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Complex Regional Pain Syndrome - Dr Venugopal Kochiyil

Complex Regional Pain Syndrome
PMR Refresher Course

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Complex Regional Pain Syndrome - Dr Venugopal Kochiyil

  1. 1. Complex Regional Pain Syndrome Dr Venugopal Kochiyil FAFRM(RACP), FFPMANZCA Medical Head – Northern Adelaide Rehabilitation Service Modbury Hospital Pain Physician – Flinders Medical Centre, Adelaide,South Australia
  2. 2. CRPS • Complex chronic pain, severe disability and reduced QoL • Perplexed and fascinated clinicians • Symptom complex include pain, sensory, autonomic, trophic and motor abnormalities • Can occur following minor trauma (fractures, sprain etc), elective surgeries, stroke etc • Spontaneous 10%
  3. 3. CRPS • CRPS Type 1 -Formerly known as RSD (1946), Sudeck dystrophy (1900) • CRPS Type 2 – Formerly known as causalgia IASP 1994 Silas Weir Mitchell
  4. 4. CRPS Type 1- IASP criteria • The presence of an initiating noxious event or a cause of immobilization • Continuing pain, allodynia or hyperalgesia disproportionate to the inciting event • Evidence at some time of edema, changes in skin blood flow or abnormal sudomotor activity in the area of pain • The diagnosis is excluded by the existence of any condition that would otherwise account for the degree of pain and dysfunction Sensitivity 1, Specificity 0.41
  5. 5. Budapest criteria 2003 • Continuing pain, which is disproportionate to any inciting event • Must report at least one symptom in three of the four following categories: Sensory: hyperesthesia and/or allodynia Vasomotor: temperature asymmetry and/or skin color changes and/or skin color asymmetry Sudomotor/ Edema: edema and/or sweating changes and/or sweating asymmetry Motor/Trophic: decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin) • Must display at least one sign at time of evaluation in two or more of the following categories: Sensory: hyperalgesia (to pinprick) and/or allodynia Vasomotor:temperature asymmetry (>1°C) and/or skin color changes and/or asymmetry Sudomotor/Edema: edema and/or sweating changes and/or sweating asymmetry Motor/Trophic: decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin) • There is no other diagnosis that better explains the signs and symptoms
  6. 6. Budapest criteria 2003 • For research purposes - atleast a symptom in each of the four symptom categories and atleast one observed sign in two or more sign categories
  7. 7. Sensitivity and specificity Decision rules Sensitivity Specificity 2+ symptoms and 2+ signs 0.94 0.36 3+ symptoms and 2+ signs 0.85 0.69 4+ symptoms and 2+ signs 0.70 0.94 2+ symptoms and 3+ signs 0.76 0.81 3+ symptoms and 3+ signs 0.70 0.83 4+ symptoms and 3+ signs 0.86 0.75 Bruehl S, Harden RN et al. Pain 1999;81:147–54.
  8. 8. Phases of CRPS • Acute phase – painful, red, warm, swelling, allodynia, hyperalgesia (mechanical, thermal), nail and hair changes, muscle weakness, negative sensory signs Marinus J, Moseley GL et al. Lancet Neurol 2011; 10: 637–48
  9. 9. Cold phase Marinus J, Moseley GL et al. Lancet Neurol 2011; 10: 637–48
  10. 10. Dystonic phase Marinus J, Moseley GL et al. Lancet Neurol 2011; 10: 637–48
  11. 11. Motor symptoms and signs • Weakness, Tremor, Decreased ROM, Difficulty in performing complex movement patterns, focal dystonia and myoclonus • Motor symptoms increase with duration of CRPS • Contractures and fibrosis • Probably associated with plastic changes in sensory and motor cortex
  12. 12. Dystonic postures in CRPS Munts et al. BMC Neurology2011,11:53
  13. 13. Spread of CRPS 1 • Contiguous spread: A gradual enlargement in the area affected over time • Independent spread (ipsilateral (32%)and diagonal (15%)): Spread of the disease from upper to lower limb, or vice versa • Mirror Spread (contralateral – 53%): Spread of pathology to the contra lateral lower limb van Rijn MA, Marinus J et al. J Neural Transm 2011; 118:1301–1309
  14. 14. Epidemiology • 5.5- 26.2 cases per 100 000 person-years • Incidence increases with age (till 70 years) • More common in women ( approx 3 times) • Arm more than legs (in adults)
  15. 15. Pathophysiology • Aberrant inflammatory mechanisms • Nociceptive sensitization • Vasomotor dysfunction • Maladaptive neuroplasticity Marinus J, Moseley GL et al. Lancet Neurol 2011; 10: 637–48
  16. 16. Inflammatory mechanisms • Activation of cutaneous nociceptors Retrograde depolarisation of primary afferents Release of neuropeptides (substance P, CGRP) • Increased Interleukins and TNFα • ? Autoimmune mechanisms
  17. 17. Vasomotor dysfunction • A common problem in CRPS • Warm (4 months), intermediate (4-15 months) and cold type • Inhibition of cutaneous sympathetic vasoconstrictor activity • Increased sensitivity to circulating catecholamines (SMP) • Endothelial dysfunction
