Extracorporeal Shockwave Therapy: What It Is, How It Works, and Which Type Is Right for Your Patient
Extracorporeal Shockwave Therapy (ESWT) has become one of the most widely used non-invasive treatment modalities in musculoskeletal and sports medicine. From stubborn tendinopathies to calcific deposits and non-healing bone fractures, ESWT offers clinicians a powerful tool to stimulate tissue repair and reduce pain without surgery or injections. But not all shockwave therapy is the same, and understanding the differences between the two main types, radial and focused, is essential for choosing the right approach for each clinical presentation.
What Is Extracorporeal Shockwave Therapy?
Shockwave therapy works by delivering high-energy acoustic waves into biological tissue. The word “extracorporeal” simply means the waves are generated outside the body and transmitted through the skin, no needles, no incisions. These acoustic waves carry mechanical energy that, when absorbed by tissue, triggers a cascade of biological responses at the cellular level, initiating repair, reducing pain, and stimulating blood vessel growth.
ESWT first emerged in the 1980s as a treatment for kidney stones (lithotripsy), where high-energy focused waves were used to break calcifications apart. Researchers noticed that the surrounding tissues healed faster than expected, prompting investigation into ESWT as a therapeutic, rather than purely destructive, tool. By the 1990s, it was being used for musculoskeletal conditions, and today its applications span orthopaedics, sports medicine, physiotherapy, podiatry, and even urology.
A shockwave is technically defined as a single, short pressure pulse, a rapid rise in pressure followed by a small negative pressure phase, that travels through tissue at the speed of sound. It is distinct from ultrasound, which uses continuous oscillating waves at much lower energy levels.
The Two Types: Radial and Focused
While both types use acoustic waves, radial and focused shockwave therapy differ significantly in how those waves are generated, how they travel through tissue, and where they deliver their energy. These physical differences have direct consequences for clinical decision-making.
Radial Shockwave Therapy (rESWT) — Also Known as Radial Pressure Wave Therapy
Radial shockwave therapy uses a pneumatic mechanism to generate its waves. Compressed air accelerates a metal projectile at high speed along a tube; the projectile then strikes a transmitter head pressed against the skin, converting its kinetic energy into an acoustic pressure wave. This wave radiates outward in a broad, divergent pattern, much like the ripples from a stone dropped in water, spreading across a wide surface area.
Because of this divergent pattern, the energy is at its highest intensity right at the skin surface and progressively diminishes the deeper it travels. Radial waves are effective to a depth of approximately 3–4 cm beneath the skin. They cannot be focused at a specific depth, they simply fan out and lose power with distance.
Key technical characteristics of radial shockwave:
Generated by a pneumatic (compressed air) mechanism
Divergent, spreading wave pattern
Maximum energy at the skin surface, decreasing with depth
Effective tissue depth: approximately 3–4 cm
Covers a broader treatment area per application
Lower peak pressure than focused shockwave
Generally well-tolerated, often comfortable to receive
More widely available and less expensive than focused devices
Focused Shockwave Therapy (fESWT)
Focused shockwave therapy uses electromagnetic, electrohydraulic, or piezoelectric mechanisms to generate its waves. Rather than diverging outward from the surface, these waves are shaped, via a lens, parabolic reflector, or crystal array, so that they converge at a precise, pre-determined focal point deep within the tissue. The energy passes through superficial tissues without causing significant disruption at the skin surface, then concentrates its force at the targeted depth.
This focal depth is adjustable and can range from approximately 2 cm to 12 cm, or even deeper with some devices, allowing the clinician to precisely target structures at varying depths, from a superficial tendon to a deep bony lesion near the hip or pelvis. The peak pressure at the focal point is significantly higher than that achievable with radial devices.
Key technical characteristics of focused shockwave:
Generated by electromagnetic, electrohydraulic, or piezoelectric mechanisms
Convergent wave pattern; energy concentrates at a precise focal point
Adjustable depth: 2–12+ cm depending on the device
High energy density at the focal point; minimal effect on overlying tissues
Small, precise treatment zone
Higher peak pressure than radial shockwave
Generally comfortable at the skin surface; potential discomfort at the focal point
Less widely available; typically more expensive
Clinical Indications: Which Type for Which Condition?
The choice between radial and focused shockwave should be guided primarily by two factors: the depth of the target tissue and the nature of the pathology. In general, radial shockwave is well suited to superficial, diffuse conditions, while focused shockwave is the preferred option for deeper structures, calcific pathology, and conditions requiring precise energy delivery.
