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Kenneth Craig, Bradley Takai, Daniel Poratt
Presenter: Kenneth Craig
Medical Director Kompass Health Associates
Kompass OrthoShock Centre of Extracorporeal Shockwave Therapy & Research
Auckland, New Zealand
Medical shockwaves a treatment option for complex / neuropathic pain
syndromes?
A compilation of case reports 2012 – 2014
Conflict of Interest Declaration
Royalties & stock options – NONE
Consulting Income – NONE
Research & Education Support – NONE
Other support - NONE
AIM
To discuss and invite more research in this area
Complex / Neuropathic Pain
-
(Dorkin et.al., 2003 & 2007; Ducreux et.al., 2006; Costigan et al., 2009; Nielson et.. al, 2008; Staud et.al., 2008; Tracey & Mantyh, 2007; Treede et. al., 2008).
Introduction
 Poorly understood
 Maladaptive
 Abnormal sensory perception
 Multifactorial propagation
 Indocile to most interventions
(Mainly symptomatic control)
 Severe impact
Peripheral hyperalgesia,
allondynia
2ndary
hyperalgesia &
allondynia
Peripheral /
Central
Ectopic
activity
To find an effective homeostatic disease modifying treatment modality that is:
 Non-invasive
 Systemically neutral
 Economically viable
The Need
ESWT?
The Answer
Our Case Series
Brief Case Description
Gender Male (n=5); Female (n=7)
Age (Mean) 44 yrs; Y(14yrs) / E (70yrs)
Inciting Event Trauma (n=10) – CRPS1; Infection (n=2) - Neuropathic
Region of Interest Foot & Ankle (n=10); Knee (n=2)
Mean Disease Duration 16 months
P & S Hyperalgesia n=12
P & S Allondynia n=12
Emotional Distress n=12
Management
Primary analgesia & NSAID’s
Secondary analgesics (TCA’s / Anticonvulsants)
Opioid analgesia (Tramadol / oxycodone)
Physical therapy
Counselling + alternative therapies (ie hypnotherapy)
Baseline Investigations
General history taking
Psychometric
POP 3 (20 pt questionnaire)
 Subjective Pain (0 – 10)
 Physical Index (% of Mobility; ADL; Vitality)
 Affective Index (% of Emotional status & Fear)
Neuropathic
questionnaire
DN4
Clinical tests DermaTemp; NeuroTip; Monofilament; Cotton-brush
Physical assessment Passive / Active ranges & movement observation
Education
Pain education
Technology education
Material s & Methods
Phamacogenic
s
All discontinued prior to Tx and remained throughout
Device Electrohydraulic (MediSpec)
Treatment # 4 at 1 week intervals
Impulse # 1500 / Tx (500 impulses over each region)
EFDL 0.08mj/mm² (initial 2); 0.10 – 0.14mj/mm² (3rd- 4th)
Tx regions Primary & secondary regions, and along neural course
0
1
2
3
4
5
6
7
8
9
10
Baseline Week 6 Week 12 Week 24
Pain (VAS)
DN4
Results
Positive response: n=10 (trauma induced)
VAS Pain score: (8.87) to 2 at w24
DN4 Score: (6.7) to 0 at w24
Results
0
10
20
30
40
50
60
70
80
90
Pre Tx Week 6 Week 12 Week 24
Physical Index
Affective Index
Physical Index: (53.47) to 2.77 at w24
Affective Index: (85.49) to10.22 at w24
Discussion
 n=2 non-respondents – infection incited (unchanged from onset)
 n=10 CRPS - Abnormal pain symptoms & sensitivity settled
 No adverse complaint to-date (n=12)
Discussion: Rational for Application
(Bee & Dickenson, 2008; Costigan et al., 2009; Keller et.al., 2007; Koban et. al., 2003; Kohno et.al., 2005; Matsuzawa-Yanagida et.al., 2008; Miraucourt et.al., 2007; Pearl, 2007; Schattschneider
et.al., 2006; Schloz et.al., 2007; Vera-Portocarrerro et.al, 2006; ).
