ISPRM Online Training Course On ESWT in PRM - Module 1

Disclaimer
This training course is intended to provide medical specialists with information regarding
the use of extracorporeal shock wave therapy (ESWT) in physical and rehabilitation
medicine (PRM). These materials are intended for education and training to help promote
a high standard of care by professionals. Use of these materials is voluntary and their
use does not confer any professional credentials or qualification to take any registration,
board or licensure examination, and neither confers nor infers competency to perform
any related professional functions.
Specialists have written and reviewed these materials but neither the authors nor ISPRM
give any guarantee that these materials are current, complete, accurate, or contain
information that is consistent with acceptable professional practice. The views expressed
in these materials represent the opinions of the authors, not ISPRM or any other
organization. The authors and ISPRM expressly disclaim any liability for any damage or
loss that may arise from relying upon or using information contained in these materials.
Specifically, these materials do not provide any specific application settings of

ESWT in PRM (including, but not limited to, device, handpiece, applicator, number
of treatments, number of shock waves per treatment, frequency of the shock
waves, and energy of the shock waves). RATHER ANY USER OF ESWT IN PRM
MUST STRICTLY ADHERE TO THE INSTRUCTIONS GIVEN IN THE INSTRUCTION
MANUAL FOR THE MEDICAL DEVICE USED, WHICH IS THE EXCLUSIVE SOURCE
OF ANY VALID INFORMATION GIVEN BY THE MANUFACTURERS OF ESWT
DEVICES.
1
Prof. Dr. Jianan Li serves as Chief Medical Officer for Beijing United Family
Rehabilitation Hospital (Beijing, China) and is also Chairman of the Department of
Rehabilitation Medicine at Nanjing Medical University (Nanjing, China) and its First
Affiliated Hospital located in Nanjing. He is also Executive Vice President and Secretary
General of Chinese Association of Rehabilitation Medicine, Chairman-elect of Chinese
Society of Physical Medicine, and Past President of the International Society of Physical
and Rehabilitation Medicine (ISPRM). Dr. Li received his Master degree in Sports
Medicine at Nanjing Medical University in 1983. He had his training in rehabilitation
medicine during 1988 to 1992 in Australia with a WHO fellowship. He also underwent 6
months of training in Moss Rehab Hospital and the Thomas Jefferson University Health
System with a fellowship from 2000 to 2001. Dr. Li has presided four National Natural
Science Funds, majoring in cardiovascular rehabilitation, as well as a number of national
education projects. He has published 326 research papers, including 16 original papers
in international journals, and served as chief editor for 20 textbooks and reference books.
He was granted the title of “Advanced Contributor” of the China Association for Science
and Technology in 2010. Dr. Li is an experienced expert in exercise training, motion
analysis and motor control, spasticity management, spinal cord injury, and cardiac
rehabilitation.
Dr. XXX
Prof. Dr. Christoph Schmitz has an extensive background in a broad range of medical
and scientific fields. His formal medical training includes a MD degree and a Ph.D.
degree equivalent (“Habilitation”) from RWTH Aachen University (Aachen, Germany). Dr.
Schmitz is Professor of Anatomy and head of the Department of Neuroanatomy at
Ludwig-Maximilians-University of Munich (Munich, Germany). He is also active in a
number of professional societies and related organizations, among them the Clinical
Sciences Committee of ISPRM. Dr. Schmitz has been awarded more than 2 million
euros in peer reviewed grants as Principal Investigator, and has published more than 30
peer-reviewed papers in the field of extracorporeal shock wave therapy of the
2
musculoskeletal system (out of more than 140 peer-reviewed papers in total).
2
Content
Chapter 1
> Essential steps of a typical treatment of a PRM indication with ESWT
> Value proposition to patients
> Short introduction into the physics of ESWT
> Short overview on molecular and cellular mechanisms of action of ESWT
> Principle of generating radial extracorporeal shock waves
> Principles of generating focused extracorporeal shock waves
Chapter 2
> PRM indications of ESWT
> Contraindications of ESWT
> Specific precautions when using ESWT in the management of wounds
Chapter 3
> PRM indications of ESWT in the PEDro database
3
4
Each treatment of a PRM indication with ESWT consists of four steps. The first one is
palpation of the painful region, guided by the patient’s biofeedback.
5
The second step is labeling of the painful region. This is particularly useful when treating
myofascial trigger points, but is also helpful when treating tendinopathies and other
indications.
6
The third step is application of coupling gel. This is absolutely essential because
extracorporeal shock waves are acoustic waves. In case these waves would need to
travel through air between the applicator of the ESWT device and the patient’s skin, most
of the energy of the acoustic waves would be reflected at the skin surface and, thus, not
reach the target region.
It is important to work exclusively with a special coupling gel that minimizes cavitation.
Use of regular ultrasound coupling gel may cause cavitation in the gel, which can cause
additional, unnecessary application pain in the patient’s skin.
In case a patient is very sensitive to application pain caused by ESWT, one can replace
the coupling gel by castor oil [1]. This effectively prevents the formation of cavitation
bubbles in the coupling medium, which can reduce application pain. However, this is
quite a greasy, grimy affair, and (to the knowledge of the authors) no ESWT device has
been approved by its manufacturer for being used in conjunction with castor oil. In any
case, castor oil must not be used in conjunction with gel pads because they can be
destroyed by the castor oil.
---
[1] Maier M, Staupendahl D, Duerr HR, Refior HJ. Castor oil decreases pain during
extracorporeal shock wave application. Arch Orthop Trauma Surg 1999;119:423-427.
7
The fourth step is application of extracorporeal shock waves.
Note that with regard to the number of treatments, number of shock waves per treatment,
frequency of the shock waves, and energy of the shock waves ANY USER OF ESWT IN
PRM MUST STRICTLY ADHERE TO THE INSTRUCTIONS GIVEN IN THE
INSTRUCTION MANUAL FOR THE MEDICAL DEVICE USED, WHICH IS THE
EXCLUSIVE SOURCE OF ANY VALID INFORMATION GIVEN BY THE
MANUFACTURERS OF ESWT DEVICES.
8
Treatment of the musculoskeletal system with ESWT...
• effectively relieves pain in more than 80 percent of patients even after just three
treatments,
• can replace surgery in many cases of diseases of the musculoskeletal system,
• requires compliance by the patient that can easily be achieved (three times five to ten
minutes treatment, usually once a week),
• can be fully performed on an outpatient basis, and
• can be combined with other PRM treatments
Accordingly, there is no medication, there are no injections (no cortisone!), and there is
no surgery involved.
ESWT is gentle and effective.
9
The first use of extracorporeal shock waves in medicine took place in urology for
cracking kidney stones (Extracorporeal Shock Wave Lithotrypsy: ESWL).
Then, urologists observed thickening of pelvic bone when they treated ureter stones with
ESWL. This was the basis for developing ESWT for treating fracture nonunions.
Later, orthopedists started to treat «orthopaedic kidney stones» (calcifying tendonitis,
heel spur) with focused ESWT (fESWT), using either ESWL devices or ESWT devices
derived from ESWL devices («first generation ESWT»). It was found that many patients
became pain-free but the «orthopaedic kidney stones» did not disappear. This was the
basis for starting intense research into the molecular and cellular mechanisms of
extracorporeal shock waves on the musculoskeletal system.
Radial ESWT (rESWT) was developed later and can be considered «second-generation
ESWT», with special devices that cannot be used for cracking kidney stones. Rather,
rESWT devices were especially developed for treatments on the musculoskeletal system
and, thus, for PRM indications.
10
According to Wikipedia,
“a shock wave (also called shock front or simply "shock") is a type of propagating
disturbance. Like an ordinary wave, it carries energy and can propagate through a
medium (solid, liquid or gas) [...]. Shock waves are characterized by an abrupt, nearly
discontinuous change in the characteristics of the medium. Across a shock there is
always an extremely rapid rise in pressure, temperature and density of the flow. [...] A
shock wave travels through most media at a higher speed than an ordinary wave.
The Encyclopedia Britannica online defines shock waves as a

„[...] strong pressure wave in any elastic medium such as air, water, or a solid
substance, produced by supersonic aircraft, explosions, lightning, or other
phenomena that create violent changes in pressure. Shock waves differ from sound
waves in that the wave front, in which compression takes place, is a region of sudden
and violent change in stress, density, and temperature. Because of this, shock waves
propagate in a manner different from that of ordinary acoustic waves. In particular,
shock waves travel faster than sound, and their speed increases as the amplitude is
raised; but the intensity of a shock wave also decreases faster than does that of a
sound wave, because some of the energy of the shock wave is expended to heat the
medium in which it travels.“
It is important to note that these definitions do not at all contribute to our

understanding of ESWT.
11
In general, extracorporeal shock waves are characterized by the development of
pressure over time. Numerous metrics have been used in the literature to characterize
extracorporeal shock waves; they are summarized here (modified from [1]):
• P+: positive peak pressure
• P-: negative peak pressure
• Tr: rise time (i.e., the time interval during which the positive pressure changes from
10% of P+ to 90% of P+)
• Tw: pulse width
• I+: time interval used to calculate the positive energy flux density
• I-: time interval used to calculate the total energy flux density
• A: duration of positive pressure
• B: duration of negative pressure
Every ESWT device generates extracorporeal shock waves with unique characteristics of
these metrics. However, it has remained largely unknown how and to which extent these
metrics determine the clinical efficacy of a particular ESWT device.
---
[1] Schmitz C, Császár NB, Rompe JD, Chaves H, Furia JP. Treatment of chronic plantar
fasciopathy with extracorporeal shock waves (review). J Orthop Surg Res. 2013;8:31-41.
12
This modern definition of therapeutic extracorporeal shock waves was proposed by
Rompe and colleagues in 2007 (modified from [1]). According to this proposal, a
therapeutic shock wave is characterized by…
• P+ between 10 and 100 Mpa,
• a rise time of less than one µs, and
• a tensile pressure component with P- approximately 10% of P+.
For some rESWT and fESWT devices it was demonstrated in the literature that they
meet these criteria (e.g., [2-5]). However, it is critical to note that meeting these criteria
does not determine the clinical efficacy of a particular ESWT device. Clinical efficacy (as
well as safety) can only be demonstrated in clinical studies.
---
[1] Rompe JD, Furia J, Weil L, Maffulli N: Shock wave therapy for chronic plantar
fasciopathy. Br Med Bull 2007a;81-82:183-208.
[2] Chitnis PV, Cleveland RO. Acoustic and cavitation fields of shock wave therapy
devices. In: Clement GT, McDannold NJ, Hynynen K, editors. Therapeutic ultrasound:
5th international symposium on therapeutic ultrasound (AIP conference proceedings).
Boston: AIP Conf Prot.; 2005. pp. 27–29.
[3] Cleveland RO, Chitnis PV, McClure SR. Acoustic field of a ballistic shock wave
therapy device. Ultrasound Med Biol. 2007; 33: 1327–1335.
[4] Perez C, Chen H, Matula TJ, Karzova M, Khokhlova VA. Acoustic field
characterization of the Duolith: measurements and modeling of a clinical shock wave
therapy device. J Acoust Soc Am 2013;134:1663-1674.
[5] Császár NB, Angstman NB, Milz S, Sprecher CM, Kobel P, Farhat M, Furia JP,
Schmitz C. Radial shock wave devices generate cavitation. PLoS One
2015;10:e0140541.
13
This figure shows the schematic representation of the mode of operation of the
handpiece of a ballistic/pneumatic rESWT device (modified from [1]). Compressed air (1)
is used to fire a projectile (2) within a guiding tube (3) that strikes a metal applicator (4)
placed on the patient’s skin. The projectile generates stress waves in the applicator that
transmit pressure waves (5) into tissue.
---
[1] Schmitz C, Császár NB, Milz S, Schieker M, Maffulli N, Rompe JD, Furia JP. Efficacy
and safety of extracorporeal shock wave therapy for orthopedic conditions: a systematic
review on studies listed in the PEDro database. Br Med Bull 2015;116:115-138.
14
This graph shows the pressure as a function of time of a radial extracorporeal shock
wave published in the literature (modified from [1]). The radial extracorporeal shock wave
was generated with the «Radial» handpiece of a Swiss DolorClast device (Electro
Medical Systems, Nyon, Switzerland) and the 15-mm concave applicator, operated at 4
bar air pressure. Pressure was measured in water at a distance of 10 mm to the
applicator. Note that the negative peak pressure was much more than 10% of the
positive peak pressure, as stated in the modern definition of therapeutic shock waves
proposed by Rompe and colleagues in 2007 (outlined above; [2]).
---
[1] Chitnis PV, Cleveland RO. Acoustic and cavitation fields of shock wave therapy
devices. In: Clement GT, McDannold NJ, Hynynen K, editors. Therapeutic ultrasound:
5th international symposium on therapeutic ultrasound (AIP conference proceedings).
Boston: AIP Conf Prot.; 2005. pp. 27–29.
[2] Rompe JD, Furia J, Weil L, Maffulli N: Shock wave therapy for chronic plantar
fasciopathy. Br Med Bull 2007a;81-82:183-208.
15
This movie shows the propagation of a radial extracorporeal shock wave in water,
generated with the «Radial» handpiece of a Swiss DolorClast device (Electro Medical
Systems) and the 15-mm concave applicator, operated at 4 bar air pressure. The movie
itself was constructed from a series of shadowgraph images, taken with a high speed
camera that can capture up to 100.000 frames per second. Shadowgraph imaging is a
visual process that is used to photograph the flow of fluids of varying density. The movie
covers a time period of approximately one millisecond.
16
This shadowgraph image shows the propagation of a radial extracorporeal shock wave in
water, generated with the «Radial» handpiece of a Swiss DolorClast device (Electro
Medical Systems) and the 15-mm standard (convex) applicator, operated at 4 bar air
pressure (modified from [1]). The wave front, the hydrophone (for triggering the high
speed camera), cavitation bubbles generated during the phase of negative pressure, and
ring-like secondary shock waves (generated by collapse of a cavitation bubble at the end
of the phase of negative pressure) are indicated.
---
17
This figure shows a schematic representation of the mode of operation of the handpiece
of an electrohydraulic focused ESWT device (modified from [1]). A high voltage
discharges rapidly across two electrode tips (spark-gap) (1) that are positioned in water.
The spark-gap serves as the first focal point (1). The heat generated by this process
vaporizes the surrounding water. This generates a gas bubble centered on the first focal
point, with the gas bubble being filled with water vapor and plasma. The result of the very
rapid expansion of this bubble is a sonic pulse, and the subsequent implosion of this
bubble causes a reverse pulse, manifesting a shock wave. By means of reflectors of
certain shape (2), this shock wave can be converted into a convergent/focused acoustic
pressure wave/shock wave with a point of highest pressure at the second focal point (3).
---
18
of an electromagnetic focused ESWT device (modified from [1]). A strong, variable
magnetic field is generated by passing a high electric current through a coil (1). This
causes a high current in an opposed metal membrane (2), which causes an adjacent
membrane (3) with surrounding liquid to be forced rapidly away. Because the adjacent
membrane is highly conductive, it is forced away so rapidly that the compression of the
surrounding liquid generates a shock wave within the liquid. By means of an acoustic
lens (4) of certain shape, this shock wave can be converted into a convergent/focused
acoustic pressure wave/shock wave with a point of highest pressure at a focal point (5).
---
19
of a piezoelectric focused ESWT device (modified from [1]). A large number of
piezocrystals (1) are mounted in a bowl-shaped device (2); the number of piezocrystals
can vary from a few to several thousands (typically between 1,000 and 2,000). When
applying a rapid electrical discharge, the piezocrystals react with a deformation
(contraction and expansion), which is known as the piezoelectric effect. This induces an
acoustic pressure puls in the surrounding water that can steep into a shock wave.
Because of the design of the bowl-shaped device an acoustic pressure wave/shock wave
can emerge with a point of highest pressure at a focal point (3).
---
20
This graph shows the pressure as a function of time of a focused extracorporeal shock
wave, generated with a Swiss PiezoClast device (Electro Medical Systems) that was
operated at medium energy settings (intensity level 10; maximum intensity level: 20)
(modified from [1]). Pressure was measured in water at the position of the focal point
according to IEC-61846:1998 (Ultrasonics—Pressure pulse lithotripters—Characteristics
of fields). Note that the positive peak pressure was much higher than the positive peak
pressure of the radial extracorporeal shock wave device shown above.
---
[1] Internal documentation of Richard Wolf (Knittlingen, Germany).
21
This movie shows the propagation of a focused extracorporeal shock wave in water,
generated with a Swiss PiezoClast device (Electro Medical Systems) that was operated
at maximum energy settings (intensity level 20). The movie itself was constructed from a
series of shadowgraph images, taken with a high speed camera that can capture up to
100.000 frames per second. Shadowgraph imaging is a visual process that is used to
photograph the flow of fluids of varying density. The movie covers a time period of
approximately one millisecond.
22
This shadowgraph image shows the propagation of a focused extracorporeal shock wave
in water, generated with a Swiss PiezoClast device (Electro Medical Systems) that was
operated at maximum energy settings (modified from [1]). The figure was constructed by
mounting five shadowgraph images taken each at 12 μs apart into one figure. The
position of the focal point, cavitation bubbles generated during the phase of negative
pressure, and ring-like secondary shock waves (generated by collapse of a cavitation
bubble at the end of the phase of negative pressure) are indicated.
---
23
This figure shows the cavitation field caused by a focused extracorporeal shock wave in
water that was generated with a Swiss PiezoClast device (Electro Medical Systems),
operated at maximum energy settings (modified from [1]). The cavitation field has an
elliptic shape with equatorial diameter of approximately 2 cm and polar diameter of
approximately 5 cm.
---
24
Due to the physical characteristics of radial and focused extracorporeal shock waves,
superficial indications are the domain of rESWT and deep indications the domain of
fESWT.
Only a very few studies in the literature addressed ESWT for myofascial trigger points so
far. Accordingly, one cannot decide at the present point in time whether trigger point
treatment should preferably done with fESWT or rESWT.
There is anecdotal evidence that patients who did not respond to either rESWT or
fESWT showed improved results when switching to the other modality (i.e., from rESWT
to fESWT or the other way round). However, the reason for this phenomenon has
remained unclear. It may primarily be a psychological issue rather than a biomedical one.
25
This is a very simplified summary of the main molecular and cellular mechanisms of
action of ESWT. Details will be provided in Module 2 (”Comprehensive background of
ESWT in PRM”).
26
When planning and performing treatments with ESWT in PRM, the recommendations
provided in these materials should be considered - as well as the individual experience of
the therapist and the individual feedback of the patient.
When performing treatments of the musculoskeletal indications presented here, the