Indications for Radial Shockwave Therapy (rESWT)
Radial shockwave is the more widely used of the two modalities, and for many common musculoskeletal presentations it delivers excellent results. Its broader coverage makes it particularly well suited to diffuse conditions and larger treatment areas.
Common clinical indications:
Plantar fasciitis / plantar heel pain — the plantar fascia is superficial and the broad coverage of radial waves suits this condition well
Achilles tendinopathy (midportion) — the Achilles tendon sits within the 3–4 cm effective range
Patellar tendinopathy (jumper’s knee) — accessible superficially at the inferior pole of the patella
Lateral epicondylitis (tennis elbow) — superficial extensor origin at the lateral elbow
Medial epicondylitis (golfer’s elbow)
Rotator cuff tendinopathy (non-calcific) — accessible in many patients though depth varies
Myofascial trigger points — radial waves are highly effective for releasing trigger points across large muscle chains
Iliotibial band syndrome
Shin splints / medial tibial stress syndrome
Trochanteric bursitis / greater trochanteric pain syndrome (in patients where the target depth is accessible)
Radial shockwave is also well suited to treating broad areas, its coverage allows the clinician to treat systematically across a region rather than targeting a single precise point.
Indications for Focused Shockwave Therapy (fESWT)
Focused shockwave comes into its own for deeper pathologies, calcific conditions, and presentations that require precisely directed high-energy delivery to a specific anatomical target.
Common clinical indications:
Calcific rotator cuff tendinopathy, the focused high-energy wave is particularly effective at breaking down calcium deposits within tendons
Proximal hamstring tendinopathy, the hamstring origin at the ischial tuberosity is deep within the buttock, well beyond the range of radial waves
Gluteal tendinopathy / greater trochanteric pain syndrome (where depth is significant)
Non-union and delayed-union bone fractures — focused waves stimulate osteogenesis and are an established treatment for fractures that fail to heal
Chronic plantar fasciitis (resistant cases) — some evidence that focused ESWT produces superior results in chronic, established cases
Bone stress reactions and stress fractures
Avascular necrosis (early-stage)
Deep tendinopathies (e.g., iliopsoas, adductor)
Peyronie’s disease and erectile dysfunction — low-intensity focused shockwave is used urologically for these conditions
Patients who cannot tolerate radial treatment, because focused shockwave spares the skin surface, it is sometimes better tolerated by patients with acute or sensitised presentations
It is worth noting that for many common tendinopathies, such as patellar tendinopathy and tennis elbow. Clinical trials have shown comparable outcomes between the two modalities. The choice in these cases can reasonably be based on availability, cost, and the clinician’s experience. However, for deep pathology and calcific conditions, focused shockwave is clearly the superior option and radial waves are insufficient.
Some clinicians combine both modalities in the same treatment session: focused shockwave to address deep-seated pathology, followed by radial shockwave to treat the surrounding soft tissue and muscle. This combined approach is increasingly supported by clinical experience.
Cellular and Biological Effects of ESWT
Understanding why shockwave therapy works requires looking at what happens at the cellular level when acoustic energy is delivered to tissue. The biological effects of ESWT are multifactorial — no single mechanism accounts for its therapeutic effects, and different tissues respond to the same mechanical stimulus in different ways. Below is a summary of the key established cellular responses.
1. Mechanotransduction — Turning Force Into Biology
The starting point for all ESWT effects is mechanotransduction: the process by which cells convert a mechanical stimulus into a biochemical signal. When a shockwave passes through tissue, it creates rapid pressure changes that deform cell membranes, open mechanosensitive ion channels, and trigger intracellular signalling cascades. This is the fundamental “switch” that activates the biological cascade. One important signalling pathway activated is ERK1/2 (extracellular signal-regulated kinase), which is linked to cell proliferation and tissue repair. ESWT also triggers the release of ATP from cells, which then binds to purinergic receptors, further amplifying the ERK1/2 signalling cascade and accelerating cell division and wound healing.
2. Neovascularisation (New Blood Vessel Formation)
One of the most clinically significant effects of ESWT is its ability to stimulate the growth of new blood vessels, a process known as neovascularisation or angiogenesis. This is particularly relevant in tendinopathy, where chronic pathology is associated with poor blood supply and impaired healing capacity.
