPS
  • Pathophysiology may vary from one patient to
    another

20
Too many targets
  • Network dysfunction other factors
  • NO magic bullet
  • Often opiate resistant

21
Approaches to the drug treatment of CRPS
  • Standard WHO pain ladder

22
World Health Organization Pain Ladder
Freedom from cancer pain
Opioid for moderate to severe pain / -
Non-opioid / - Adjuvant
Morphine Paracetamol NSAID
3
Pain persisting or increasing
Opioid for mild to moderate pain / -
Non-opioid / - Adjuvant
Codeine Paracetamol NSAID
2
Pain persisting or increasing
Non-opioid / - Adjuvant
1
Paracetamol NSAID
23
Individualised Approach
  • Symptom based
  • Systems based

24
Analgesics
  • Start with WHO
  • KEEP IT SIMPLE (if drugs dont work, dont give
    em)
  • If peaks troughs in pain control
  • Consider slow release preparations
  • If opioids are helping
  • Consider transdermal patches - matrix patch
    (buprenorphine, fentanyl)
  • Keeping patch on change over nausea titration
    up down heat drug release

25
Opioids
  • If they dont help, STOP them!
  • Dont keep increasing dose will not help
  • Opioid doped patients dont rehab!
  • Some patients will be keen to come off others
    wont let the crutch go.

26
Adjuvant Medications
  • NSAIDS
  • COX I / COX II
  • Slight increased risk of stroke heart
    attack
  • True for any NSAID ?
  • GI ulceration
  • Risk / benefit analysis

27
Neuromodulatory
  • Anticonvulsant medications
  • Gabapentin, Pregabalin, Carbamazepine, Phenytoin,
    Topiramate, Valproate etc
  • Side effects drowsiness, weight gain

28
Antidepressants
  • Tricyclics (nortriptyline, amitriptyline)
  • SSRI (fluoxetine), SNRI (venlafaxine), NARI
    (reboxetine)
  • Useful for BOTH pain and anxiety / depression
    related problems
  • Different dosages for pain
  • May help with poor sleep pattern
  • Give nor/amitriptyline at 8 pm

29
Muscle relaxants
  • Muscle spasm dystonia in CRPS
  • Baclofen
  • SE sedation, hypotonia
  • Benzodiazepines
  • SE habituation, drowsiness

30
NMDA receptor antagonists
  • Ketamine
  • Ketamine coma

31
Calcium modulating
  • Calcitonin nasal, s/c
  • Pamidronate infusion

32
Immunomodulatory
  • Anti-TNF
  • IV-immunoglobulins
  • Steroids

33
Interventional
  • Nerve / sympathetic blocks
  • Local eg.stellate ganglion
  • Regional use of cuff
  • Agents lignocaine, clonidine, baclofen,
    guanethidine
  • Sympathectomy chemical, surgical
  • (risk of abnormal sweating, increased pain)
  • Spinal column stimulator
  • Intrathecal drugs baclofen, clonidine, opioids
  • Amputation

34
Sympathectomy
  • Cochrane review Authors' conclusions
  • The practice of surgical and chemical
    sympathectomy is based on poor quality evidence,
    uncontrolled studies and personal experience.
    Furthermore, complications of the procedure may
    be significant, in terms of both worsening the
    pain or producing a new pain syndrome and
    abnormal forms of sweating (compensatory
    hyperhidrosis and pathological gustatory
    sweating).

35
Non-Pharmaceutical
  • Occupational therapy
  • Desensitisation techniques
  • Physiotherapy, hydrotherapy
  • Mirror Visual Feedback
  • Graded Motor Imagery
  • Pain management
  • Clinical psychology

36
Key Points
  • Opiates may not work
  • Keep drug treatment simple
  • There is very little evidence for the beneficial
    effect of most treatments for CRPS
  • Non-drug treatments are a powerful, underused tool

37
My Research
38
Background knowledge
Cortical reorganisation in CRPS Confirmed by
imaging studies Reverses with resolution of
disease (Flor)
39
Conflicting sensory information
  • May cause pain (Harris)
  • Cortical reorganisation as a cause
  • Can cause pain in healthy volunteers
  • Can worsen pain in FMS

Allocentric/egocentric integration
40
Allodynia
  • When a normally non-noxious stimulus is perceived
    as noxious ie. painful

41
ARC Grant Work
  • Allodynia in CRPS, RA, OA
  • Autonomic dysfunction in CRPS
  • Allocentric/egocentic mismatch susceptibility
  • Correlation of the above
  • Guide treatment approach