energy of the shock waves should be adjusted such that the patient experiences some
discomfort at least during the first treatment – but does not feel pain. The discomfort
indicates that the peripheral nervous system is activated by the shock waves. During the
following treatments the patient might not experience discomfort anymore, despite the
possibility to increase the energy of the shock waves.
The energy of the shock waves should be adjusted as high as possible (i.e., until the
patient feels some discomfort – but no pain – during the treatment). This will improve the
treatment success (reviewed in [1]).
The tissue to be treated with shock waves should not be subjected to local anesthesia
prior to the application of shock waves. This may cause failure of the shock wave
treatment [2]. This is most probably due to the fact that local anesthesia may block the
mechanisms of action of shock waves on the C nerve fibers. In this case, shock waves
may not be able to activate the C nerve fibers anymore [3].
Approximately 80% of all patients report a substantial improvement of the clinical

situation (pain) after two treatment sessions. This is a good sign with respect to the
prognosis of treatment outcome. Accordingly, it is possible to predict the treatment
outcome after two treatment sessions – but not before.
In any case, the recommendations provided here do not determine any specific
application settings of ESWT in PRM (including, but not limited to, device,
handpiece, applicator, number of treatments, number of shock waves per
treatment, frequency of the shock waves, and energy of the shock waves).
RATHER ANY USER OF ESWT IN PRM MUST STRICTLY ADHERE TO THE
27
INSTRUCTIONS GIVEN IN THE INSTRUCTION MANUAL FOR THE MEDICAL DEVICE USED,
WHICH IS THE EXCLUSIVE SOURCE OF ANY VALID INFORMATION GIVEN BY THE
MANUFACTURERS OF ESWT DEVICES.
---
[1] Schmitz C, Császár NB, Milz S, Schieker M, Maffulli N, Rompe JD, Furia JP. Efficacy and
safety of extracorporeal shock wave therapy for orthopedic conditions: a systematic review on
studies listed in the PEDro database. Br Med Bull 2015;116:115-138.
[2] Rompe JD, Meurer A, Nafe B, Hofmann A, Gerdesmeyer L. Repetitive low-energy shock wave
application without local anesthesia is more efficient than repetitive low-energy shock wave
application with local anesthesia in the treatment of chronic plantar fasciitis. J Orthop Res
2005;23:931-941.
[3] Klonschinski T, Ament SJ, Schlereth T, Rompe JD, Birklein F. Application of local anesthesia
inhibits effects of low-energy extracorporeal shock wave treatment (ESWT) on nociceptors. Pain
Med 2011;12(10):1532-1537.
27
Most of the energy of extracorporeal shock waves is delivered at the boundary
between soft and hard tissue. This is the anatomical location of the entheses, i.e.,
where tendons meet bone. This is the main reason why ESWT is so effective in the
treatment of insertional tendinopathies. Furthermore, the boundary between soft and
hard tissue is also the anatomical location of the periosteum that has nociceptive
nerve endings, making it very sensitive to manipulation including the application of
extracorporeal shock waves.
*, these indications are shown on the following pages as examples.
29
Myofascial pain syndrome and trigger points
Myofascial trigger points (MFTPs) are a very common condition, especially in the cervical
musculature. Up to 85% of back pain and approximately 55% of neck pain and
headaches are caused by myofascial pain. The predominant age is 30 to 50 years.
Women are more affected than men. Very often MFTPs are associated with poor
posture. Notably MFTPs frequently produce neurological complaints including headache,
dizziness, sensory symptoms, as well as gastrointestinal problems. They are localized
segments of muscle that are thought to be subjected to trauma by acute injury or
microtrauma from repetitive stress. MFTPs can occur in any skeletal muscle.
Diagnosis of MFTPs, established by Simons et al. [1] and used in many studies, is
essentially based on five major criteria:
i. regional pain,
ii. referred pain (specific for each individual muscle),
iii. palpable taut band,
iv. tenderness point at taut band, and
v. restricted range of motion.
Furthermore, at least one minor diagnostic criteria must be met:

i. stimulated pain when applying pressure on MFTPs,
ii. local twitch response on palpation or injection into MFTPs, and
iii. symptom improvement by stretching or injection into MFTPs.
It has been hypothesized that muscle injury or stress disrupts the sarcoplasmic reticulum
within muscle fibers, releasing free calcium ions. These free calcium ions causes the
actin and myosin of the muscle fibers to lock into place as long as adenosine
triphosphate is available. The resulting contraction of small parts of the muscle leads to
diminished blood flow with subsequent ischemia and release of painful substances such
as serotonin, histamine and prostaglandins in the affected area. Several studies revealed
30
biochemical alterations in MFTPs including more acidic pH in active MFTPs than in normal muscle
tissue, and increased levels of inflammatory markers including bradykinin, substance P, tumor
necrosis factor, interleukin (IL) -1, IL-6, IL-8, CGRP, serotonin, and norepinephrine. These
alterations are particularly found in active MFTPs.
The treatment of MFTPs should start with a manual technique that involves applying pressure to a
trigger point to release the pathologic contraction of the muscle segment and to stretch the
segment to restore normal muscle fiber length. This can be accompanied by acupuncture, stress
management and relaxation techniques. Pharmacologic treatment is unspecific and may comprise
muscle relaxants, nonsteroidal anti-inflammatory drugs (NSAIDs), anticonvulsants, or topical
application of local anesthetics or botulinum toxin.
ESWT is very effective for MFTPs and may mimic manual therapy in applying pressure to a trigger
point to release the pathologic contraction of the muscle segment. Prevention of recurrence should
focus on appropriate ergonomic changes in patients’ day-to-day activities to avoid repetitive stress
to the injured muscles.
Tension-type headache
Tension-type headache (TTH) is characterized by a bilateral, pressing, tightening pain of mild to
moderate intensity, and is the most featureless of the primary headaches. TTH can occur in short
episodes of variable duration (episodic forms) or continuously (chronic form). Infrequent Episodic
TTH (< 1 day of headache per month) usually does not require medical treatment except of simple
analgesics. In contrast, both patients with Frequent Episodic TTH (ETTH; between 12 and 180
days of headache per year) and Chronic TTH (CTTH; at least 189 days of headache per year) may
encounter considerable disability and warrant specific intervention. The lifetime prevalence of TTH
is approximately 78%, with 24% to 37% of the patients suffering from TTH several times a month,
10% weekly, and 2% to 3% of the population suffering from CTTH which usually lasts for the
greater part of a lifetime.
Because many secondary headaches may mimic TTH, a diagnosis of TTH requires exclusion of
other organic diseases. In most patients, TTH develops from the episodic form to the chronic form,
and prolonged peripheral nociceptive stimuli from pericranial myofascial tissues seem to be
responsible for the conversion of ETTH to CTTH.
TTH is considered the prototype of headaches in which myofascial pain plays an important role.
Many studies have reported an increased number of active and latent myofascial trigger points in
pericranial muscles in patients with ETTH and CTTH. These active and latent myofascial trigger
points can be found in the suboccipital, splenius capitis, splenius cervicis, semispinalis capitis,
semispinalis cervicis, levator scapulae and upper trapezius muscles. Short-term relief of headache
by myofascial trigger point release has been successfully demonstrated in CTTH.
Both ETTH and CTTH can be treated with ESWT when focusing on the treatment of active and
latent myofascial trigger points in the suboccipital, splenius capitis, splenius cervicis, semispinalis
capitis, semispinalis cervicis, levator scapulae and upper trapezius muscles.
---
[1] Simons DG, Travell JG, Simons LS. Travell & Simons' Myofascial Pain and Dysfunction: The
Trigger Point Manual (2-Volume Set), 2nd edition. Philadelphia: Lippincott Williams & Wilkins;
1998.
30
Osteoarthritis (OA) is the most common cause of pain and disability worldwide,
especially in the elderly population. It is a chronic disease characterized by the
progressive degeneration of cartilage, producing pain and loss of articular function.
OA cartilage contains a higher percentage of cells undergoing apoptosis than normal