ESWT achieves this by upregulating the expression of key angiogenic growth factors, including:
VEGF (Vascular Endothelial Growth Factor) — the primary driver of new blood vessel formation
eNOS (Endothelial Nitric Oxide Synthase) — stimulates nitric oxide (NO) production, which causes vasodilation and promotes vascular growth
Animal studies consistently demonstrate increased numbers of neovessels at treated tendon–bone junctions following ESWT, and this improved blood supply is thought to be an important factor in accelerating tendon healing and remodelling.
3. Stimulation of Growth Factors and Collagen Production
ESWT upregulates the expression of several growth factors that are critical to tissue repair:
TGF-β1 (Transforming Growth Factor Beta-1) — stimulates fibroblast proliferation and collagen synthesis; plays a central role in tendon healing
IGF-I (Insulin-Like Growth Factor I) — promotes tenocyte (tendon cell) proliferation and matrix production
PCNA (Proliferating Cell Nuclear Antigen) — a marker of active cell division, upregulated in tenocytes following ESWT
These effects combine to drive fibroblast proliferation and the synthesis of new collagen, both Type I (the dominant structural collagen in tendons) and Type III (involved in early repair). Research confirms that gene expression for collagen is upregulated in the weeks following shockwave treatment, consistent with active tissue regeneration.
4. Pain Modulation — Multiple Pathways
ESWT achieves pain relief through several distinct mechanisms:
Substance P depletion: Substance P is a neuropeptide that plays a key role in pain transmission, vasodilation, and neurogenic inflammation. Shockwave therapy produces an initial increase and then a sustained decrease in substance P levels at the treated site. This reduction is closely linked to the clinical pain relief observed after treatment, and unlike NSAIDs, this effect is localised to the treatment region rather than systemic.
CGRP suppression: Calcitonin gene-related peptide (CGRP), another pro-nociceptive neuropeptide, is also reduced in dorsal root ganglia following ESWT, contributing to reduced pain signalling at the spinal level.
Hyperstimulation analgesia: High-energy shockwaves can overstimulate nociceptors, temporarily blocking pain signals through a gate-control mechanism — similar in concept to other physical modalities such as TENS.
Disruption of the pain-inflammation cycle: By reducing substance P and prostaglandin E2 levels in the peritendinous tissues, ESWT helps break the chronic inflammatory cycle that sustains pain in long-standing tendinopathy without the gastrointestinal side effects associated with NSAIDs.
5. Calcification Breakdown (Focused Shockwave Specifically)
At higher energy levels, only achievable with focused shockwave devices, ESWT can mechanically fragment and disintegrate calcific deposits within tendons and other soft tissues. This is the same principle originally used for kidney stone lithotripsy. As calcium deposits break down, they can be reabsorbed by the body, reducing pain and restoring normal mechanical function to the tendon. This is particularly relevant in calcific rotator cuff tendinopathy, where focused ESWT is a well-evidenced first-line treatment before surgical options are considered.
6. Cavitation — A Focused-Shockwave Effect
A unique feature of focused shockwave therapy is the phenomenon of cavitation, the formation and rapid collapse of microscopic bubbles in fluid within the tissue at the focal point. This collapse generates localised microtrauma and releases nitric oxide (NO), contributing to the anti-inflammatory and angiogenic effects described above. Cavitation is far more pronounced with focused shockwave, given the high energy concentration at the focal point, and is thought to contribute to its superior efficacy for deep-seated and calcific pathology.
7. Shared Effects of Both Radial and Focused ESWT
While the mechanisms above may vary in magnitude between the two modalities, research confirms that both radial and focused shockwave share the following biological effects:
Increased cell membrane permeability, enhancing the uptake of ions and nutrients
Stimulation of microcirculation (both blood and lymphatic)
Promotion of fibroblast proliferation and connective tissue remodelling
Release of substance P (with subsequent depletion and pain relief)
Anti-inflammatory effects via modulation of inflammatory mediators
Macrophage activation: ESWT has been shown to shift macrophage phenotype toward a healing-promoting (M2) state, reducing chronic inflammation and improving tissue resolution
The Neuromodulatory Effects of Shockwave Therapy
Beyond its well established effects on tendon, bone, and soft tissue, ESWT exerts a rich and increasingly well understood set of effects on the nervous system. These neuromodulatory properties are relevant not just for conditions traditionally considered “neurological”. They are central to understanding why shockwave therapy reduces pain, improves motor function, and can produce lasting clinical change well beyond what would be expected from simple tissue repair alone.