Peripheral abnormaly (Increased
nociceptive barrage, aberrant
inflammatory, immunological interactions
etc.)
Central abnormaly (sensitisation &
aberrant inflammatory, immunological
interactions etc.)
Reduced descending inhibition
Reduced inhibitory polarisation modulators
Neuro-transcription (pain memory)
Nutritive vessel hypoxia =
small fiber damage
ESWT proposed mechanics of action:
 Modulates inflammatory substances
 Modulates immune response
 Improves perfusion – hypoxic correction
 Regenerative and restorative capacity
 Unique stimulus – cognitive capturing / arousing
 Certainly more research is warranted
Future Direction & Conclusion
Continue to monitor these cases
Research collaboration with pain
centres (ie TREND / TARPS)
More measurable Tx. outcomes
(dorsaVi) to help expand recognition
and use of ESWT
Certainly worthwhile investigating
THANK YOU
1. Angehrn, F., Kuhn, C., Sonnabend, O. & Voss, A. (2008). Impact of extracorporeal shock waves on the human skin with cellulite: A case study of an unique instance.
Clinical Interventions in Ageing, 3(1) 175 – 182
2. Bee LA, Dickenson AH. 2008. Descending facilitation from the brainstem determines behavioural and neuronal hypersensitivity following nerve injury and efficacy of
pregabalin. Pain 140(1):209–23
3. Costigan, M., Scholz, J. & Woolf, C. J. (2009). Neuropathic Pain: A Maladaptive Response of the Nervous System to Damage. Annual Review of Neuroscience, 32, 1
– 32.
4. Ducreux, D., Attal, N., Parker, F. & Bouhassira, D. (2006). Mechanisms of central neuropathic pain: a combined psychophysical and fMRI study in syringomyelia.
Brain 129(part4), 963 – 976.
5. Dworkin RH, Backonja M, Rowbotham MC, Allen RR, Argoff CR, et al. 2003. Advances in neuropathic pain: diagnosis, mechanisms, and treatment recommendations.
Arch. Neurol. 60:1524–34
6. Dworkin, R. H., O‘Connor, A. B., Backonja, M., Farrar, J. T., Finnerup, N. B., Jensen, T. S., Wallece, M. S. (2007). Pharmacologic management of neuropathic pain:
evidence-based recommendations. Pain, 132(3), 237 – 251.
7. Finnerup, N. B., Sindrup, S. H. & Jensen, T. S. (2010). The evidence of pharmacological treatment of neuropathic pain. Pain, 150(3), 573 – 581.
8. Kembler M. A., De Vet H. C.W., Barendse G.A., Van Den Wildenberg F. A. J . M, Van Kleef M. (2008). Effect of Spinal Cord Stimulation for Complex Regional Pain
Syndrome Type -1: a five year final follow-up of patients in a randomised controlled trial. Journal of Neurosurgery, 108(2), 292 – 298.
9. Koban M, Leis S, Schultze-Mosgau S, Birklein F. Tissue hypoxia in complex regional pain syndrome. Pain 2003;104:149–57.
10. Kohno T, Ji RR, Ito N, Allchorne AJ, Befort K, et al. 2005. Peripheral axonal injury results in reduced mu opioid receptor pre- and post-synaptic action in the spinal
cord. Pain 117:77–87
11. Kroenke, K., Krebs, E. E. & Blair, M. J. (2009). Pharmacotherapy of chronic pain: a synthesis of recommendatins from systemic reviews. General Hospital Psychiatry,
31(3), 206 – 219.
12. Kumar K., Rizvi S. & Bnurs S. B. (2011). Spinal Cord Stimulation Is Effective in Management of Complex Regional Pain Syndrome 1: Fact or Fiction. Neurosurgery,
69(3), 566 – 580.