42
Methods
The problem of qualia (is what I call green the
same as what you see as green?) QST Semmes
Weinstein monofilaments for mechanical detection
thresholds
43
QST gadgets
44
Body Map
MDT thresholds (grams) Allodynia Paraesthesia Refe
rred sensations
45
Laser Doppler Flowmetry
CRPS
Healthy
46
What does the patient tell us ?
  • Foreigness of the limb
  • Dislike/hatred of the limb
  • Hiding/neglecting the limb
  • Distorted body image
  • Touch sensitivity beyond the limb
  • Clumsiness/lack of control
  • Visual disturbance
  • Language/numerical problems
  • Sensitivity to other sensory modalities
  • Protective zone

47
Bizarre symptoms as organic phenomena
  • Chronic pain as a network dysfunction
  • No single pain centre
  • Somatotopic maps S1,S2, beyond
  • Many brain areas can be activated
    (fMRIconsistently spinal cord, thalamus, S1, S2,
    insula, anterior cingulate and prefrontal cortex
    ALSO hippocampus, posterior parietal lobe, basal
    ganglia and brainstem)

48
Referred sensations
49
FACE BESIDE HANDS
50
CRPS
  • Expansion of receptive fields in somatosensory
    cortex.Cortical reorganization

51
Visual Pathways
52
Dorsal / ventral pathways
Old / unconscious / where
New / conscious / what
53
Conflicting visual information
54
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55
What happens in CRPS ?
  • Disturbed pain matrix
  • Add visual incongruence
  • Result PAIN

56
Duck / rabbit
Conscious object recognition Memory
dependent Top-down bias
Ventral pathway
57
Necker cube
Perspective, depth, scaling rules Object
recognition Bottom up bias
Dorsal pathway
58
CRPS visual disturbances
  • Movement of stable objects
  • Dorsal pathway network dysfunction ( parietal
    lobe)
  • Asymmetric autonomic sympathetic responses to
    AVS independent of baseline function

59
Parietal lobe function
  • Left sensory integrative processing important
    for normal language and maths
  • Right sensory integrative processing related
    to the use of spatial information in
    perceptual, cognitive motor behaviours

60
Parietal Lobe
  • Left sided lesions
  • Conduction aphasia
  • Tactile agnosia
  • Dysphasia
  • R-L disorientation
  • Finger agnosia
  • Agraphia
  • Body image disorders
  • Sensory extinction
  • Astereognosis
  • Alexia
  • Dysgraphaesthesia

61
Right sided lesions
  • Anosognosia (lack of awareness of disease)
  • Neglect
  • Tactile agnosia
  • Asomatognosia
  • Constructional dyspraxia

62
Parietal Dysfunction?
  • In CRPS patients there may be
  • Neglect like phenomena
  • Body dysmophia
  • Motor dyspraxias
  • Unusual sensory patterns extinction, allochiria
  • Parietal abnormalities on formal detailed bed
    side testing

63
CRPS
  • Distorted body image
  • Expanded peripersonal space
  • Feel touch above body surface

64
Phantom Limb
65
Organic basis for the Bizarre
  • Severe allodynia breeze is painful
  • Cortical reorganisation referred sensations,
    phantom limb-like sensations
  • Sensory conflict as basis for pain
  • Chronic pain sensitised system (peripheral
    central) lowered thresholds
  • Brain network dysfunction eg. Parietal
    dysfunction
  • Role of psychological distress in chronic severe
    pain

66
Translation of research into clinical practice
  • Understanding of chronic pain mechanisms
  • Which ones are more dominant in this patient?
  • Individualise treatment
  • Allodynia in chronic pain conditions
    (eg.fibromyalgia) translation of understanding
    treatment techniques

67
The pain personality
  • Brain network dysfunction
  • What if there were similar dysfunctional cortical
    networks in chronic pain.
  • A common personality might emerge

68
Acknowledgements
  • Funding Bodies Other Partners
  • Arthritis Research Campaign
  • Gwen Bush Foundation
  • RSD-UK
  • Royal National Hospital for Rheumatic Diseases
    Donated Funds
  • CRPS Clinical Research Team
  • Professor David Blake
  • Dr. Helen Cohen
  • Mrs Carole Dyer
  • Dr. Jane Hall
  • Dr. Nigel Harris
  • Ms Keri Johnson
  • Ms. Jenny Lewis
  • Dr. Karen Rodham
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