cartilage. Nitric oxide (NO) is an important inducer of apoptosis and has been
hypothesized to be an important mediator of chronic articular lesions in OA. The
inhibition of NO synthesis can slow cartilage degeneration.
Symptoms of OA include stiffness and pain that limits weight-bearing activities such as
walking, going up and down stairs, and standing up from a chair.
Women are more frequently affected than men, and hip and knee are mostly affected.
Despite the high prevalence and negative impact on the quality of life of affected
individuals, there is no cure for OA.
Therapeutic measures aim to relieve painful symptoms and maximize functional capacity
and quality of life, while minimizing adverse effects from drugs and invasive
interventions. Several conservative treatment strategies are available for OA, among
them nonsteroidal anti-inflammatory drugs (NSAID), weight loss, participation in self-
management programs, neuromuscular education, valgus directing force braces, lateral
wedge insoles, intraarticular (IA) corticosteroids, IA hyaluronic acid, and IA platelet rich
plasma (PRP).
Recently a number of experimental studies on animal models indicated that ESWT may
be effective in treating disabling pain due to primary OA. Specifically, it has been
suggested that ESWT may inhibit the production of NO in knee synovia and reduce
chondrocyte apoptosis. Accordingly, ESWT for OA may have disease-modifying activity.
Moreover, several randomized controlled trials showed that ESWT can successfully be
used to alleviate pain in patients with knee OA.
31
Ultimately, patients suffering from OA and complaining of severe disabling and refractory pain are
usually referred to a total or partial joint arthroplasty.
31
The Taskforce on Childhood Motor Disorders of the U.S. National Institutes of Health
(NIH) defined spasticity in 2001 as hypertonia in which one or both of the following signs
are present:
i. resistance to externally imposed movement that increases with increasing speed of
stretch and varies with the direction of joint movement; and
ii. resistance to externally imposed movement that rapidly rises above a threshold
speed of joint angle.
Spasticity is caused by damage to the central motor pathways that control voluntary
movement. Effects of spasticity range from mild muscle stiffness to severe, painful
muscle contractures and repetitive spasms that reduce mobility and substantially impede
normal activities of daily living. Spasticity can prevent or hamper function, cause pain,
disturb sleep, and present major difficulties for hygiene care. However, it must not be
forgotten that spasticity can also be useful, perhaps allowing a person to stand or walk
when weakness would not otherwise permit it. With these issues in mind, it is imperative
that management of spasticity is always patient- and function focused, rather that aimed
at the reduction of spasticity only. In children, spasticity impacts on muscle and bone
growth. Subsequently it interferes with motor development, hand functions, gait and
balance and also causes significant musculoskeletal complications such as hip
dislocation and scoliosis as well as pain. A particular problem is spasticity of plantar
flexor muscles in very young children because it causes toe walking.
The Quality Standards Subcommittee of the American Academy of Neurology and the
Practice Committee of the Child Neurology Society pointed out in 2010 that the Modified
Ashworth Scale measures a broader set of neural and musculoskeletal factors of non-
velocity-dependent hypertonia in addition to spasticity itself. According to some authors
the Tardieu scale (TS) is a tool that is more consistent with the proposed definition of
spasticity provided by the NIH Taskforce on Childhood Motor Disorders. The TS
accounts for the joint angle measure of the spastic phenomenon at different velocities of
32
joint movement.
The management of spasticity is complex and poses a major challenge to the neurorehabilitation
team. The ultimate goal of any therapy program must be to achieve the patient’s maximum
potential in motor skills. Neurorehabilitation is always prescribed as physical and occupational
therapy, as well as orthoses and gait aids. Unfortunately, the scientific evidence for various
physical therapy treatment options for patients with spasticity is limited. Botulinum neurotoxin
(BoNT) is a widely used and effective pharmacological treatment for focal muscle overactivity. An
alternative to BoNT treatment is focal intramuscular treatment with phenol and alcohol, with the aim
to improve activity limitations and other outcomes in patients with spasticity. However, focal
intramuscular injection of BoNT, phenol and alcohol is not without problems:
i. BoNT is expensive and not available in many countries;
ii. a significant risk of focal intramuscular injection of alcohol and phenol is persisting pain; and
iii. all these procedures are invasive and, thus, not without risk when applied under difficult
hygienic conditions.
With regard to post-stroke spasticity, a recent Cochrane review concluded that, at best, there was
'low level' evidence for the effectiveness of outpatient multidisciplinary rehabilitation in improving
active function and impairments following BoNT treatment for upper limb spasticity in patients with
chronic stroke.
Orthopedic surgery is considered a last resort in managing spasticity in children, but is not an
option for managing spasticity per se. Instead, it is used to help correct the secondary problems
that occur with growth alongside spastic muscles and poor motion control. Those problems include
muscle shortening, joints contractures and bony deformities.
Recently, ESWT has become an alternative in the treatment of spasticity. Among others, ESWT
can produce physiological responses in treated tissue such as changes of nitric oxide (NO)
formation. NO is involved in neuromuscular junction formation in the peripheral nervous system
and in important physiological functions of the central nervous system, including
neurotransmission, memory, and synaptic plasticity. Furthermore, many other mechanisms of
extracorporeal shock waves (ESW) may mediate their beneficial effects in spasticity, such as:
i. effects of ESW on the neuromuscular junction;
ii. mechanical relaxation of muscle fibers by means of ESW;
iii. decreased spinal excitability without long-lasting clinical or neurophysiologic effects after
continuous or intermittent pressure on tendons; and
iv. direct effects of ESW on fibrosis and the rheological properties of chronic hypertonic muscles.
32
Idiopathic low back pain
Low back pain without sciatica, stenosis or severe spinal deformation (henceforth
referred to as idiopathic low back pain, ILBP) is common and affects people of all ages. It
is second only to the common cold as the most common affliction of mankind and is
among the leading complaints bringing patients to physicians’ offices. Its reported point
prevalence is as high as 33 percent, its one-year prevalence as high as 73 percent and
its lifetime prevalence exceeds 70% in most industrialized countries, with an annual
incidence of 15-20% in the United States. In physically active adults not seeking medical
attention, the annual incidence of clinically significant ILBP with functional impairment is
approximately 10-15%. An alarming increase in the prevalence of chronic ILBP has been
observed in industrialized countries over the last years, affecting both men and women
and across all ages and racial and ethnic groups.
The social and economic impact of ILBP is substantial. It is the most frequent cause of
disability for people under age 45. Acute ILBP (lasting three to six weeks) usually
resolves in several weeks, although recurrences are common and low-grade symptoms
are often present years after an initial episode. Risk factors for the development of
disabling chronic or persistent ILBP (variously defined as lasting more than three months
or more than six months) include pre-existing psychological distress, disputed
compensation issues, other types of chronic pain and job dissatisfaction. Diagnosis is
based on clinical features.
Diagnostic imaging should be considered to rule out other causes of lower back pain
(particularly in chronic cases) or to establish the diagnosis of ILBP when in doubt.
The goals of management for patients with ILBP are to

i. decrease the pain,
ii. restore mobility,
iii. hasten recovery so the patient can resume normal daily activities as soon as
33
possible,
iv. prevent development of a chronic recurrent condition, and
v. restore and preserve physical and financial independence and comfort.
However, management for patients with ILBP is challenged by the following problems:
i. most back pain has no recognizable cause;
ii. an underlying systemic disease is rare;
iii. most episodes of back pain are unpreventable; and, most importantly,
iv. few if any treatments have been proven effective for ILBP.
Among those treatments are limited bed rest, exercise, nonsteroidal anti-inflammatory drugs
(NSAIDs) and acetaminophen (Tylenol), muscle relaxants and opioids (if acetaminophen or
NSAIDs do not relieve the pain), chirotherapy, physiotherapy and, ultimately, surgery (in cases of
cauda equina syndrome, infections, tumors and fractures compressing the spinal cord, mechanical
instability of the back, and, perhaps, intractable pain with a positive straight-leg-raising test and no
response to conservative therapy). However, the analgesic effects of many treatments for non-
specific low back pain are small and do not differ in populations with acute or chronic symptoms.
ESWT is an alternative to conservative treatment and should be applied before considering

surgery.
Pseudoradicular syndrome
Radicular and pseudoradicular lower back pain are different types of pain that radiate distally at the
legs. Radicular pain radiates below the knee and is thought to stem from disorders associated with
nerve root compression which is often felt in distal dermatomes below the knee (projected pain).
In contrast, pseudoradicular pain does not radiate below the knee and is thought to be associated
with local proximal disorders that do not affect any nerves or nerve roots. These disorders include
facet joint affection, piriformis syndrome and several other conditions. The associated pain is
perceived in proximal dermatomes within the thigh (referred pain, head zones). In many cases of
pseudoradicular lower back pain, it is impossible to find the underlying disease characterizing
these cases as idiopathic.
The distinction between radicular and pseudoradicular lower back pain is clinically relevant for
several reasons:
i. Radicular pain has always a neuropathic component because it always involves damage or
irritation of peripheral nerves or nerve roots. In contrast, pseudoradicular pain may occur
without damage or irritation of peripheral nerves or nerve roots and, thus, might be purely
nociceptive. This distinction is very important when evaluating the results of neurophysiologic
examinations.
ii. Radicular pain (neuropathic pain) is predominantly sensitive to antidepressants and
anticonvulsants. In contrast, pseudoradicular pain (nociceptive pain) is predominantly sensitive
to nonsteroidal anti-inflammatory drugs (NSAIDS).
Diagnosis is based on the clinical features. Diagnostic imaging should be considered to rule out
other causes of lower back pain or to establish the diagnosis of radicular or pseudoradicular lower
back pain when in doubt. However, it should be noted that abnormalities found in radiological
examinations in the lumbar spine poorly correlate with clinical symptoms.
ESWT is a very effective alternative to conservative treatment in pseudoradicular lower back pain.
33
Calcifying tendinitis of the shoulder
Calcifying tendinitis of the shoulder is an acute or chronic painful disorder that is
characterized by calcifications in rotator cuff tendons. The main clinical symptom is
shoulder pain, often aggravated by lying on the shoulder or elevation of the arm above
shoulder level. The patient may be awoken from sleep by the pain. Other complaints may
be weakness, stiffness, snapping or catching of the shoulder.
Diagnosis is based on the clinical features of the disease and on imagery. The
calcifications occur most commonly in the supraspinatus tendon (51%–90%) and least
commonly in the subscapularis tendon (3%). The etiology is largely unknown. It has been
hypothesized that the condition may be related to hypovascularity-induced fibrosis and
necrosis within the tendon with subsequent degeneration. The characteristics of an
existing, symptomless calcific deposit may be changed by minor traumatic episodes,
leading to acute symptoms. The condition may also be related to mechanical irritation by
deposits when the arm is abducted and deposits impinge on the acromion.
The disease usually presents in four stages:

i. precalcific stage (usually without symptoms), involving fibrocartilaginous metaplasia
within the tendon;
ii. formative phase (with or without pain), with calcific deposits formed in the
fibrocartilaginous matrix;
iii. resorptive phase (massive pain), with deposits disappearing by cell-mediated
resorption (inflammatory response); and
iv. final stage (with or without pain), involving healing and rotator cuff repair.
Notably this cycle can be blocked at any one stage in chronic calcifying tendinitis.
The incidence is approximately 3% in the healthy population, and approximately 7% in

those with shoulder pain. The predominant age is 30 to 50 years. Women are two times
34
more affected than men.
The initial treatment should be conservative including rest, physiotherapy, and nonsteroidal anti-
inflammatory drugs.
In later stages, extracorporeal shock wave therapy (ESWT) should be considered (not in the
resorptive phase), or subacromial infiltration with corticosteroids. Surgery should be considered for
recalcitrant cases of calcifying tendinitis of the shoulder.
Subacromial pain syndrome

The term subacromial shoulder pain is often used synonymously with the terms rotator cuff
disease, rotator cuff tendinosis, and shoulder impingement syndrome. As calcifying tendinitis of the
shoulder (details are provided in the corresponding Section) can also present with shoulder pain,
the subacromial pain syndrome can also comprise calcifying tendinitis of the shoulder.
Sometimes the term rotator cuff tendinitis is confused with the term shoulder bursitis, but both
terms refer to an inflammation of a particular area within the shoulder joint (i.e., the subacromial
space) that is causing a common set of symptoms and is named shoulder impingement syndrome
(SIS). The term SIS is descriptive and refers to pinching of the tendons and bursa of the rotator cuff
between bones (i.e., in the subacromial space). In most acute cases SIS is a combination of
inflammation of the rotator cuff tendons (tendinitis) and inflammation of the bursa that surrounds
these tendons (bursitis). In many cases of SIS the subacromial space is reduced because of
different shape of the bones compared to healthy control people. The condition is often caused by
an initial injury, starting the inflammatory process. This may cause thickening of the tendons or
bursa, taking up more space and pinching these structures even more, resulting in more
inflammation. Accordingly, the problem can be self-exacerbating, resulting in a vicious circle of
inflammation, thickening of the tendons and bursa, pinching of these structures, more inflammation,
and so on.
Diagnosis is based on the clinical features of the disease. Diagnostic imaging should be considered
to rule out other causes of shoulder pain (including calcifying tendinitis of the shoulder) or to
establish the diagnosis of SIS when in doubt. SIS is the most common form of shoulder pain, and
repetitive activity at or above the shoulder during work or sports (including swimming, throwing,
tennis, weightlifting, golf, volleyball, and gymnastics) represents the main risk factor for SIS.
Increasing age predisposes to SIS.
With respect to therapy, three different stages of SIS are distinguished:

> Stage 1 (acute inflammation, edema and hemorrhage in the rotator cuff): conservative
treatment including rest, icing, physiotherapy, and nonsteroidal anti-inflammatory drugs;
> Stage 2 (continuum of Stage 1, with the rotator cuff tendon progressing to fibrosis and
tendinitis): conservative treatment, ESWT, or surgery when conservative treatment and ESWT
fail; and
> Stage 3 (mechanical disruption of the rotator cuff tendon and/or changes in the coracoacromial
arch with osteophytosis along the anterior acromion): surgery.
34
Tennis elbow is a tendinopathy of the common extensor origin of the lateral elbow. In
former times the condition was usually named "lateral epicondylitis". However, the
pathology is no longer thought to be inflammatory. Nowadays the accurate description
wound be "partially reversible but degenerative overuse-underuse tendinopathy".
Because of the complexity of this description, usually the term "tennis elbow" is used.
The main clinical symptoms are pain on resisted movements (particularly resisted third
finger extension) and tenderness at the lateral epicondyle, with normal elbow range of
motion.
Diagnosis is based on the clinical features of the disease. Diagnostic imaging should be
considered to rule out other causes of elbow pain or to establish the diagnosis of tennis
elbow when in doubt. As with other tendinopathies the pathology of tennis elbow is
complex and not fully understood. Similar to calcifying tendinitis of the shoulder, sudden
overload may alter the structure of the tendons at the common extensor origin, leading to
a degenerative process. However, calcifications are rare in tennis elbow. Involvement of
neurogenic inflammation in tennis elbow has also been suggested.
The population prevalence is approximately 2%, with peak incidence occurring at 40 to