Reference
14 Matsuzawa-Yanagida K, Narita M, Nakajima M, Kuzumaki N, Niikura K, et al. 2008. Usefulness of antidepressants for improving the neuropathic pain-like state and
pain-induced anxiety through actions at different brain sites. Neuropsychopharmacology 33:1952–65
15 McGeeney, B. E. (2009). Pharmacological Management of Neuropathic Pain in Older Adults: An Update on Peripherally and Centrally Acting Agents. Journal of Pain
and Symptom Management. 38(2S), S15 – S27.
16 Miraucourt LS, Dallel R, Voisin DL. 2007. Glycine inhibitory dysfunction turns touch into pain through PKCgamma interneurons. PLoS ONE 2:e1116
17 Nielsen CS, Stubhaug A, Price DD, Vassend O, Czajkowski N, Harris JR. 2008. Individual differences in pain sensitivity: genetic and environmental contributions.
Pain 136:21–29
18 Notarnicola, A., Moretti, L., Tafuri, S., Panella, A., Filipponi, M., Casalino, A., Panella, M. & Moretti, B. (2010). Shockwave therapy in the management of complex
regional
19 Perl ER. 2007. Ideas about pain, a historical view. Nat. Rev. Neurosci. 8:71–80
20 Saginni, R., Figus, A., Troccola, A., Cocco, V., Saggini, A. & Scuderi, N. (2008). EXTRACORPOREAL SHOCK WAVE THERAPY FOR MANAGEMENT OF CHRONIC
ULCERS IN THE LOWER EXTREMITIES. Ultrasound in Medicine & Biology, 34(8),1261–1271.
21 Sandkuhler J. Models and Mechanisms of Hyperalgesia and Allondynia. Physiological Reviews. 2009; 89(2):707–758.
22 Sansone, R. A. & Sansone, L. A. (2008). Pain, Pain, Go Away: Antidepressants and Pain Management. Psychiatry, 5(12), 16 – 19.
23 Staud R, Craggs JG, Perlstein WM, Robinson ME, Price DD. 2008. Brain activity associated with slow temporal summation of C-fiber evoked pain in fibromyalgia
patients and healthy controls. Eur. J. Pain 12(8):1078–89
24 Schaden, W., Thiele, R., Kölpl, C., Pusch, M., Nissan, A., Attinger, C. E., Maniscalo-The berge, M. E., Peoples, G. E., Elster, E. A. & Stojadinovic , A. (2007). Shock
Wave Therapy for Acute and Chronic Soft Tissue Wounds: A Feasibility Study, 143 (1) 1 – 12.
25 Tracey, I & Mantyh, P. W. (2007). The Cerebral Signature for Pain Perception and Its Modulation. Neuron, 55(2), 377 – 391.
26 Treede RD, Jensen TS, Campbell JN, Cruccu G, Dostrovsky JO, et al. 2008. Neuropathic pain: redefinition and a grading system for clinical and research purposes.
Neurology 70:1630–35
27 Vera-Portocarrero LP, Zhang ET, Ossipov MH, Xie JY, King T, et al. 2006. Descending facilitation from the rostral ventromedial medulla maintains nerve injury-induced
