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• High-energy versus low-energy protocols of shock wave application
  Jan D. Rompe
  Published on: 4 October 2004

• Published on: 4 October 2004

  High-energy versus low-energy protocols of shock wave application

  • Jan D. Rompe, Orthopaedic Surgeon

  Dear Editor,

  I read with interest the article “Extracorporeal shock wave therapy for plantar fasciitis: randomised controlled multicentre trial” by John Ogden (Br J Sports Med 38: 382, 2004).

  I strongly contradict his suggestion that multiple dosed, low-energy, non-anaesthetically based treatments [9] cannot accomplish the same clinical outcome and patient satisfaction as single dosed, high-energy, ana...

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  Dear Editor,

  I read with interest the article “Extracorporeal shock wave therapy for plantar fasciitis: randomised controlled multicentre trial” by John Ogden (Br J Sports Med 38: 382, 2004).

  I strongly contradict his suggestion that multiple dosed, low-energy, non-anaesthetically based treatments [9] cannot accomplish the same clinical outcome and patient satisfaction as single dosed, high-energy, anaesthetically based treatments [1,7,14].

  Not a single study has been published directly comparing high-energy with low-energy treatment protocols for chronic plantar fasciitis!

  What is more the alleged efficacy of these single dosed, high-energy, anaesthetically based treatments have already been discussed in an exhaustive way by Buchbinder [2]: Regarding the HealthTronics sponsored FDA trial [7] Buchbinder critizised that the presence of plantar fasciitis was determined solely on clinical grounds. It was uncertain whether the 2 groups in the trial were comparable at baseline. In the “results” section none of 4 success criteria was statistically significant in favor of the active treatment. Regarding the Dornier sponsored FDA trial [1,14] Buchbinder wrote while a statistical significant difference favoring the active group in improvement of morning pain was reported to be evidence of efficacy of ESWT, it could be argued that a difference of 0.7 on a 10-cm VAS pain scale may not be clinically significant. And, there was no statistically significant difference between groups in the proportion of participants with at least 60% improvement in morning pain, AOFAS Ankle-Hindfoot-Scale, and SF12 Health Status Questionnaire.

  When discussing a possible working mechanism of shock wave application it is important to focus not only on differences of shock wave devices in clinical use. There are also different pathways for the effects of high- versus low-energy shock waves.

  It is important to know that the current literature [5,6,12,13] indicates that shock waves may selectively lead to dysfunction of peripheral sensory unmyelinated nerve fibers without affecting nerve fibers responsible for motor function (large myelinated fibers).

  For high-energy treatment with 0.9 mJ/mm², this selective destruction of unmyelinated sensory nerve fibers within the focal zone of ESWT may contribute to clinically evident long-term analgesia (5).

  For low-energy application with 0.1 mJ/mm², analgesia may be a result of a shock wave-induced release of neuropeptides, such as CGRP, resulting in a local neurogenic inflammation in the focal area with subsequent prevention of sensory nerve endings from reinnervating this area [6,12]. A second application accentuated these inflammatory changes and therefore prevented reinnervation [13].

  Centrally, the common findings of a reduction in the number of neurons immunoreactive to CGRP and substance P without a reduction of the total number of neurons within the lower lumbar DRG probably are a secondary effect following the (primarily induced) decrease of the number of sensory nerve fibers in the focal zone of shock wave application. So the peripheral and central nervous system may both play a pivotal role in mediating shock wave induced long-term analgesia.

  Recently, Wang [15] showed that low-energy shock wave application resulted in increased neovascularization at the tendon-bone junction in rabbits. Chen [4] treated rats with a collagenease-induced Achilles tendinitis with a single low-energy shock wave treatment with 0, 200, 500 and 1000 impulses. Shock wave application with 200 impulses restored biomechanical and biochemical characteristics of healing tendons 12 weeks after treatment. However, shock wave treatments with 500 and 1000 impulses elicited inhibitory effects on tendinitis repair. Together, low-energy shock wave effectively promoted tendon healing.

  In my view it is clear from these experimental data that with increasing energy applied there is a chance of side effects that my well inhibit healing of an already diseased fascia or tendon.

  It is also clear that even low-energy shock waves may induce a positive local reaction regarding down-regulation of pain transmitters, and up-regulation of cell proliferation factors. I am not aware of any such studies with regard to energy flux densities of about 0.3 mJ/mm² as used by Ogden [7] or Theodore [14].

  Accordingly, I cannot agree with Ogden´s [8] and Theodore´s [14] statement that high energy shock waves initiate a more effective and quicker clinical response than low-energy shock waves. I would like the authors to support this statement with results from experimental studies or from prospective controlled clinical trials.

  I agree with Speed [11] that some regimes of ESWT are a potentially helpful addition to the options for the management of soft-tissue conditions such as chronic plantar fasciitis. Like Ogden [8] and Theodore [14] I am opposed to the opinion of Buchbinder [3]. Contrary to her I strongly recommend that these regimes of ESWT - producing virtually no complications, allowing immediate full weight bearing without splints - should be given priority before surgery [10].

  References

  (1). Buch M et al. Extracorporeal shockwave therapy in symptomatic heel spurs. Orthopade 31:637-644, 2002.

  (2). Buchbinder R et al. Ultrasound-guided extracorporeal shock wave therapy for plantar fasciitis: a randomized controlled trial. JAMA 288:1364-1372, 2002.

  (3). Buchbinder R. Clinical practice. Plantar fasciitis. N Engl J Med 350:2159-2166, 2004.

  (4). Chen YJ et al. Extracorporeal shock waves promote healing of collagenase-induced Achilles tendinitis and increase TGF-beta1 and IGF-I expression.J Orthop Res 22:854-861, 2004.

  (5). Maier M et al. Substance P and prostaglandin E2 release after shock wave application to the rabbit femur. Clin Orthop 406:237-245, 2003.

  (6). Ohtori S et al. Shock wave application to rat skin induces degeneration and reinnervation of sensory nerve fibres. Neurosci Lett 315:57-60, 2001.

  (7). Ogden JA et al. Shock wave therapy for chronic proximal plantar fasciitis. Clin Orthop 387: 47-59, 2001.

  (8). Ogden JA. Extracorporeal shock wave therapy for plantar fasciitis: randomised controlled multicentre trial. Br J sports Med 38: 382, 2004.

  (9). Rompe JD et al. Shock wave application for chronic plantar fasciitis in running athletes – a prospective, randomized, placebo- controlled trial. Am J Sports Med 31:268-275, 2003.

  (10). Rompe JD. Letter to the editor. N Engl J Med 351: 834; 2004.

  (11). Speed CA. Extracorporeal shock-wave therapy in the management of chronic soft-tissue conditions. JBJS 86-B:165-171, 2004.

  (12). Takahashi N et al. Application of shock waves to rat skin decreases calcitonin gene-related peptide immunoreactivity in dorsal root ganglion neurons. Auton Neurosci 107:81-84, 2003.

  (13). Takahashi N et al. The mechanism of pain relief in extracorporeal shock wave therapy. Poster # 448, AAOS Annual Meeting San Francisco, 2004. http://www.aaos.org/wordhtml/anmt2004/poster/p448.htm.

  (14). Theodore GH et al. Extracorporeal shock wave therapy for the treatment of plantar fasciitis. Foot Ankle Int 25:290-297, 2004.

  (15). Wang CJ. Shock wave therapy induces neovascularization at the tendon-bone junction. A study in rabbits. J Orthop Res 21:984-989, 2003.

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  Conflict of Interest:
  None declared.

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