50 years of age. Approximately 40% of all tennis players report problems with their
elbow, but only a quarter of them consider the symptoms to be disabling and severe.
Notably most patients with tennis elbow do not play tennis. This is due to the fact that
many tennis players have a weekly training routine that regularly loads the tendons and
keeps them healthy. Rather, the injury usually occurs in people who have been sedentary
for years and then overuse a previously underused and atrophied tendon by exercising at
the gym, doing gardening, or even just carry heavy luggage. When the injury is caused
by playing tennis it is the backhand stroke that leads to excessive loading of the tendons
at the common extensor origin.
The initial treatment should be conservative including rest, physiotherapy, and
35
nonsteroidal anti-inflammatory drugs. As in case of chronic Achilles tendinopathy and chronic
plantar fasciopathy, eccentric (lengthening only) exercises have become the mainstay of
rehabilitation programmes for tennis elbow.
An attractive alternative is ESWT. In most circumstances, cortisone injections should not be used.
This is due to the fact that cortisone leads to very good results in the short term (six weeks) but has
been demonstrated to be harmful in the longer term (more than three months). Surgery should be
considered when conservative treatment fails.
35
Greater trochanteric pain syndrome (GTPS) includes a number of disorders of the lateral
peritrochanteric space of the hip such as tears of the gluteus medius and minimus,
trochanteric bursitis, and external coxa saltans.
The main clinical symptoms are pain and reproducible tenderness in the region of the
greater trochanter and/or the buttock or lateral thigh. Diagnosis is based on the clinical
features of the disease. Diagnostic imaging should be considered to rule out other
causes of hip pain or to establish the diagnosis of GTPS when in doubt. The greater
trochanter is the site of attachment for the tendons of five muscles: the gluteus medius
and gluteus minimus laterally, and the piriformis, obturator externus and obturator
internus medially. As in the shoulder, injury and subsequent degeneration may occur in
the components of the rotator cuff of the hip, starting with tendinitis, tendinosis, and
eventual tear. This process is occuring more commonly in the gluteus medius than the
gluteus minimus. Furthermore, there are three bursas present around the lateral aspect
of the greater trochanter, i.e., the subgluteus maximus bursa, the subgluteus medius
bursa and the gluteus minimus bursa. These bursas are believed to serve as cushioning
for the gluteus tendons, the iliotibial band, and the tensor fascia latae. Trochanteric
bursitis occurs mostly secondary to repetitive friction between the greater trochanter and
the iliotibial band with hip flexion and extension. Trochanteric bursitis is also often
associated with overuse, trauma, or other conditions that may alter normal gait patterns.
GTPS has been reported to affect between 10% and 25% of the general population, with
an increased prevalence in women compared to men.
Therapy of symptomatic tendon tears comprises rest, antiinflammatory medications and

physiotherapy focusing on range of motion and strengthening exercises. Trochanteric
bursitis is usually self-limiting and responds to rest, ice, antiinflammatory medications
and physiotherapy focusing on stretching, flexibility, strengthening and gait mechanics.
When symptoms persist despite these interventions, bursal injections of local anesthetics
and corticosteroid can provide effective pain relief.
36
Radial extracorporeal shock wave therapy (rESWT) has been demonstrated to be efficient for
recalcitrant GTPS. In case of inefficacy of rESWT, surgical intervention may be considered in
cases in which other potential sources of the patient’s symptoms have been ruled out.
36
The patellar tendon connects the lower pole of the patella to the tibia. Patellar
tendinopathy (PT), often referred to as jumper’s knee, is a chronic overuse injury of the
patellar tendon. The main clinical symptom is pain at the inferior pole of the patella.
considered to rule out other causes of knee pain or to establish the diagnosis of PT when
in doubt. Similar to other tedinopathies, the etiology of PT is not completely understood,
but repetitive overload is thought to be an important factor. Histologic examination of
biopsy specimens from patients undergoing patellar tendon surgery for chronic
symptoms has shown that chronic PT is associated with degenerative changes in the
tendon. Accordingly, the disease is better characterized as “tendinopathy” than
“tendinitis”, resembling the situation in other overuse tendon problems such as Achilles
tendinopathy.
Athletes have a very high prevalence of PT, i.e., up to 40% among elite basketball and
volleyball players. The condition can be debilitating and may prevent athletes to return to
sport for long periods between 6 months and more than 2 years.
The treatment of PT should start with conservative treatment modalities including rest,
physiotherapy, eccentric strengthening, bracing and non-steroidal anti-inflammatory
drugs.
Patients not responding to conservative treatment for six months should then be
subjected to ESWT.
Surgery should be considered for recalcitrant cases of PT. Numerous arthroscopic and
open procedures were described, but a consensus agreement about the best option is
not available.
37
Medial tibial stress syndrome (MTSS) - commonly known as ‘‘shin splints” – is a
frequent overuse injury or repetitive-stress injury of the lower extremity. The condition is
one of the most common causes of exertional leg pain in athletes, and usually presents
as diffuse pain of the lower extremity, along the middle-distal tibia associated with
exertion. Early courses of MTSS are characterized by pain that (i) gets worse at the
beginning of exercise, (ii) gradually subsides during training, and (iii) stops within minutes
after exercise. Later, pain may present with less activity and may even occur at rest.
considered to rule out other causes of exertional leg pain, or to establish the diagnosis of
MTSS when in doubt. Training errors (“too much, too fast”) appear to be the most
common factors involved in MTSS. The condition is most often found in runners, soccer
and basketball players, and in dancers. Notably MTSS is almost always associated with
biomechanical abnormalities of the lower extremity including knee abnormalities, tibial
torsion, femoral anteversion, foot arch abnormalities or a leg-length discrepancy.
However, improper footwear (including worn-out shoes) can also contribute to shin
splints. A variety of tibial stress injuries can be involved in MTSS including tendinopathy,
periostitis, and dysfunction of the tibialis posterior, tibialis anterior and soleus muscles.
Women appear to be more affected than men, and have an approximately threefold risk
for progression to stress fractures.
The treatment of MTTS should start with rest and ice in the acute phase, followed by low-
impact and cross-training exercises during rehabilitation and a modified training program
(decreased intensity, frequency, and duration, regular stretching and strengthening
exercises, wearing proper-fitting shoes with good shock absorption). Orthotics, manual
therapy, injections and acupuncture may also help to alleviate the symptoms.
Patients not responding to conservative treatment should be subjected to rESWT.
Surgery should also be considered for recalcitrant cases of MTSS.
38
The Achilles tendon is the combination of tendons of the soleus and gastrocnemius
muscles and connects these muscles to the back of the heel. Mid-portion Achilles
tendinopathy (MPAT) is an acute or chronic, painful disorder of the Achilles tendon.
Several terms have been used to describe this condition including tendinosis, tendinitis
and peritendinitis. However, histologic examination of biopsy specimens from patients
undergoing surgery for chronic symptoms has shown that chronic MPAT is associated
with degenerative changes in the tendon. Accordingly, the disease is better characterized
as tendinopathy than tendinitis or tendinosis. The Achilles tendon is (together with the
plantaris tendon) surrounded by a paratenon. In many cases of Achilles tendinopathy the
condition is accompanied by paratendinopathy.
Diagnosis is based on the clinical features of the disease, with the location of the pain as
an important discriminating factor. The spot of maximum pain and painful swelling in
MPAT is located 2 to 6 cm proximal to the insertion, whereas in case of insertional
Achilles tendinopathy, the spot of maximum pain is at the tendon-bone junction.
Symptoms can be exacerbated when getting up after a period of rest. In isolated
paratendinopathy, there is local thickening of the paratenon, and the area of swelling
does not move with dorsiflexion and plantarflexion of the ankle. In contrast, the area of
swelling moves with dorsiflexion and plantarflexion of the ankle in case of isolated
tendinopathy. Diagnostic imaging should be considered to rule out other causes of
Achilles tendon pain, or to establish the diagnosis of MPAT when in doubt.
As in case of insertional Achilles tendinopathy, the etiology of MPAT is likely

multifactorial and may include advanced age, obesity, hypertension, diabetes, and
steroid use, to mention only a few. Particularly in athletes the onset of MPAT may also be
influenced by poor training habits including excessive training, training on hard or sloping
surfaces, and abrupt changes in scheduling. It has been hypothesized that healing of
injuries of the Achilles tendon as a result of overuse involves the penetration of small
blood vessels from the paratenon into the tendon in order to increase healing by
providing improved blood flow. However, these small blood vessels are accompanied by
39
small nerve fibers with high concentrations of nociceptive substances including glutamate,
substance P, and calcitonin gene-related peptide (CGRP). These small nerve fibers are considered
the cause of pain in chronic MPAT. The lifetime risk of an Achilles tendon injury in elite long-
distance runners is approximately 50%. However, individuals of all activity levels and all ages
present with similar complaints, and approximately 30% of all patients have a sedentary lifestyle.
The treatment of MPAT should start with conservative treatment modalities including rest, icing,
physiotherapy, stretching (eccentric loading), exercises, orthoses, heel lifts and non-steroidal anti-
inflammatory drugs.
Patients not responding to conservative treatment shall be subjected to ESWT.
Surgery should be considered for recalcitrant cases of MPAT, with different surgical strategies
aiming at debridement or tenotomy of the tendon itself).
39
The Achilles tendon is the combination of tendons of the soleus and gastrocnemius
muscles and connects these muscles to the back of the heel. Insertional Achilles
tendinopathy (IAT) is an acute or chronic painful disorder of the Achilles tendon at its
insertion onto the calcaneus. Several terms have been used to describe this condition
including tendinosis, tendinitis and peritendinitis. However, histologic examination of
biopsy specimens from patients undergoing surgery for chronic symptoms has shown
that chronic IAT is associated with degenerative changes in the tendon. Accordingly, the
disease is better characterized as tendinopathy than tendinitis or tendinosis.
Diagnosis is based on the clinical features of the disease, with the location of the pain as
an important discriminating factor. The spot of maximum pain in IAT is located at the
tendon-bone junction, whereas in case of noninsertional Achilles tendinopathy, the spot
of maximum pain is 2 to 6 cm proximal to the insertion. Symptoms can be exacerbated
by running on hard surfaces and climbing stairs. Diagnostic imaging should be
considered to rule out other causes of Achilles tendon pain and heel pain, or to establish
the diagnosis of IAT when in doubt.
The etiology of IAT is likely multifactorial and may include advanced age, obesity,
hypertension, diabetes, hyperpronation and steroid use, to mention only a few.
Particularly in athletes the onset of IAT may also be influenced by poor training habits
including excessive training, training on hard or sloping surfaces, and abrupt changes in
scheduling. It has been hypothesized that healing of injuries of the Achilles tendon as a
result of overuse involves the penetration of small blood vessels into the tendon in order
to increase healing by providing improved blood flow. However, these small blood
vessels are accompanied by small nerve fibers with high concentrations of nociceptive
substances including glutamate, substance P, and calcitonin gene-related peptide
(CGRP). These small nerve fibers are considered the cause of pain in chronic IAT.
Runners comprise the largest group of patients with chronic pain in the Achilles tendon.
The annual incidence of IAT among athletes is approximately 8%. However, individuals
40
of all activity levels and all ages present with similar complaints.
The treatment of IAT should start with conservative treatment modalities including rest, icing,
physiotherapy, stretching (eccentric loading), exercises, orthoses, heel lifts and non-steroidal anti-
inflammatory drugs. In certain cases braces and immobilization with a cast or a pneumatic walking
boot may improve the situation.
Patients not responding to conservative treatment shall be subjected to ESWT.
Surgery should be considered for recalcitrant cases of IAS, with different surgical strategies
described in the literature.
Prevention of recurrence should focus on appropriate exercise habits, wearing low-heeled shoes
and eccentric strengthening exercises.
40
Plantar fasciopathy (PF) is an acute or chronic, painful disorder of the plantar fascia that
spans between the medial calcaneal tubercle and the proximal phalanges of the toes. It
is the most common cause of plantar heel pain and accounts for approximately 11-15%
of foot symptoms presenting to physicians.
The main clinical symptom is heel pain, particularly in the morning or after a period of
rest. Often patients report improvement of pain after walking. Pain is usually located at
the origin of the plantar fascia, i.e., at the medial calcaneal tubercle. Passive dorsiflexion
of the toes may aggravate the pain in some patients, particularly in those with chronic
PF. Patients suffering from chronic PF may also present with heel pad swelling.
considered to rule out other causes of plantar heel pain or to establish the diagnosis of
PF when in doubt. Histologic examination of biopsy specimens from patients undergoing
plantar fascia release surgery for chronic symptoms has shown that chronic PF is
associated with degenerative changes in the fascia. Accordingly, the disease is better
characterized as “fasciopathy” than “fasciitis”, resembling the situation in overuse tendon
problems.
In the United States, more than two million individuals are treated for PF on an annual
basis. Up to 10% of the population will experience plantar heel pain during the course of
a lifetime. Both athletes and the elderly commonly present to physicians with PF.
The treatment of PF should start with conservative treatment modalities including rest,
physiotherapy, stretching, exercises, shoe inserts/orthotics, night splints, non-steroidal
anti-inflammatory drugs, and local corticosteroid injections.
Patients not responding to conservative treatment (between 10% and 20% of all patients)
shall be subjected to ESWT.
41
Surgery should be considered for recalcitrant cases of PF.
41
Osgood Schlatter disease (OSD) involves the tibial tuberosity in growing children. The
conditon is characterized by local pain, swelling and tenderness of the tuberosity. OSD is
thought to be caused by repetitive strain and chronic avulsion of the secondary
ossification center of the tibial tuberosity, i.e., by small injuries due to repeated overuse
before the area has finished growing. The repetitive strain is from the strong pull of the
quadriceps muscle produced during sporting activities, particularly during running,
jumping and climbing. Accordingly, OSD is common in adolescents who play soccer,
basketball and volleyball, and who participate in gymnastics. The tibial tuberosity
avulsion continues to grow, ossify and enlarge. The intervening area may become
fibrous, creating a localized nonunion, or may show complete bony union with mild
enlargement of the tibial tuberosity. In any case, the result is a traction apophysitis of the
tibial tubercle.
Diagnosis is based on the clinical features of the disease and on diagnostic imaging.
Particularly in unilateral cases of OSD plain radiographs of the knee are recommended to
rule out other conditions such as acute tibial apophyseal fracture, infection, or tumor.
The true incidence of OSD is unknown. The predominant age is between 12 and 15
years in boys and between 8 and 12 years in girls, coinciding with periods of growth
spurts. Boys are more affected than girls (approximately 3:1). In 20-30% of all cases
OSM presents bilaterally.
The treatment of OSD should start with conservative treatment modalities including rest,
icing, modification of activities, and rehabilitation exercises.
Patients not responding to conservative treatment (approximately 10% of all patients)

shall be subjected to ESWT.
Surgery should be considered for recalcitrant cases of OSD in skeletally mature patients,
aiming at surgical excision of the ossicle (in case of a localized nonunion) and/or free
42
cartilaginous material.
42
Diabetic foot ulcer, pressure ulcer and venous stasis ulcer are the most common chronic
skin and soft tissue wounds. A chronic wound is usually one that has failed to heal within
three months.
Diagnosis is based on the clinical features of the disease. The incidence is approximately
1%, with chronic wounds mostly affecting people 60 years or older. Accordingly, the
number of chronic wounds will rise as the population ages. Factors that contribute to
chronic wounds include poor circulation, (diabetic) neuropathy, bacterial colonization and
infection, systemic illnesses, age, repeated trauma, vasculitis, immune suppression
(including the use of steroids over a long period), but also emotional stress.
According to the University of Texas Wound Classification system, wounds are