central sensitization. Neuroscience 140:1311– 20
28 Woolfe, C. J. & Ma, Q. (2007). Nociceptors – Noxious Stimulus Detectors. Neuron, 55(2), 353 – 364.
Reference

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ISMST - 2014 Presentation Final Presentation

  • 1. Kenneth Craig, Bradley Takai, Daniel Poratt Presenter: Kenneth Craig Medical Director Kompass Health Associates Kompass OrthoShock Centre of Extracorporeal Shockwave Therapy & Research Auckland, New Zealand Medical shockwaves a treatment option for complex / neuropathic pain syndromes? A compilation of case reports 2012 – 2014
  • 2. Conflict of Interest Declaration Royalties & stock options – NONE Consulting Income – NONE Research & Education Support – NONE Other support - NONE
  • 3. AIM To discuss and invite more research in this area
  • 4. Complex / Neuropathic Pain - (Dorkin et.al., 2003 & 2007; Ducreux et.al., 2006; Costigan et al., 2009; Nielson et.. al, 2008; Staud et.al., 2008; Tracey & Mantyh, 2007; Treede et. al., 2008). Introduction  Poorly understood  Maladaptive  Abnormal sensory perception  Multifactorial propagation  Indocile to most interventions (Mainly symptomatic control)  Severe impact Peripheral hyperalgesia, allondynia 2ndary hyperalgesia & allondynia Peripheral / Central Ectopic activity
  • 5. To find an effective homeostatic disease modifying treatment modality that is:  Non-invasive  Systemically neutral  Economically viable The Need ESWT? The Answer Our Case Series
  • 6. Brief Case Description Gender Male (n=5); Female (n=7) Age (Mean) 44 yrs; Y(14yrs) / E (70yrs) Inciting Event Trauma (n=10) – CRPS1; Infection (n=2) - Neuropathic Region of Interest Foot & Ankle (n=10); Knee (n=2) Mean Disease Duration 16 months P & S Hyperalgesia n=12 P & S Allondynia n=12 Emotional Distress n=12 Management Primary analgesia & NSAID’s Secondary analgesics (TCA’s / Anticonvulsants) Opioid analgesia (Tramadol / oxycodone) Physical therapy Counselling + alternative therapies (ie hypnotherapy)
  • 7. Baseline Investigations General history taking Psychometric POP 3 (20 pt questionnaire)  Subjective Pain (0 – 10)  Physical Index (% of Mobility; ADL; Vitality)  Affective Index (% of Emotional status & Fear) Neuropathic questionnaire DN4 Clinical tests DermaTemp; NeuroTip; Monofilament; Cotton-brush Physical assessment Passive / Active ranges & movement observation Education Pain education Technology education
  • 8. Material s & Methods Phamacogenic s All discontinued prior to Tx and remained throughout Device Electrohydraulic (MediSpec) Treatment # 4 at 1 week intervals Impulse # 1500 / Tx (500 impulses over each region) EFDL 0.08mj/mm² (initial 2); 0.10 – 0.14mj/mm² (3rd- 4th) Tx regions Primary & secondary regions, and along neural course
  • 9. 0 1 2 3 4 5 6 7 8 9 10 Baseline Week 6 Week 12 Week 24 Pain (VAS) DN4 Results Positive response: n=10 (trauma induced) VAS Pain score: (8.87) to 2 at w24 DN4 Score: (6.7) to 0 at w24
  • 10. Results 0 10 20 30 40 50 60 70 80 90 Pre Tx Week 6 Week 12 Week 24 Physical Index Affective Index Physical Index: (53.47) to 2.77 at w24 Affective Index: (85.49) to10.22 at w24
  • 11.
  • 12. Discussion  n=2 non-respondents – infection incited (unchanged from onset)  n=10 CRPS - Abnormal pain symptoms & sensitivity settled  No adverse complaint to-date (n=12)
  • 13. Discussion: Rational for Application (Bee & Dickenson, 2008; Costigan et al., 2009; Keller et.al., 2007; Koban et. al., 2003; Kohno et.al., 2005; Matsuzawa-Yanagida et.al., 2008; Miraucourt et.al., 2007; Pearl, 2007; Schattschneider et.al., 2006; Schloz et.al., 2007; Vera-Portocarrerro et.al, 2006; ). Peripheral abnormaly (Increased nociceptive barrage, aberrant inflammatory, immunological interactions etc.) Central abnormaly (sensitisation & aberrant inflammatory, immunological interactions etc.) Reduced descending inhibition Reduced inhibitory polarisation modulators Neuro-transcription (pain memory) Nutritive vessel hypoxia = small fiber damage
  • 14. ESWT proposed mechanics of action:  Modulates inflammatory substances  Modulates immune response  Improves perfusion – hypoxic correction  Regenerative and restorative capacity  Unique stimulus – cognitive capturing / arousing  Certainly more research is warranted
  • 15. Future Direction & Conclusion Continue to monitor these cases Research collaboration with pain centres (ie TREND / TARPS) More measurable Tx. outcomes (dorsaVi) to help expand recognition and use of ESWT Certainly worthwhile investigating
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