  18. 18. Central nervous system • Central sensitization • Structural changes to emotional centres • Impaired motor control – dystonia (GABAergic mechanisms) • Descending facilitation > descending inhibition • Distortion of mental image of affected area • Cortical reorganisation (S1 and M1)
  19. 19. Risk factors in CRPS • No definite evidence of psychological risk factors • Immobilisation of injured limb • Use of ACE inhibitors • Asthma and migraine
  20. 20. Genetic factors in CRPS • Familial form of CRPS • Patients younger than 50 years has increased risk of sibling with CRPS (de Rooij et al. J Pain 2009;10:1250–1255) • Association with different HLA factors
  21. 21. Bruehl S. Anesthesiology 2010; 113:713–25
  22. 22. Models of CRPS • Animal chronic post-ischemia pain (CPIP) model - produced by prolonged hindpaw ischemia and reperfusion in the rat • Human forearm immobilisation model
  23. 23. Outcome of CRPS • Issues with what is the definition of recovery in CRPS • Usually monophasic but 2% relapsing remitting • 30% completely recovered, 53% stable • 15% no improvement, 30% not gone back to work de Mos M, Huygen FJ et al. Clin J Pain 2009;25: 590-7
  24. 24. Management • Patient information and education • Pain relief • Physical Rehabilitation • Psychological and Vocational rehabilitation
  25. 25. Medications • Nifedipine in acute phase – Level 4 • Short course of steroids in acute phase – Level 1 • Intravenous bisphosphonates in acute phase – Level 1 • IVIg – no evidence • Opioids • Neuropathic pain medications • Baclofen or clonazepam for dystonia • Intravenous ketamine infusion (continuous/intermittent – inpatient/outpatient)
  26. 26. Biologicals • Infliximab study was withdrawn
  27. 27. Rehabilitation • Aim at activating premotor and primary motor cortices • Functional restoration • Desensitization • Gradual weight bearing
  28. 28. Graded motor imagery • Three stages Left/Right discrimination Explicit motor imagery Mirror therapy • Activate cortical networks involved in sensory motor processing
  29. 29. Recognise online www.gradedmotorimagery.com
  30. 30. Evidence in CRPS • Limited data (all available data for upper limb) • Decreased pain experience, improved grip force, improved global impression of change but no change in perception of upper extremity function (Laqueux E, Charest J et al. Int J Rehabil Res. 2012 Jun;35(2):138-45) • No improvement in pain scores but some partial functional improvement. Real world response is variable (Johnson S, Hall J et al. Eur J Pain. 2012;16(4):550-61)
  31. 31. In CRPS • Three RCTs by Moseley – NNT for 50% reduction in pain was 2, NNT for 4/10 improvement in function was 3 (Pain 2004a;108:192–8, Pain 2005;114:54–61, Neurology 2006b;67:2129–34)
  32. 32. Invasive interventions • Appropriately timed and selected interventional therapy has an adjunctive role • Measured steps
  33. 33. Nerve blocks/sympathetic block • Patients with mechanical allodynia, burning pain, temperature and colour changes might benefit • Repeat block if there is benefit • Stellate ganglion block and lumbar sympathetic block • ? Benefit in differentiating SMP from SIP • Limited evidence • Continuous/intermittent spinal infusions (epidural/intrathecal)
  34. 34. Sympathectomy • Chemical and surgical • Regeneration of sympathetic chain • Post sympathectomy neuralgia (44%) • Compensatory hyperhidrosis, phantom sweating and pathologic gustatory sweating
  35. 35. Implantable pumps (IT) • Case reports • If no response to SCS • Patient selection • Trial • Medications (opioids, clonidine, local anaesthetic, baclofen)
  36. 36. Spinal cord stimulation • SCS + Physio was better than PT alone (Kemler et al NEJM 2000, J Neurosurg 2008) but no difference in functional outcome • ? Long term benefit • ? Benefit in allodynia and hyperalgesia • Benefit with sympathetic block may indicate better results • Patient selection and trial • Ideally within 12 to 16 weeks
  37. 37. Stanton-Hicks M et al. Cli J Pain 1998;14:155-66
  38. 38. Prevention
  39. 39. Vitamin C and CRPS • 4 Studies – 3 after upper limb surgery and one after foot and ankle surgery • Atleast 500mg started immediately after surgery and continued for 45 to 50 days Shibuya N, Humpers JM. J Foot Ankle Surg. 2013;52(1):62-6
  40. 40. Other options • Multimodal analgesia • Nerve blocks • Calcitonin 100 units a day for four weeks
  41. 41. Surgery in a patient with CRPS • What is the risk? • Avoid surgery till acute symptoms have subsided • No evidence that any preventive methods actually prevent re-initiation or aggravation of CRPS

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