ISMST - 2014 Presentation Final Presentation

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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

Transcript of ISMST - 2014 Presentation Final Presentation

Page 1: ISMST - 2014 Presentation Final Presentation

Kenneth Craig, Bradley Takai, Daniel Poratt

Presenter: Kenneth CraigMedical 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

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Conflict of Interest Declaration

Royalties & stock options – NONE

Consulting Income – NONE

Research & Education Support – NONE

Other support - NONE

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AIM

To discuss and invite more research in this area

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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 impactPeripheral hyperalgesia,

allondynia

2ndary

hyperalgesia &

allondynia

Peripheral /

Central

Ectopic

activity

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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

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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)

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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

questionnaireDN4

Clinical tests DermaTemp; NeuroTip; Monofilament; Cotton-brush

Physical assessment Passive / Active ranges & movement observation

EducationPain education

Technology education

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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

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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

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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

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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)

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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

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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

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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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THANK YOU

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