Peripheral Nerve Pain Modulation
The most immediately clinically relevant neuromodulatory effect of ESWT is its ability to reduce pain through direct action on peripheral nociceptors and pain-signalling pathways. This goes beyond the simple Substance P depletion described in the cellular effects section above, and involves several distinct mechanisms acting in parallel.
When shockwaves are delivered at sufficient intensity, they produce hyperstimulation of nociceptors — an overstimulation of the very pain receptors responsible for signalling discomfort. This temporarily saturates the pain pathway, blocking further transmission through a gate-control mechanism. The effect is similar in concept to how firm pressure applied to a painful area can temporarily override that pain. Importantly, this hyperstimulation is followed by a period of reduced nociceptor sensitivity — essentially a resetting of the local pain threshold downward — which contributes to the sustained pain relief observed in the hours and days after treatment.
ESWT also acts on the calcitonin gene-related peptide (CGRP) system. CGRP is a powerful vasodilator and pain-amplifying neuropeptide that is released at the site of tissue injury and plays a key role in maintaining chronic pain states. Research has shown that ESWT reduces CGRP expression in both the treated peripheral tissue and in the dorsal root ganglia (the cell bodies of sensory nerves that relay pain signals to the spinal cord). This reduction in CGRP activity at the spinal level suggests that shockwave therapy can influence not just local peripheral pain, but the central processing of pain signals, helping to interrupt the chronic pain cycle at multiple levels simultaneously.
Peripheral Nerve Regeneration
One of the most exciting and clinically significant developments in shockwave research is growing evidence that ESWT can actively promote peripheral nerve regeneration, not just reduce pain in existing nerve tissue, but stimulate structural repair of damaged nerves.
The key mechanism here involves Schwann cells (the specialised glial cells that produce myelin) the insulating sheath around peripheral nerve fibres that is essential for fast, accurate nerve conduction. After nerve injury, Schwann cells must proliferate, clear debris through Wallerian degeneration, and lay down new myelin around regenerating axons. ESWT has been shown to significantly accelerate this process through several pathways:
ESWT triggers ATP release from treated cells, which activates purinergic receptors and downstream ERK/MAPK signalling, directly stimulating Schwann cell proliferation
This Schwann cell proliferation is associated with upregulation of key neurotrophic factors, particularly BDNF (Brain-Derived Neurotrophic Factor), NGF (Nerve Growth Factor), and GDNF (Glial Cell-Derived Neurotrophic Factor) — all of which are critical for axonal survival, regrowth, and functional recovery
ESWT activates the PERK pathway in Schwann cells, which in turn enhances ATF4 expression and increases BDNF production, supporting both the survival of damaged neurons and the re-myelination of regenerating axons
Animal studies have demonstrated increased numbers of nerve fibres and thicker myelin sheaths in ESWT-treated peripheral nerve injuries compared to untreated controls, alongside measurable improvements in functional recovery
These findings have clinical implications for conditions such as peripheral nerve entrapment (including carpal tunnel syndrome), diabetic peripheral neuropathy, post-surgical nerve injuries, and other peripheral neuropathies where nerve conduction is impaired. Research into carpal tunnel syndrome in particular has shown that ESWT, both radial and focused, can improve sensory nerve conduction velocity and reduce distal latency, suggesting genuine structural and functional improvement in nerve conduction, not simply pain relief.
Improvement in Nerve Conduction
Directly related to the above, a 2024 systematic review and meta-analysis confirmed that ESWT produces measurable improvements in nerve conduction parameters, particularly in sensory nerve studies. In the acute phase of nerve entrapment or injury, shockwaves are thought to improve nerve conduction by facilitating the drainage of fluid trapped within peripheral nerve bundles, reducing intraneural pressure and fascicular oedema. In chronic cases, ESWT helps counteract fibrotic changes within the nerve, promoting vascularisation of the nerve fascicles, and improving the oxygen and nutrient supply to the affected tissue.
Spasticity Reduction
ESWT is now an established intervention for spasticity — the abnormal increase in muscle tone that follows upper motor neurone injury in conditions such as stroke, cerebral palsy, multiple sclerosis, and spinal cord injury. The International Society for Medical Shockwave Treatment (ISMST) recognises spasticity as an expert indication for ESWT.