categorized into four stages:
A: without infection and ischemia;
B: with infection;
C: with ischemia; and
D: with infection and ischemia)
According to the same classification system wounds are also categorized into four
grades:
0: pre- or postulcerative lesion completely epithelialized;
1: superficial wounds, not involving tendon, capsule or bone;
2: wounds penetrating to tendon or capsule; and
4: wound penetrating to bone or joint.
Wound healing is classically divided into four phases:

i: hemostasis;
ii: inflammation;
iii: proliferation; and
iv: remodeling.
43
There is considerable overlapping among individual phases. These phases are controlled by a
wealth of growth factors that are involved in wound healing such as vascular endothelial growth
factor (VEGF), epidermal growth factor (EGF) and transforming growth factors α and β (TGF-α and
-β), to mention only a few. Inadequate levels of growth factors may also contribute to the formation
of chronic wounds.
Therapeutic strategies for chronic wounds aim at preventing and treating infection, fighting
ischemia, and replacing and/or stimulating growth factors. This can be achieved by surgical wound
debridement, application of hyperbaric oxygen, negative pressure wound therapy, and topical and
systemic application of molecules such as cell adhesion proteins, cytokines, enzymes, or EGF-like
growth factor. Mesenchymal stem cell therapy has become another potential future target for
intervention.
Recently ESWT was introduced into the management of chronic wounds (Stages/Grades A1 and
A2, as well as C1 and C2 with great care), based on its proven abilities to improve the functional
microvasculature, stimulate expression of growth factors such as VEGF, and increase cell
proliferation. ESWT is particularly interesting for those chronic wounds that are too small for
negative pressure wound therapy.
43
Lymphedema may be primary or secondary. Primary lymphedema is a lymphatic
malformation developing during the later stage of lymphangiogenesis. In contrast,
secondary lymphedema is the result of disruption or obstruction of the lymphatic system.
Secondary lymphedema can occur as a consequence of tumors, surgery, infection,
inflammation, radiation therapy and trauma. Secondary lymphedema is one of the most
significant complications after the surgical treatment of breast cancer, with significant
impact on the quality of life.
A substantial number of women develop secondary lymphedema after surgical treatment

of breast cancer, with reported incidence between 6% and 63% depending on the
population studied, the measurement criteria used and the reported length of follow-up.
Lymphedema is divided into the following stages:

> Stage IA (latent lymphedema) presents without clinical evidence of edema, but with
impaired lymph transport capacity.
> Stage IB (initial lymphedema) is characterized by edema that totally or partially
decreases by rest and draining position.
> In Stage IIA (increasing lymphedema) vanishing lymph transport capacity is seen
and fibroindurative skin changes appear.
> Stage IIB (column shaped limb fibrolymphedema) presents with lymphostatic skin
changes and worsening disability.
> In Stage IIIA (elephantiasis) scleroindurative pachydermitis and papillomatous
lymphostatic verrucosis is observed together with life-threatening disability
> Stage IIIIB is extreme elephantiasis with total disability.
Diagnosis of lymphedema is based on the clinical features of the disease (extremity

circumference measurement before and after surgery; a difference of more than 2 cm
points to the development of lymphedema). Diagnostic imaging (plain radiographs,
duplex ultrasonography, radionuclide lymphoscintigraphy and other imaging modalities)
should be considered to rule out other causes of increased extremity circumferences, or
44
to establish the diagnosis of lymphedema when in doubt.
Treatment should start with manual lymphatic drainage and compression bandage-centered
decongestive lymphatic therapy. An alternative is sequential intermittent pneumatic compression
using pumping devices.
Radial shock wave therapy (rESWT) has been demonstrated being efficient for lymphedema
stages IIA and IIB.
Surgery should be considered for recalcitrant cases of lymphedema not responding or responding
poorly to the aforementioned treatment options. Surgical options include lympho-venous or
lympho-venous-lymphatic bypass anastomosis, lympho-lymphatic segmental interposition, free
lymph node transplantation, and ablative surgery in case of massive limb changes or fibrotic
induration.
44
Note that with regard to contraindications of ESWT ANY USER OF ESWT IN PRM
MUST STRICTLY ADHERE TO THE INSTRUCTIONS GIVEN IN THE INSTRUCTION
MANUAL FOR THE MEDICAL DEVICE USED, WHICH IS THE EXCLUSIVE SOURCE
OF ANY VALID INFORMATION GIVEN BY THE MANUFACTURERS OF ESWT
DEVICES.
45
Note:
NEVER treat an infected wound with shock waves!

The shock waves might disseminate bacteria from the wound into the body, possibly
resulting in systemic infection and ultimately sepsis.
NEVER treat a Grade III wound with shock waves!

Direct exposure of bones or joints to shock waves leads to incalculable risks.
Be careful with ischemic wounds, and NEVER treat a necrotic wound with shock
waves!
Necrotic tissue cannot regenerate and must be removed.
---
[1] Armstrong DG, Lavery LA, Harkless LB. Validation of a diabetic wound classification
system. The contribution of depth, infection, and ischemia to risk of amputation. Diabetes
Care 1998;21:855-859.
46
47
This study is a striking example demonstrating the absolute need for testing the efficacy
and safety of any therapy in PRM in high-quality randomized controlled trials (RCTs).
48
(This publication is available for free to download at
http://bmb.oxfordjournals.org/content/116/1/115.long. It contains the full references of all
studies cited in this chapter.)
PEDro is the Physiotherapy Evidence Database (note that the term „physiotherapy“
refers here to the vocabulary used in countries like Australia, Norway or The
Netherlands).
PEDro is a free database of over 35,000 randomized clinical trials (RCTs), systematic
reviews and clinical practice guidelines in physiotherapy. For each trial, review or
guideline, PEDro provides the citation details, the abstract and a link to the full text,
where possible. All trials on PEDro are independently assessed for quality. These quality
ratings are used to quickly guide users to trials that are more likely to be valid and to
contain sufficient information to guide clinical practice. PEDro is produced by the Centre
for Evidence-Based Physiotherapy at The George Institute for Global Health, affiliated
with the University of Sydney (Sydney, Australia).
These are the criteria for inclusion of RCTs in PEDro:

> The trial must involve comparison of at least two interventions. One of these
interventions could be a no treatment control, or a sham treatment.
> At least one of the interventions being evaluated must be currently part of
physiotherapy practice or could become part of physiotherapy practice. However, the
study need not be carried out by physiotherapists.
> The interventions should be applied to subjects who are representative (or who are
intended to be representative) of those to whom the intervention might be applied in
the course of physiotherapy practice.
> The trial should involve random allocation or intended-to-be-random allocation of
subjects to interventions.
> The paper must be a full paper (not an abstract) in a peer-reviewed journal.
PEDro is using the following criteria for assessing the quality of RCTs:
49
(Eligibility criteria were specified).
1. Subjects were randomly allocated to groups.
2. Allocation was concealed.
3. The groups were similar at baseline regarding the most important prognostic indicators.
4. There was blinding of all subjects.
5. There was blinding of all therapists who administered the therapy.
6. There was blinding of all assessors who measured at least one key outcome.
7. Measures of at least one key outcome were obtained from more than 85% of the subjects
initially allocated to groups.
8. All subjects for whom outcome measures were available received the treatment or control
condition as allocated or, where this was not the case, data for at least one key outcome was
analysed by “intention to treat”.
9. The results of between-group statistical comparisons are reported for at least one key
outcome.
10. The study provides both point measures and measures of variability for at least one key
outcome.
All but two of the PEDro scale items are based on the Delphi list, developed by Verhagen et al. [1].
The reliability of the PEDro scale for rating the quality of randomised controlled trials was
demonstrated by Maher et al. [2].
Bhogal et al. [3] showed that at least for the stroke rehabilitation literature the PEDro scale provides
a more comprehensive measure of methodological quality than the Jadad scale.
De Morton [4] confirmed the validity of the PEDro scale.
---
[1] Verhagen AP, de Vet HC, de Bie RA, Kessels AG, Boers M, Bouter LM, Knipschild PG. The
Delphi list: a criteria list for quality assessment of randomized clinical trials for conducting
systematic reviews developed by Delphi consensus. J Clin Epidemiol 1998;51:1235-1241.
[2] Maher CG, Sherrington C, Herbert RD, Moseley AM, Elkins M. Reliability of the PEDro scale for
rating quality of randomized controlled trials. Phys Ther 2003;83:713-721.
[3] Bhogal SK, Teasell RW, Foley NC, Speechley MR. The PEDro scale provides a more
comprehensive measure of methodological quality than the Jadad scale in stroke rehabilitation
literature. J Clin Epidemiol 2005;58:668-673.
[4] De Morton NA. The PEDro scale is a valid measure of the methodological quality of clinical
trials: a demographic study. Aust J Physiother 2009;55:129-133.
49
a. As of January 1, 2017.
This figure shows the number of publications on fESWT (red bars) and rESWT (blue
bars) in the PEDro database as a function of the year of publication. Focused ESWT was
developed earlier than rESWT.
50
a. As of January 1, 2017
This figure shows the systematic review flow chart of a search for the key words “shock
wave” and “shockwave” in the PEDro database according to the PRISMA (Preferred
Reporting Items for Systematic Reviews and Meta-Analyses) guidelines [1] (deadline:
January 1, 2017).
Abbreviations:
> rESWT+: RCT on rESWT with positive outcome (i.e., rESWT statistically significantly
better than either placebo or alternative treatment modalities)
> rESWT-: RCT on rESWT with negative outcome (i.e., rESWT not statistically
significantly better than either placebo or alternative treatment modalities)
> fESWT+: RCT on fESWT with positive outcome (i.e., fESWT statistically significantly
better than either placebo or alternative treatment modalities)
> fESWT-: RCT on fESWT with negative outcome (i.e., rESWT not statistically
significantly better than either placebo or alternative treatment modalities)
*, one study [2] addressed both radial and focused ESWT and, thus, was listed in both
categories rESWT+ and fESWT+.
Methodological details:
A total of n=246 records were identified in the PEDro database (deadline: January 1,
2017) of which n=51 were duplicates. All reviews (n=56) were excluded, as well as
records that did not address ESWT. Furthermore, all ESWT studies on wound healing
and chronic decubitus were excluded. The remaining records (n=124) were distributed
into studies on
> rESWT with positive outcome (i.e., rESWT significantly better statistically than either
placebo or alternative treatment modalities) (rESWT+; n=31),
51
> rESWT with negative outcome (i.e., rESWT not significantly better statistically than either
placebo or alternative treatment modalities) (rESWT-; n=8),
> fESWT with positive outcome (fESWT+; n=67), and
> fESWT with negative outcome (fESWT-; n=19) (note that one RCT [2] addressed both rESWT
and fESWT and, thus, was listed in both groups rESWT+ and fESWT+).
For each of the groups rESWT+, rESWT-, fESWT+, and fESWT- mean and standard error of the
mean (SEM) of the following variables was calculated:
> number of treatment sessions;
> interval between treatment sessions for those RCTs with more than one treatment session;
> number of shock waves per treatment session;
> energy flux density (EFD) of the shock waves;
> total energy flux density that was applied (calculated as the product of the number of treatment
sessions, the number of shock waves per treatment session, and the energy flux density of the
shock waves); and
> PEDro score (between 0 and 10).
Comparison of groups was performed using Kruskal-Wallis test (nonparametric analysis of

variance) followed by pairwise comparisons using Dunn’s multiple comparison test. A p value <
0.05 was considered statistically significant.
It is of note that in many RCTs in PEDro it was not specified whether the reported EFD was the
positive EFD (EFD+) or the total EFD (EFDTotal) (details about EFD+ and EFDTotal are provided in,
e.g., [3, 4]). Accordingly, calculations of mean EFDs were based on mixed EFD+ and EFDTotal data.
Furthermore, absolute and relative numbers of studies performed with respectively

electrohydraulic, electromagnetic, or piezoelectric shock wave generators we calculated. This was
done separately for the groups fESWT+ and fESWT-. Comparison of groups was performed using
Chi-square test. Again, a p value < 0.05 was considered statistically significant.
The results of this analysis are shown on the following pages.
---
[1] Liberati A, Altman DG, Tetzlaff J, Mulrow C, Gøtzsche PC, Ioannidis JP, Clarke M, Devereaux
PJ, Kleijnen J, Moher D. The PRISMA statement for reporting systematic reviews and meta-
analyses of studies that evaluate healthcare interventions: explanation and elaboration. Br Med J
2009;339:b2700.
[2] Lohrer H, Nauck T, Dorn-Lange NV, Schöll J, Vester JC. Comparison of radial versus focused
extracorporeal shock waves in plantar fasciitis using functional measures. Foot Ankle Int
2010;31:1-9.
[3] Ogden JA, Tóth-Kischkat A, Schultheiss R: Principles of shock wave therapy. Clin Orthop Rel
Res 2001a;(387):8-17.
[4] Gerdesmeyer L, Maier M, Haake M, Schmitz C: Physikalisch-technische Grundlagen der

extrakorporalen Stosswellentherapie (ESWT) [Physical-technical principles of extracorporeal
shockwave therapy (ESWT)]. Orthopade 2002;31:610-617.
51
a) As of January 1, 2017
This figure shows mean and standard error of the mean (SEM) of the number of
treatment sessions (Panel A), interval between treatment sessions (Panel B), number of
impulses per treatment session (Panel C), energy flux density of the impulses (Panel D),
total energy flux density that was applied (Panel E), and the PEDro score of all RCTs
(Panel F) on radial (rESWT) and focused (fESWT) extracorporeal shock wave therapy
with positive (+) or negative (-) outcome listed in the PEDro database (deadline: January
1, 2017).
The results of this analysis can be summarized as follows:

