1. Medical shockwaves a treatment option for complex and neuropathic pain syndromes?
A compilation of case reports.
Kenneth Craig
Medical Director, KompassOrthoShockCentre for Medical Shockwave Therapy & Research, Auckland.
Introduction
The impervious nature of complex and neuropathic pain syndromes that are often indocile to conventional treatments2,4,5,6warrants the exploration of treatment methods that limit intrinsic risk while modifying disease patterns.2This compilation of four case-reports discusses the use of medical shock waves for the treatment of complex and neuropathic painsyndromes of the lower extremity.
Aim
To determine if further investigation is warranted to explore the use of medical shockwaves for the treatment of certain types of neuropathic and complex pain conditions.
Method
Three treatments of medium-low intensity extracorporeal-shockwaves (ESW) propagated by an electro –
hydraulic generator (MediSpec, Germantown) were administered at one week intervals. Energy density
flux levels ranged from 0.08mj/mm² -0.20mj/mm². Pain, function and emotional measures were
performed utilizing visual analogue scale (VAS), Neuropathic Pain Diagnostic Questionnaire (DN4),
and Pain Outcomes Profile (POP) questionnaire at baseline and post-treatment.
Use of anti-inflammatory and pain medications were ceased prior to treatment and remained discontinued
throughout the 24 week follow-up period.
Result
Improvements in function and stress levels along with reduction of the pain experience was observed post-treatment. Mean average subjective pain scores (VAS) reduced from (baseline 8.87/10 to post-treatment 2/10). Average DN4 (baseline 5.6/10) scored (0/10 post-treatment). POP questionnaire recorded improvements in both the Physical Index (baseline 53.47; post- treatment 2.77), and the Affective Index (baseline 85.49; post-treatment 10.22) respectively.
Discussion
The exact mechanism of ESWT is yet to be fully elucidated, however a dose and stimulus dependant shockwave triggers a neuro-bio-chemical regulatory cascade resulting in the resolution of the associated neuro-physical pathology and cognitive response in the subjects of this case series (Figure 2).
Conclusion
The findings of these case-reports corroborates with the findings of earlier investigations utilizing shockwaves for complex regional pain syndrome of the knee conducted by Nortarnicolaand colleagues (2010). ESW may provide a non-invasive, non-pharmacogenicdisease modifying treatment option for periheralneuropathic and complex pain conditions. This encourages further investigations of ESW to be conducted on neuropathic and complex pain syndromes of the upper and lower extremity.
Reference
1.CarmelietP & Tessier-LavigneM. Common mechanisms of nerve and blood vessel wiring. Nature. 2005; 436(7048): 193 –200.
2.CostigaM, ScholzJ, Woolf CJ. Neuropathic Pain: A Maladaptive Response of the Nervous System to Damage. AnnuRev Neurosci. 2009; 32;1-32.
3.Craig K & Miller A. Extracorporeal Shockwave Therapy (ESWT), an option for chronic tendinopathymanagement: a clinical perspective. New Zealand Pain Society Publication. 2011; 8 –16.
4.Harden R N, BruelS & Stanton-Hicks M. Proposed New Diagnostic Criteria for Complex Regional Pain Syndrome. Pain Medicine. 2007; 8(4): 326 –331.
5.Lopes P, LisboaB, FrattiniF, et al. Enhancement of sciatic nerve regeneration after vascular endothelial growth factor (VEGF) gene therapy. Neuropathology and Applied Neurobiology. 2011, 37: 600 –612.
6.NortanicolaA, MorretiL, TafuriS et al. Shockwave therapy in the management of CRPS of the femoral condyleof the knee. Ultrasound Med Biol. 2010; 36(6):874-9.
7.OmoiguiS. The Biochemical Origin of Pain –Proposing a new law of Pain: The origin of all Pain is Inflammation and the Inflammatory Response. Part 1 of 3 –A unifying law of pain. Med Hyptheses. 2007; 69(1): 70 –82.
8.SandkuhlerJ. Learning and memory in pain pathways. Pain 2000;88: 113 –118.
9.SandkuhlerJ. Models and Mechanisms of Hyperalgesiaand Allondynia. Physiological Reviews. 2009; 89(2):707 –758.
10.Stanton-Hicks M. Complex Regional Pain Syndrome: Manifestations and the Role of Neurostimulationin Its Management. Journal of Pain and Symptom Management. 2006; 31(45): S20 –S24.
Figure 1.
Illustrates a sound wave propagated electrohydraulicallyby a controlled underwater explosion, which is then targeted onto the region of interest. Ultrasound coupling gel is used to assist with transmission of the shockwaves into tissue.
Case
Inciting
Event
Disease
Duration
Signs,Symptoms & Complaint
PreTx
VAS
Hyperalgesia
Allondynia
Ectopic
activity
Previous Tx. & Working Diagnosis (WDX)
Female
32yrs
Trauma
18mths
•Severe Pain
•Mild Inflammation
8.5
Present
Absent
Present
•Physical therapy
•NSAID’s (WDX: Neuropathic pain)
•Cortisone
Male
56yrs
Trauma
48mths.
•SeverePain
•Feels like standing on
broken glass.
•Inflammation
•Discoloration
•Tropic change (nails)
•>Temperature
•< ROM
•Involvement of
contralaterallimb
9.0
Present
Present
Present
•Physical therapy
•NSAID’s
•Foot orthotics
•Cortisone (1)
•Local block (WDX: CRPS1)4,10
•TENS
•Amitriptylin*
Female
42yrs
Trauma
24mths.
•Severe Pain
•Inflammation
•>Temperature
•Unable to weight bear
•Dystonia& weakness
•< ROM
9.0
Present
Absent
Present
•Physical therapy
•NSAID’s
•Foot orthotics (WDX: CRPS1)4,10
•Cortisone (5)
•GABA**
Female
44yrs
Trauma
24mths.
•Severe Pain
•Inflammation
•Discoloration
•Tropic change (nails)
•>Temperature
•Dystonia& weakness
•Required walking aid
•< ROM
9.0
Present
Present
Present
•Physical therapy
•NSAID’s
•Foot orthotics (WDX: CRPS1)4,10
•Amitriptylin*
Table 1.
Presenting signs & symptoms and treatments prior to ESWT.
Cortisone (1) –single course.
Cortisone (5) –five courses.
* Treatment discontinued upon patients
request.
** Treatment discontinued due to adverse
reaction.
0
10
20
30
40
50
60
70
80
90
Pre Tx
Week 6
Week 12
Week 24
Physical Index
Affective Index
Table 2. Averagesubjective pain score using VAS demonstrates improvement in pain levels at 24 weeks
from baseline. DN4 scores demonstrates absence of abnormal sensory activity / perception
as of week 12.
Table 3. Average Physical and Affective index scores using POP demonstrates improvements
in each domain respectively at 24 weeks from baseline.
Figure 2. Illustrates the proposed mechanism of ESW discussed above.
Increases cellular permeability & neuronal signaling.3,6
Stimulates angiogenesis = improved microcirculation. Regulates chemical & immuno- mediators of the inflammatory response (ienNOS, eNOS, SP, CGRP, TNFα, IL1B, IL6 etc).3,6
Cellular expression of growth proliferators enhancing neurotrophicand neuroprotectiveeffects.1,3,6,7
= neural desensitization
& physiological resolution.
Selective erasure of the pathological memory / response reflex6,8
& resolution of aberrant pain perception.
0
1
2
3
4
5
6
7
8
9
10
Pre-Tx
Week 6
Week 12
Week 24
VAS
DN4