The mechanisms by which shockwave reduces spasticity are not yet fully understood, but several hypotheses have been proposed. Shockwaves appear to directly reduce the excitability of the stretch reflex arc by acting on muscle spindles and Golgi tendon organs (the proprioceptive sensors that regulate muscle tone). The mechanical energy delivered to spastic muscle may also disrupt the abnormal collagen cross-linking and fibrotic changes that develop in chronically shortened muscles, improving viscoelastic properties and reducing passive resistance to movement. Simultaneously, the reduction in Substance P and other pain-associated neuropeptides may reduce the hyperexcitability of the spinal cord circuitry that underlies spasticity. Clinical studies have consistently shown measurable reductions in Modified Ashworth Scale scores (the standard clinical measure of spasticity) following ESWT, with effects typically lasting several weeks and potentially prolonged with repeated treatment.
BDNF and Central Neuroplasticity
Perhaps the most intriguing frontier in shockwave neuroscience is the growing evidence that ESWT upregulates BDNF not just in peripheral nerve tissue, but potentially in ways that influence central nervous system plasticity. BDNF is often described as the brain’s own “fertiliser”. It plays a foundational role in neuronal survival, synaptic plasticity, learning, and the brain’s capacity to reorganise in response to injury or rehabilitation.
The connection to the work of researchers like Ebonie Rio is worth noting here: Rio’s research demonstrated that tendinopathy involves measurable changes in cortical excitability and inhibition in the motor cortex, and that effective rehabilitation needs to address these central neurological changes, not just the tendon itself. ESWT’s ability to upregulate BDNF and stimulate Schwann cell activity suggests it may complement neuroplastic approaches to tendon rehabilitation by creating a more favourable neurological environment for motor re-learning. While direct research on ESWT’s effects on cortical excitability in tendinopathy specifically is still emerging, the biological groundwork is compelling and represents an important area for future investigation.
Implications for Clinical Practice
The neuromodulatory effects of ESWT have several important practical implications:
Pain relief is not purely mechanical. The rapid pain relief often reported by patients after even a single shockwave session, sometimes within minutes, cannot be explained by structural tissue repair alone. Neuromodulation, including nociceptor hyperstimulation and Substance P depletion, is the primary driver of this immediate analgesic effect.
ESWT can be used for nerve entrapment conditions such as carpal tunnel syndrome, where improving nerve conduction and reducing perineural fibrosis may offer a genuine alternative to injection or surgery in appropriate patients.
Spasticity management is a clinically validated application that sits at the intersection of musculoskeletal and neurological physiotherapy, and ESWT should be considered as part of a comprehensive rehabilitation programme for patients with upper motor neurone conditions.
The combination of ESWT with active neuroplastic rehabilitation — such as the exercise-based approaches described by Rio and Malliaras — is likely to be more effective than either approach alone, given their complementary mechanisms of action at the tissue, peripheral nerve, and central nervous system levels.
Contraindications and Safety
ESWT has an excellent safety profile in the vast majority of patients. Common temporary side effects include localised redness, mild bruising, and transient soreness at the treatment site, all of which typically resolve within 24–48 hours.
Absolute contraindications include:
Malignancy in or near the treatment area
Pregnancy (over the treatment area)
Blood clotting disorders or anticoagulant therapy
Open wounds or active infection at the treatment site
Treatment directly over growth plates in skeletally immature patients
Implanted electronic devices (e.g. pacemakers) near the treatment area
Relative contraindications include:
Corticosteroid injection at the site within the preceding 6 weeks
Acute inflammatory conditions at the treatment site
Nerve tissue in the direct treatment path (for high-energy focused ESWT)
Summary
Extracorporeal shockwave therapy is one of the most versatile and biologically active non-invasive tools available to musculoskeletal clinicians. Understanding the physical differences between radial and focused modalities, particularly around depth, precision, and energy delivery, is essential for choosing the right treatment for each patient.
Radial shockwave is effective, accessible, and well-suited to superficial and diffuse conditions. Focused shockwave is the modality of choice for deeper pathologies, calcific conditions, and presentations that require precise energy targeting beyond the reach of radial waves.
At the cellular level, both modalities share a rich set of biological effects, stimulating neovascularisation, collagen production, fibroblast activity, and pain modulation, while focused shockwave adds the specific mechanisms of cavitation and calcification disruption that make it uniquely suited to particular clinical presentations.
When used appropriately and in conjunction with a well-designed rehabilitation programme, ESWT offers patients a meaningful, evidence-based pathway to recovery from some of the most persistent and frustrating musculoskeletal conditions.
For a deeper dive into shockwave therapy evidence across specific conditions, speak to your physiotherapist or musculoskeletal clinician.
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