Panel A: the average number of treatment sessions among all RCTs on ESWT in PEDro
was 2.98 ± 0.14 (mean ± SEM; range: 1 to 12), with highest numbers in RCTs on
rESWT+ and lowest numbers in RCTs on fESWT+. The difference in the mean number
of treatment sessions between these two groups was statistically significant (p<0.001).
Panel B: among those RCTs on ESWT in PEDro with more than one treatment session,
the average interval between treatment sessions was 8.45 ± 0.58 days (range: 1 to 42
days). On average, the longest intervals between treatment sessions were reported for
Group fESWT- and the shortest intervals for Group rESWT+. However, there were no
statistically significant (p<0.05) differences between the groups.
Panel C: the average number of shock waves per treatment session among all RCTs on
ESWT in PEDro varied only slightly among the groups rESWT+, rESWT-, fESWT+, and
fESWT-, with a mean value of 1957 ± 85 (range: 250 to 6000). There were no statistically
significant (p<0.05) differences between the groups.
Panel D: the energy flux density of the shock waves applied in all RCTs on ESWT in
52
PEDro was on average 0.19 ± 0.01 mJ/mm2 (range: 0.03 to 0.78), with the highest mean value in
Group fESWT+ and the lowest mean value in Group rESWT+. The difference in the mean energy
flux density between these two groups was statistically significant (p<0.05). However, one cannot
exclude that this was (at least in part) due to the fact that for many RCTs in Groups fESWT+ and
fESWT-, it remained unclear whether the reported EFD was EFD+ or EFDTotal (which is higher than
EFD+; c.f. [1, 2]). In contrast, for most studies in Groups rESWT+ and rESWT- it was known that
the reported EFD was EFD+.
Panel E: among all RCTs on ESWT in PEDro the average total energy flux density that was
applied (calculated as the product of the number of treatment sessions, the number of shock waves
per treatment session, and the energy flux density of the shock waves) was 0.99 ± 0.07 J/mm2
(range: 0.01 to 3.72 J/mm2), with the highest mean value in Group rESWT- and the lowest mean
value in Group rESWT+. However, there were no statistically significant (p<0.05) differences
between the groups.
Panel F: the average PEDro score among all RCTs on ESWT in PEDro was 6.22 ± 0.15 (range: 1
to 9), with the highest mean score in Group fESWT- and the lowest mean score in Group fESWT+.
However, there were no statistically significant (p<0.05) differences between the groups.
Furthermore, in 17 RCTs on fESWT with positive outcome in PEDro an electrohydraulic (EH)

device was used, in 41 RCTs an electromagnetic (EM) device, in 6 RCTs a piezoelectric (PE)
device, in one RCT both an EH and a PE device, and in one RCT both an EH and an EM device.
For the RCTs on fESWT with negative outcome in PEDro the corresponding numbers were 1 (EH),
16 (EM), 1 (PE), 1 (EM + PE) and 0 (EH + EM). The distribution of numbers of EH, EM and PE
devices was not statistically significant (p=0.25) between RCTs on fESWT with positive outcome
and RCTs on fESWT with negative outcome.
These data can be interpreted as follows:

> ESWT is efficacious: 79.5% (31 out of 39) of all RCTs on rESWT and 77.9% (67 out of 86) of
all RCTs on fESWT listed in the PEDro database had positive outcome (i.e., rESWT or fESWT
resulted in statistically significantly better clinical outcome than either placebo or alternative
treatment modalities). Because of substantial differences between RCTs, however, it was not
possible to calculate collective percentages of “good” or “excellent” results in the RCTs on
rESWT+ and fESWT+ listed in the PEDro database.
> ESWT is safe: in no RCT on rESWT and fESWT listed in the PEDro database a severe
adverse event was reported.
> RCTs on ESWT with either positive or negative outcome had almost the same averaged
PEDro scores.
> When applied appropriately there appears to be no difference between rESWT and fESWT
with respect to treatment outcome.
> The distinction between rESWT as “low-energy ESWT” and fESWT as “high-energy ESWT” is
not correct and should be abandoned.
> When using the generalized terms rESWT and fESWT one has to consider that there is no
scientific basis for the assumption that all or most radial extracorporeal shock wave devices (or
all or most focused extracorporeal shock wave devices, respectivley) are comparable to each
other. However, when using the generalized terms rESWT and fESWT, the studies listed in the
PEDro database do not indicate an advantage of fESWT over rESWT and vice versa.
> Furthermore, the studies on fESWT listed in the PEDro database do not indicate an advantage
of a certain principle of generating focused shock waves.
One should also consider the following:

> For most of the rESWT and fESWT devices currently used in the practice-based sector only a
very few studies or no any study have been listed in the PEDro database demonstrating
effectiveness of these devices.
> This does not necessarily imply that evidence for effectiveness of these devices has not been
52
demonstrated in RCTs. Rather, it is possible that the corresponding studies (i) have not been
published, (ii) were published but do not meet the criteria for inclusion in PEDro, or (iii) were
published but not included in PEDro due to other reasons.
> In this respect, it should be pointed out that according to Council Directive 93/42/EEC of 14
June 1993 it is not mandatory to demonstrate effectiveness for a certain medical product in a
RCT – despite the fact that Council Directive 93/42/EEC is considered one of the most
important instruments for demonstrating safety and effectiveness of medical devices in the
European Economic Area.
In order to assess the relevance of ESWT in PRM compared to other treatment modalities, a
second search of the PEDro database was performed. Details of this second search are
outlined on the following pages.
---
[1] Ogden JA, Tóth-Kischkat A, Schultheiss R: Principles of shock wave therapy. Clin Orthop Rel
Res 2001a;(387):8-17.
[2] Gerdesmeyer L, Maier M, Haake M, Schmitz C: Physikalisch-technische Grundlagen der

extrakorporalen Stosswellentherapie (ESWT) [Physical-technical principles of extracorporeal
shockwave therapy (ESWT)]. Orthopade 2002;31:610-617.
52
a. As of January 1, 2017
Abbreviations used in this table:
> Records, total number of records.

> Reviews, number of reviews.
> RCTs, number of RCTs.
> Ps, PEDro score.
> A, absolute number of RCTs addressing the corresponding indication (i.e., plantar
fasciopathy, Achilles tendinopathy, lateral epicondylitis, non-calcific supraspinatus
tendinopathy, calcifying tendonitis of the shoulder, subacromial pain, and spasticity),
split up according to PEDro scores.
> B, relative number of RCTs on ESWT addressing the corresponding indication, split
up according to PEDro scores.
> CE, currently evaluated by PEDro.
> Total-1, total and relative numbers of RCTs in categories A and B.
> Total-2, total and relative numbers of RCTs in categories A and B with a PEDro score
of 6 or higher.
> n/a, not applicable.
Methodological details:
This search addressed the question which indications were repeatedly (i.e., more than
three times) addressed in the RCTs on ESWT in the PEDro database retrieved during
the first search (outlined in detail above). This was the case for the indications plantar
fasciopathy, Achilles tendinopathy, lateral epicondylitis, subacromial pain syndrome, non-
calcific supraspinatus tendinopathy, calcifying tendonitis of the shoulder and spasticity.
On this basis the second search in the PEDro database was performed. To this end for
53
each of the key terms plantar, Achilles, epicondylitis, subacromial, non-calcific, calcifying and
spasticity the following metrics were calculated:
> total number of records;
> number of reviews and number of RCTs;
> number of RCTs that addressed the corresponding indication; and
> number of RCTs on ESWT in PEDro that addressed the corresponding indication.
Full-text articles were not assessed for eligibility during the second search.
These data can be interpreted as follows:

> For the key word plantar, 99 out of 286 RCTs (34.6%) in the PEDro database were RCTs on
plantar fasciopathy (“a” in the table), of which 52 (52/99 = 52.5%) had a PEDro score of 6 or
higher (“b” in the table).
> For the other key words the corresponding numbers were as follows:
• Achilles: 47/109 = 43.1% RCTs on Achilles tendinopathy, among them 28/47 = 60.3%
with PEDro score ≥ 6.
• Epicondylitis: 113/113 = 100% RCTs on lateral epicondylitis, among them 54/113 =
47.8% with PEDro score ≥ 6.
• Non-calcific: 3/5 = 60% RCTS on non-calcific supraspinatus tendinopathy, among them
2/3 = 66.6% with PEDro score ≥ 6.
• Calcifying: 16/16 = 100% RCTs on calcifying tendonitis of the shoulder, among them
9/16 = 56.3% with PEDro score ≥ 6.
• Subacromial: 81/84 = 96.4% RCTS on subacromial pain syndrome, among them 52/81
= 64.2% with PEDro score ≥ 6.
• Spasticity: 270/270 = 100% RCTs on spasticity, among them 124/270 = 45.9% with
PEDro score ≥ 6.
> For plantar fasciopathy, 44.4% of the RCTs listed in the PEDro database were RCTs on ESWT
(57.7% of the RCTs with PEDro score ≥ 6) (“c” and “d” in the table).
> For the other indications the corresponding relative numbers of RCTs on ESWT were as
follows:
• Achilles tendinopathy: 12.8% of all RCTs, and 17.9% of those RCTs with PEDro score
≥ 6.
• Lateral epicondylitis: 21.2% of all RCTs, and 24.1% of those RCTs with PEDro score ≥
6.
• Non-calcific supraspinatus tendinopathy: 100% of all RCTs.
• Calcifying tendonitis of the shoulder: 81.3% of all RCTs, and 77.8% of those RCTs with
PEDro score ≥ 6.
• Subacromial pain syndrome: 4.9% of all RCTs, and 3.8% of those RCTs with PEDro
score ≥ 6.
• Spasticity: 1.9% of all RCTs, and 2.4% of those RCTs with PEDro score ≥ 6.
> Collectively these data show that for certain indications RCTs on ESWT have become the
predominant type of RCT listed in the PEDro database and/or obtained the highest
PEDro scores among all investigated treatment modalities. Both criteria (i.e., predominant
type of RCT listed in the PEDro database, and highest PEDro scores among all investigated
treatment modalities) were fulfilled for the indications plantar fasciopathy, non-calcific
supraspinatus tendinopathy, and calcifying tendonitis of the shoulder. For Achilles tendinopathy
and lateral epicondylitis, respectively 12.8 and 21.2% of all RCTs listed in the PEDro database
were RCTs on ESWT, but these RCTs also obtained among the highest PEDro scores among
all investigated treatment modalities for these conditions.
> For other indications (greater trochanteric pain syndrome, patellar tendinopathy, knee
osteoarthritis, long bone fracture, osteonecrosis of the femoral head, proximal hamstring
tendinopathy, primary long bicipital tenosynovitis, myofascial pain syndrome, myogelosis of the
masseter muscle, and spasticity) the RCTs listed in the PEDro database have demonstrated
53
efficacy and safety when treating these conditions with ESWT; however, there are not enough
RCTs on ESWT listed in PEDro to draw meaningful conclusions regarding the significance of
ESWT for the corresponding conditions.
On the following pages details of all RCTS on ESWT listed in the PEDro database are
summarized. These data are for documentation purposes only. There is no need to read
through these data in detail.
53
b) Outcome of the study:

+: positive outcome of ESWT compared to either placebo or alternative treatment
modalities;
-: negative outcome of ESWT compared to either placebo or alternative treatment
modalities
c) Energy flux density; EFD+: positive energy flux density; EFDTotal: total energy flux
density
d) Not specified
Note that this table is for documentation purposes only. There is no need to read
---
[1] Cacchio A, Paoloni M, Barile A, Don R, de Paulis F, Calvisi V, Ranavolo A, Frascarelli
M, Santilli V, Spacca G. Effectiveness of radial shock-wave therapy for calcific tendinitis
of the shoulder: single-blind, randomized clinical study. Physical Therapy 2006;86:672–
682.
[2] Kolk A, Yang KG, Tamminga R, van der Hoeven H. Radial extracorporeal shock-wave
therapy in patients with chronic rotator cuff tendinitis: a prospective randomised double-
blind placebo-controlled multicentre trial. Bone Joint J 2013;95-B:1521-1526.
[3] Engebretsen K, Grotle M, Bautz-Holter E, Ekeberg OM, Juel NG, Brox JI. Supervised
exercises compared with radial extracorporeal shock-wave therapy for subacromial
shoulder pain: 1-year results of a single-blind randomized controlled trial. Phys Ther
2011;91(1):37-47.
[4] Hussein AZ, Donatelli RA. The efficacy of radial extracorporeal shockwave therapy in
54
shoulder adhesive capsulitis: a prospective, randomised, double-blind, placebo-controlled, clinical
study. Eur J Physiother 2016;18:63-76.
[5] Liu S, Zhai L, Shi Z, Jing R, Zhao B, Xing G. Radial extracorporeal pressure pulse therapy for
the primary long bicipital tenosynovitis a prospective randomized controlled study. Ultrasound Med
Biol 2012;38:727-735.
[6] Damian M, Zalpour C. Trigger point treatment with radial shock waves in musicians with
nonspecific shoulder-neck pain: data from a special physio outpatient clinic for musicians. Med
Probl Perform Art 2011;26(4):211-217.
[7] Gündüz R, Malas FÜ, Borman P, Kocaoğlu S, Özçakar L. Physical therapy, corticosteroid
injection, and extracorporeal shock wave treatment in lateral epicondylitis. Clinical and
ultrasonographical comparison. Clin Rheumatol 2012;31(5):807-812.
[8] Spacca G, Necozione S, Cacchio A. Radial shock wave therapy for lateral epicondylitis: a
prospective randomised controlled single-blind study. Eura Medicophys 2005;41:17-25.
[9] Capan N, Esmaeilzadeh S, Oral A, Basoglu C, Karan A, Sindel D. radial extracorporeal shock
wave therapy is not more effective than placebo in the management of lateral epicondylitis: a
double-blind, randomized, placebo-controlled trial. Am J Phys Med Rehabil 2016;95:495-506.
[10] Lee SS, Kang S, Park NK, Lee CW, Song HS, Sohn MK, Cho KH, Kim JH. Effectiveness of
initial extracorporeal shock wave therapy on the newly diagnosed lateral or medial epicondylitis.
Ann Rehabil Med 2012;36:681-687.
[11] Wu YT, Ke MJ, Chou YC, Chang CY, Lin CY, Li TY, Shih FM, Chen LC. Effect of radial shock
wave therapy for carpal tunnel syndrome: A prospective randomized, double-blind, placebo-
controlled trial. J Orthop Res 2016;34:977-984.
[12] Rompe JD, Segal NA, Cacchio A, Furia JP, Morral A, Maffulli N. Home training, local
corticosteroid injection, or radial shock wave therapy for greater trochanter pain syndrome. Am J
Sports Med 2009;37:1981-1990.
[13] Weckström K, Söderström J. Radial extracorporeal shockwave therapy compared with manual
therapy in runners with iliotibial band syndrome. J Back Musculoskel Rehab 2016;29:161-170.
[14] Rompe JD, Nafe B, Furia JP, Maffulli N: Eccentric loading, shock-wave treatment, or a wait-
and-see policy for tendinopathy of the main body of tendo Achillis: a randomized controlled trial.
Am J Sports Med 2007;35:374-383.
[15] Rompe JD, Furia J, Maffulli N: Eccentric loading compared with shock wave treatment for
chronic insertional achilles tendinopathy. A randomized, controlled trial. J Bone Joint Surg Am
2008;90:52-61.
[16] Rompe JD, Furia J, Maffulli N: Eccentric loading versus eccentric loading plus shock-wave
treatment for midportion achilles tendinopathy: a randomized controlled trial. Am J Sports Med
2009;37:463-470.
54

modalities;
modalities
c) Energy flux density; EFD+: positive energy flux density; EFDTotal: total energy flux
density
d) Not specified
e) Joeunmedical, Korea
---
[1] Chow IH, Cheing GL: Comparison of different energy densities of extracorporeal
shock wave therapy (ESWT) for the management of chronic heel pain. Clin Rehabil
2007;21:131-141.
[2] Gerdesmeyer L, Frey C, Vester J, Maier M, Weil L Jr, Weil L Sr, Russlies M, Stienstra
J, Scurran B, Fedder K, Diehl P, Lohrer H, Henne M, Gollwitzer H. Radial extracorporeal
shock wave therapy is safe and effective in the treatment of chronic recalcitrant plantar
fasciitis: results of a confirmatory randomized placebo-controlled multicenter study. Am J
Sports Med 2008;36:2100-2109.
[3] Ibrahim MI, Donatelli RA, Schmitz C, Hellman MA, Buxbaum F. Chronic plantar
fasciitis treated with two sessions of radial extracorporeal shock wave therapy. Foot
55
Ankle Int. 2010;31:391–397.
[4] Rompe JD, Cacchio A, Weil L Jr, Furia JP, Haist J, Reiners V, Schmitz C, Maffulli N. Plantar
fascia-specific stretching versus radial shock-wave therapy as initial treatment of plantar
fasciopathy. J Bone Joint Surg Am 2010;92:2514-2522.
2010;31:1-9.
[6] Shaheen AAM. Comparison of three different treatment protocols of low-energy radial
extracorporeal shock wave therapy for management of chronic plantar fasciitis. Ind J Physiother
Occup Ther 2010;4:8-12.
[7] Rompe JD, Furia J, Cacchio A, Schmitz C, Maffulli N. Radial shock wave treatment alone is
less efficient than radial shock wave treatment combined with tissue-specific plantar fascia-
stretching in patients with chronic plantar heel pain. Int J Surg 2015;24:135-142.
[8] Konjen N, Napnark T, Janchai S. A comparison of the effectiveness of radial extracorporeal
shock wave therapy and ultrasound therapy in the treatment of chronic plantar fasciitis: a
randomized controlled trial. J Med Assoc Thai 2015;98:S49-S56.
[9] Eslamian F, Shakouri SK, Jahanjoo F, Hajialiloo M, Notghi F. Extra corporeal shock wave
therapy versus local corticosteroid injection in the treatment of chronic plantar fasciitis, a single
blinded randomized clinical trial. Pain Med 2016;17:1722-1731.
[10] Krukowska J, Wrona J, Sienkiewicz M, Czernicki J. A comparative analysis of analgesic
efficacy of ultrasound and shock wave therapy in the treatment of patients with inflammation of the
attachment of the plantar fascia in the course of calcaneal spurs. Arch Orthop Trauma Surg
2016;136:1289-1296.
[11] Mehra A, Zaman T, Jenkin AI: The use of a mobile lithotripter in the treatment of tennis elbow
and plantar fasciitis. Surgeon 2003;1:290-292.
[12] Cho YS, Park SJ, Jang SH, Choi YC, Lee JH, Kim JS. Effects of the combined treatment of
extracorporeal shock wave therapy (ESWT) and stabilization exercises on pain and functions of
patients with myofascial pain syndrome. J Physical Ther Sci 2012;24(11):1319-1323
[13] Lee JH, Han EY. A Comparison of the effects of PNF, ESWT, and TPI on pain and function of
patients with myofascial pain syndrome. J Phys Ther Sci 2013;25:341-344.
[14] Li JW, Zheng S, Zhang JC, Huang J. 不同频率冲击波针灸对膝骨性关节炎患者疼痛及功能活
动的影响 [Effect of acupuncture plus different frequency shock-wave interventions on pain
reactions and motor function in knee osteoarthritis patients]. Acupunct Res 2015;40:300-303).
[15] Vidal X, Morral A, Costa L, Tura M. Radial extracorporeal shock wave therapy (rESWT) in the
treatment of spasticity in cerebral palsy: A randomized, placebo-controlled clinical trial.
NeuroRehabilitation 2011;29:413-419.
[16] Dymarek R, Taradaj J, Rosińczuk J. The effect of radial extracorporeal shock wave stimulation
on upper limb spasticity in chronic stroke patients: a single-blind, randomized, placebo-controlled
study. Ultrasound Med Biol 2016;42:1862-1875.
55

modalities;
modalities
c) Principle of generating focused shock waves (PE, piezoelectric; EH, electrohydraulic;

EM, electromagnetic)
d) Energy flux density (EFD+: positive energy flux density; EFDTotal: total energy flux
density; ?, not specified whether the reported energy flux density was EFD+ or
EFDTotal
e) Not specified
---
[1] Rompe JD, Bürger R, Hopf C, Eysel P. Shoulder function after extracorporal shock
wave therapy for calcific tendinitis. J Shoulder Elbow Surg 1998;7:505-509.
[2] Seil R, Rupp S, Hammer DS, Ensslin S, Gebhardt T, Kohn D. Extrakorporale
Stosswellentherapie bei der Tendionosis calcarea der Rotatorenmanschette: Vergleich
verschiedener Behandlungsprotokolle. [Extracorporeal shockwave therapy in tendionosis
calcarea of the rotator cuff: comparison of different treatment protocols] [Article in
German]. Z Orthop Ihre Grenzgeb 1999;137:310-315.
[3] Loew M, Daecke W, Kusnierczak D, Rahmanzadeh M, Ewerbeck V. Shock-wave
56
therapy is effective for chronic calcifying tendinitis of the shoulder. J Bone Joint Surg Br
1999;81:863-867.
[4] Schmitt J, Haake M, Tosch A, Hildebrand R, Deike B, Griss P. Low-energy extracorporeal
shock-wave treatment (ESWT) for tendinitis of the supraspinatus. A prospective, randomised
study. J Bone Joint Surg. Br. 2001;83–B:873–876.
[5] Haake M, Deike B, Thon A, Schmitt J. Exact focusing of extracorporeal shock wave therapy for
calcifying tendinopathy. Clin Orthop Relat Res. 2002;(397):323–331.
[6] Cosentino R, De Stefano R, Selvi E, Frati E, Manca S, Frediani B, Marcolongo R.
Extracorporeal shock wave therapy for chronic calcific tendinitis of the shoulder: single blind study.
Ann Rheum Dis 2003;62:248-250.
[7] Gerdesmeyer L, Wagenpfeil S, Haake M, Maier M, Loew M, Wörtler K, Lampe R, Seil R, Handle
G, Gassel S, Rompe JD. Extracorporeal shock wave therapy for the treatment of chronic calcifying
tendonitis of the rotator cuff: a randomized controlled trial. JAMA. 2003;290:2573-2580.
[8] Perlick L, Luring C, Bathis H, Perlick C, Kraft C, Diedrich O. Efficacy of extracorporal shock-
wave treatment for calcific tendinitis of the shoulder: experimental and clinical results. J Orthop Sci
2003;8:777-783.
[9] Pan PJ, Chou CL, Chiou HJ, Ma HL, Lee HC, Chan RC. Extracorporeal shock wave therapy for
chronic calcific tendinitis of the shoulders: a functional and sonographic study. Arch Phys Med
Rehabil. 2003;84:988-993.
[10] Peters J, Luboldt W, Schwarz W, Jacob V, Herzog C, Vogl TJ. Extracorporeal shock wave
therapy in calcific tendinitis of the shoulder. Skeletal Radiology 2004;33:712–718.
[11] Sabeti M, Dorotka R, Goll A, Trieb K. Extracorporeal shock wave therapy in the treatment of
calcific tendinitis of the rotator cuff. Am J Sports Med. 2005;33:1365–1368.
[12] Hsu CJ, Wang DY, Tseng KF, Fong YC, Hsu HC, Jim YF. Extracorporeal shock wave therapy
for calcifying tendinitis of the shoulder. J Shoulder Elbow Surg 2008;17(1):55-59.
[13] Hearnden A, Desai A, Karmegam A, Flannery M. Extracorporeal shock wave therapy in
chronic calcific tendonitis of the shoulderd – is it effective? Acta Orthop Belg. 2009;75:25–31.
[14] Tornese D, Mattei E, Bandi M, Zerbi A, Quaglia A, Melegati G. Arm position during
extracorporeal shock wave therapy for calcifying tendinitis of the shoulder: a randomized study.
Clin Rehabil. 2011;25:731–739.
[15] Ioppolo F, Tattoli M, Di Sante L, Attanasi C, Venditto T, Servidio M, Cacchio A, Santilli V.
Extracorporeal shock-wave therapy for supraspinatus calcifying tendinitis: a randomized clinical
trial comparing two different energy levels. Phys Ther 2012;92:1376-85
56

modalities;
modalities

EFDTotal
e) Not specified
---
[1] Haake M, Sattler A, Gross MW, Schmitt J, Hildebrandt R, Muller HH. Comparison of
extracorporeal shockwave therapy (ESWT) with roentgen irradiation in supraspinatus
tendon syndrome -- a prospective randomized single-blind parallel group comparison. Z
Orthop Ihre Grenzgeb. 2001;139:397–402.
[2] Groß MW, Sattler A, Haake M, Schmitt J, Hildebrandt R, Müller HH, Engenhart-
Cabillic R. The value of radiotherapy in comparison with extracorporeal shockwave
therapy for supraspinatus tendinitis. Strahlenther Onkol. 2002;178:314–320.
[3] Schmitt J, Tosch A, Hünerkopf M, Haake M. Die extrakorporale Stosswellentherapie
57
(ESWT) als therapeutische Option beim Supraspinatussehnensyndrom? Ein-Jahres-Ergebnisse
einer placebokontrollierten Studie. [Extracorporeal shockwave therapy (ESWT) as therapeutic
option in supraspinatus tendon syndrome? One year results of a placebo controlled study] [Article
in German]. Orthopade 2002;31:652-657.
[4] Speed CA, Richards C, Nichols D, Burnet S, Wies JT, Humphreys H, Hazleman BL.
Extracorporeal shock-wave therapy for tendonitis of the rotator cuff. A double-blind, randomised,
controlled trial. J Bone Joint Surg Br. 2002b;84:509-512.
[5] Saggini R, Cavezza T, Di Pancrazio L, Pisciella V, Saladino G, Zuccaro MC, Bellomo RG.
Treatment of lesions of the rotator cuff. J Biol Regul Homeost Agents 2010;24:453-459.
[6] Galasso O, Amelio E, Riccelli DA, Gasparini G. Short-term outcomes of extracorporeal shock
wave therapy for the treatment of chronic non-calcific tendinopathy of the supraspinatus: a double-
blind, randomized, placebo-controlled trial. BMC Musculoskeletal Disord. 2012;13:86.
[7] Santamato A, Panza F, Notarnicola A, Cassatella G, Fortunato F, de Sanctis JL, Valeno G,
Kehoe PG, Seripa D, Logroscino G, Fiore P, Ranieri M. Is extracorporeal shockwave therapy
combined with isokinetic exercise more effective than extracorporeal shockwave therapy alone for
subacromial impingement syndrome? A randomized clinical trial. J Orthop Sports Phys Ther
2016;46:714-725.
57

modalities;
modalities

EFDTotal
---
[1] Rompe JD, Hope C, Küllmer K, Heine J, Bürger R. Analgesic effect of extracorporeal
shock-wave therapy on chronic tennis elbow. J Bone Joint Surg Br 1996;78:233-237.
[2] Rompe JD, Hopf C, Küllmer K, Heine J, Bürger R, Nafe B. Low-energy extracorporal
shock wave therapy for persistent tennis elbow. Int Orthop 1996;20:23-27.
[3] Rompe JD, Eysel P, Hopf C, Krischek O, Vogel J, Burger R, Jage J, Heine J.
Extrakorporale Sstosswellentherapie in der Orthopädie. Positive Ergebnisse beim
Tennisellenbogen und der Tendinosis calcarea der Schulter [Extracorporeal shockwave
therapy in orthopedics. Positive results in tennis elbow and tendinosis calcarea of the
shoulder] [Article in German]. Fortschr Med 1997;115:26,29-33
[4] Rompe JD, Krischek O, Eysel P, Hopf C, Jage J. Chronische Insertionstendopathie
58
am lateralen Epicondylus humeri. Ergebnisse der extrakorporalen Stosswellenapplikation [Results
of extracorporeal shock-wave application in lateral elbow tendopathy] [Article in German]. Schmerz
1998;12:105-111.
[5] Crowther MA, Bannister GC, Huma H, Rooker GD. A prospective, randomised study to
compare extracorporeal shock-wave therapy and injection of steroid for the treatment of tennis
elbow. J Bone Joint Surg Br 2002;84:678-679.
[6] Haake M, Konig IR, Decker T, Riedel C, Buch M, Muller H. Extracorporeal shock wave therapy
in the treatment of lateral epicondylitis: a randomized multicenter trial. J Bone Joint Surg Am.
2002;84–A:1982–1991.
[7] Haake M, Böddeker IR, Decker T, Buch M, Vogel M, Labek G, Maier M, Loew M, Maier-
Boerries O, Fischer J, Betthäuser A, Rehack HC, Kanovsky W, Müller I, Gerdesmeyer L, Rompe
JD. Side-effects of extracorporeal shock wave therapy (ESWT) in the treatment of tennis elbow.
Arch Orthop Trauma Surg. 2002;122:222–228.
[8] Speed CA, Nichols D, Richards C, Humphreys H, Wies JT, Burnet S, Hazleman BL.
Extracorporeal shock wave therapy for lateral epicondylitis – a double blind randomised controlled
trial. J Orthop Res. 2002;20:895–898.
[9] Melikyan EY, Shahin E, Miles J, Bainbridge LC. Extracorporeal shock-wave treatment for tennis
elbow. A randomised double-blind study. J Bone Joint Surg Br 2003;85:852-855.
[10] Rompe JD, Decking J, Schoellner C, Theis C. Repetitive low-energy shock wave treatment for
chronic lateral epicondylitis in tennis players. Am J Sports Med. 2004;32:734–743.
[11] Chung B, Wiley JP. Effectiveness of extracorporeal shock wave therapy in the treatment of
previously untreated lateral epicondylitis: a randomized controlled trial. Am J Sports Med.
2004;32:1660–1667.
[12] Melegati G, Tornese D, Bandi M, Rubini M. Comparison of two ultrasonographic localization
techniques for the treatment of lateral epicondylitis with extracorporeal shock wave therapy: a
randomized study. Clin Rehabil 2004;18:366-370.
[13] Pettrone FA, McCall BR. Extracorporeal shock wave therapy without local anesthesia for
chronic lateral epicondylitis. J Bone Joint Surg Am. 2005;87:1297–1304.
[14] Ozturan KE, Yucel I, Cakici H, Guven M, Sungur I. Autologous blood and corticosteroid
injection and extracoporeal shock wave therapy in the treatment of lateral epicondylitis.
Orthopedics 2010;33:84-91.
58

modalities;
modalities

EFDTotal
---
[1] Rompe JD, Kullmer K, Riehle H-M, Herbsthofer B, Eckardt A, Burger R, Nafe B, Eysel
P. Effectiveness of low-energy extracorporal shock waves for chronic plantar fasciitis.
Foot Ankle Surg 1996;2:215-221
[2] Rompe JD, Hopf C, Nafe B, Burger R. Low-energy extracorporeal shock wave
therapy for painful heel: a prospective controlled single-blind study. Arch Orthop Trauma
Surg 1996;115:75-79.
[3] Krischek O, Rompe JD, Herbsthofer B, Nafe B. Symptomatische niedrig-energetische
Stosswellentherapie bei Fersenschmerzen und radiologisch nachweisbarem plantaren
Fersensporn [Symptomatic low-energy shockwave therapy in heel pain and radiologically
detected plantar heel spur] [Article in German]. Z Orthop Ihre Grenzgeb 1998;136:169-
59
174.
[4] Cosentino R, Falsetti P, Manca S, De Stefano R, Frati E, Frediani B, Baldi F, Selvi E,
Marcolongo R. Efficacy of extracorporeal shock wave treatment in calcaneal enthesophytosis. Ann
Rheum Dis 2001;60:1064-1067.
[5] Ogden JA, Alvarez R, Levitt R, Cross GL, Marlow M. Shock wave therapy for chronic proximal
plantar fasciitis. Clin Orthop Relat Res. 2001;387:47¬59.
[6] Buch M, Knorr U, Fleming L, Theodore G, Amendola A, Bachmann C, Zingas C, Siebert WE.
Extrakorporale Stosswellentherapie beim symptomatischen Fersensporn. Eine Übersicht
[Extracorporeal shockwave therapy in symptomatic heel spurs. An overview] [Article in German].
Orthopaede 2002;31:637–644.
[7] Buchbinder R, Ptasznik R, Gordon J, Buchanan J, Prabaharan V, Forbes A. Ultrasound-guided
extracorporeal shock wave therapy for plantar fasciitis: a randomized controlled trial. J Am Med
Assoc 2002;288:1364-1372.
[8] Rompe JD, Schoellner C, Nafe B. Evaluation of low-energy extracorporeal shock-wave
application for treatment of chronic plantar fasciitis. J Bone Joint Surg Am 2002;84:335–341.
[9] Haake M, Buch M, Schoellner C, Goebel F, Vogel M, Mueller I, Hausdorf J, Zamzow K, Schade-
Brittinger C, Mueller HH. Extracorporeal shock wave therapy for plantar fasciitis: randomised
controlled multicentre trial. Brit Med J 2003;327:75.
[10] Hammer DS, Adam F, Kreutz A, Kohn D, Seil R. Extracorporeal shock wave therapy (ESWT)
in patients with chronic proximal plantar fasciitis: a 2-year follow-up. Foot Ankle Int 2003;24:823-
828.
[11] Rompe JD, Decking J, Schoellner C, Nafe B. Shock wave application for chronic plantar
fasciitis in running athletes. A prospective, randomized, placebo-controlled trial. Am J Sports Med.
2003;31:268–275.
59

modalities;
modalities

EFDTotal
e) Not specified
---
[1] Speed CA, Nichols D, Wies J, Humphreys H, Richards C, Burnet S, Hazleman BL.
Extracorporeal shock wave therapy for plantar fasciitis. A double blind randomised
controlled trial. J Orthop Res. 2003;21:937–940.
[2] Ogden JA, Alvarez RG, Levitt RL, Johnson JE, Marlow ME. Electrohydraulic high-
energy shock-wave treatment for chronic plantar fasciitis. J Bone Joint Surg Am.
2004;86:2216–2228.
[3] Theodore GH, Buch M, Amendola A, Bachmann C, Fleming LL, Zingas C.
Extracorporeal shock wave therapy for the treatment of plantar fasciitis. Foot Ankle Int.
60
2004;25:290–297.
[4] Rompe JD, Meurer A, Nafe B, Hofmann A, Gerdesmeyer L. Repetitive low-energy shock wave
application without local anesthesia is more efficient than repetitive low-energy shock wave
application with local anesthesia in the treatment of chronic plantar fasciitis. J Orthop Res
2005;23:931-941.
[5] Porter MD, Shadbolt B. Intralesional corticosteroid injection versus extracorporeal shock wave
therapy for plantar fasciopathy. Clin J Sport Med. 2005;15:119–124.
[6] Dorotka R, Sabeti M, Jimenez-Boj E, Goll A, Schubert S, Trieb K. Location modalities for
focused extracorporeal shock wave application in the treatment of chronic plantar fasciitis. Foot
Ankle Int 2006;27:943-947.
[7] Kudo P, Dainty K, Clarfield M, Coughlin L, Lavoie P, Lebrun C. Randomized, placebo-
controlled, double-blind clinical trial evaluating the treatment of plantar fasciitis with an
extracoporeal shockwave therapy (ESWT) device: a North American confirmatory study. J Orthop
Res. 2006;24:115–123.
[8] Gollwitzer H, Diehl P, von Korff A, Rahlfs VW, Gerdesmeyer L. Extracorporeal shock wave
therapy for chronic painful heel syndrome: a prospective, double blind, randomized trial assessing
the efficacy of a new electromagnetic shock wave device. J Foot Ankle Surg. 2007;46:348-357.
[9] Liang HW, Wang TG, Chen WS, Hou SM. Thinner plantar fascia predicts decreased pain after
extracorporeal shock wave therapy. Clin Orthop Relat Res. 2007;(460):219–225.
[10] Tornese D, Mattei E, Lucchesi G, Bandi M, Ricci G, Melegati G. Comparison of two
extracorporeal shock wave therapy techniques for the treatment of painful subcalcaneal spur. A
randomized controlled study. Clin Rehabil 2008;22:780-787.
2010;31:1-9.
[12] Saxena A, Fournier M, Gerdesmeyer L, Gollwitzer H. Comparison between extracorporeal
shockwave therapy, placebo ESWT and endoscopic plantar fasciotomy for the treatment of chronic
plantar heel pain in the athlete. Muscles Ligaments Tendons J 2013;2:312-316.
60

modalities;
modalities

EFDTotal
---
[1] Costa ML, Shepstone L, Donell ST, Thomas TL. Shock wave therapy for chronic
Achilles tendon pain: a randomized placebo-controlled trial. Clin Orthop Relat Res
2005;440:199-204.
[2] Rasmussen S, Christensen M, Mathiesen I, Simonsen O. Shockwave therapy for
chronic Achilles tendinopathy: a double-blind, randomized clinical trial of efficacy. Acta
Orthopaedica 2008;79:249–256.
[3] Wang CJ, Wang FS, Huang CC, Yang KD, Weng LH, Huang HY. Treatment for
osteonecrosis of the femoral head: comparison of extracorporeal shock waves with core
decompression and bone-grafting. J Bone Joint Surg Am 2005;87:2380-2387.
[4] Wang CJ, Liu HC, Fu TH. The effects of extracorporeal shockwave on acute high-
61
energy long bone fractures of the lower extremity. Arch Orthop Trauma Surg 2007;127:137-142.
[5] Larking AM, Duport S, Clinton M, Hardy M, Andrews K. Randomized control of extracorporeal
shock wave therapy versus placebo for chronic decubitus ulceration. Clin Rehabil 2010;24:222-
229.
[6] Kraus M, Reinhart E, Krause H, Reuther J. Niederenergetische extrakorporale
Stosswellentherapie (ESWT) zur Behandlung von Myogelosen des M. masseter. [Low energy
extracorporeal shockwave therapy (ESWT) for treatment of myogelosis of the masseter muscle].
Mund Kiefer Gesichtschir. 1999;3:20-23.
[7] Taheri P, Vahdatpour B, Andalib S. Comparative study of shock wave therapy and Laser
therapy effect in elimination of symptoms among patients with myofascial pain syndrome in upper
trapezius. Adv Biomed Res 2016;5:138.
[8] Santamato A, Notarnicola A, Panza F, Ranieri M, Micello MF, Manganotti P, Moretti B,
Fortunato F, Filoni S, Fiore P. SBOTE study: extracorporeal shock wave therapy versus electrical
stimulation after botulinum toxin type a injection for post-stroke spasticity-a prospective randomized
trial. Ultrasound Med Biol 2013;39:283-291.
[9] Abdel Gawag HA, Abdel Karim AE, Mohammed AH. Shock wave therapy for spastic plantar
flexor muscles in hemiplegic cerebral palsy children. Egypt J Med Hum Gen 2015;16:269-275.
61
Abbreviation:
> R, radial ESWT device.
62
Abbreviations:
> F-EH, focused ESWT device, electrohydraulic principle.
> F-EM, focused ESWT device, electromagnetic principle.
> F-PE, focused ESWT device, piezoelectric principle.
63
Abbreviations:
> F-EH, focused ESWT device, electrohydraulic principle.
> F-EM, focused ESWT device, electromagnetic principle.
> F-PE, focused ESWT device, piezoelectric principle.
64
* It is obvious that, for example, fESWT is more efficacious than rESWT in the treatment
of deep fracture nonunions, because the latter can not be reached with radial
extracorporeal shock waves. In this case, however, rESWT would not be used
appropriately.
** In particular, it is critical to note that most of the fESWT devices that were used in
those studies that are listed in the PEDro database are not marketed anymore today.
65

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Specifically, these materials do not provide any specific application settings of

The Encyclopedia Britannica online defines shock waves as a

It is important to note that these definitions do not at all contribute to our

When performing treatments of the musculoskeletal indications presented here, the

Approximately 80% of all patients report a substantial improvement of the clinical

Furthermore, at least one minor diagnostic criteria must be met:

OA cartilage contains a higher percentage of cells undergoing apoptosis than normal

The goals of management for patients with ILBP are to

ESWT is an alternative to conservative treatment and should be applied before considering

The disease usually presents in four stages:

The incidence is approximately 3% in the healthy population, and approximately 7% in

Subacromial pain syndrome

With respect to therapy, three different stages of SIS are distinguished:

The population prevalence is approximately 2%, with peak incidence occurring at 40 to

The initial treatment should be conservative including rest, physiotherapy, and

Therapy of symptomatic tendon tears comprises rest, antiinflammatory medications and

Patients not responding to conservative treatment should be subjected to rESWT.

Surgery should also be considered for recalcitrant cases of MTSS.

As in case of insertional Achilles tendinopathy, the etiology of MPAT is likely

Patients not responding to conservative treatment shall be subjected to ESWT.

Patients not responding to conservative treatment shall be subjected to ESWT.

Patients not responding to conservative treatment (approximately 10% of all patients)

According to the University of Texas Wound Classification system, wounds are

Wound healing is classically divided into four phases:

A substantial number of women develop secondary lymphedema after surgical treatment

Lymphedema is divided into the following stages:

Diagnosis of lymphedema is based on the clinical features of the disease (extremity

NEVER treat an infected wound with shock waves!

NEVER treat a Grade III wound with shock waves!

These are the criteria for inclusion of RCTs in PEDro:

De Morton [4] confirmed the validity of the PEDro scale.

Comparison of groups was performed using Kruskal-Wallis test (nonparametric analysis of

Furthermore, absolute and relative numbers of studies performed with respectively

The results of this analysis are shown on the following pages.

[4] Gerdesmeyer L, Maier M, Haake M, Schmitz C: Physikalisch-technische Grundlagen der

The results of this analysis can be summarized as follows:

Furthermore, in 17 RCTs on fESWT with positive outcome in PEDro an electrohydraulic (EH)

These data can be interpreted as follows:

One should also consider the following:

[2] Gerdesmeyer L, Maier M, Haake M, Schmitz C: Physikalisch-technische Grundlagen der

Abbreviations used in this table:

> Records, total number of records.

These data can be interpreted as follows:

b) Outcome of the study:

b) Outcome of the study:

b) Outcome of the study:

c) Principle of generating focused shock waves (PE, piezoelectric; EH, electrohydraulic;

b) Outcome of the study:

c) Principle of generating focused shock waves (PE, piezoelectric; EH, electrohydraulic;

b) Outcome of the study:

c) Principle of generating focused shock waves (PE, piezoelectric; EH, electrohydraulic;

b) Outcome of the study:

c) Principle of generating focused shock waves (PE, piezoelectric; EH, electrohydraulic;

b) Outcome of the study:

c) Principle of generating focused shock waves (PE, piezoelectric; EH, electrohydraulic;

b) Outcome of the study:

c) Principle of generating focused shock waves (PE, piezoelectric; EH, electrohydraulic;

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