ENTHESOPATHIES

KNOWLEDGE UPDATE
ULRICH DREISILKER

L8V8L10 Jt;
1st edition November 2020
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Author: Ulrich Dreisilker

Pictures: Oliver Kirstein, Simone Herbener
English Translation from German: Henriette Backer

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CONTENTS ESWT - an updated overview 18

Shock wave therapy vs. pressure wave therapy 23

Physical and technical differentiation 24

Shock waves: mechanism of action 28

ESWT - from mechanistic hypothesis to biological response

- angiogenesis, NO, eNOS, growth factors (VEGF etc.) 29
ESWT and biological response: analgesia 33
ESWT and biological response: growth factor
TGF-beta 1, collagen I and Ill 34
ESWT and biological response: mechanotransduction 35
ESWT and biological response: stem cells 38

Pressure waves: mechanism of action 40

Pressure wave energy, mechanotransduction 41
Pressure wave energy, myofascial trigger points 42
Pressure wave energy, fascia 44
What is EMTT® (Extracorporeal Magnetotransduction Therapy)? 45
Physical fundamentals of EMTT® 47
General treatment information and treatment fundamentals 50

Patient positioning 51
Shock wave and pressure wave dosage, shock wave navigation
by patient feedback 56
Procedural guidance for ESWT 57
Criteria for selecting shock wave or pressure wave technology 59
Combination of shock wave and pressure wave technology 60
Suggested ESWT procedure - Regimen A: combined shock wave (SW)
and pressure wave (PW) treatment 61
Suggested ESWT procedure - Regimen B: pressure wave (PW) treatment 62

Sonography 63

Long-established and newer ESWT indications 68

Introduction 69
Long-established indications 70

Shoulder impingement/tendinopathy with or without

calcifications, rotator cuff syndrome 71

Lateral and medial humeral epicondylopathy 76

lnsertional tendinopathy of distal biceps tendon 80

Achillodynia or mid-portion tendinopathy, insertional

tendinopathy of Achilles tendon 80

Plantar fasciitis - heel spur 85

Jumper's or runner's knee, patellar insertional tendinopathy 89
Other indications in sports medicine 93
Hamstring tendinopathy (ischiocrural muscles) 94
Hip adductor tendinopathy 97

lliotibial band tendinopathy 99

Anterior tibial syndrome 102

Shin splint (medial tibial stress syndrome and tendinopathy

of the peroneal tendons) 103

lnsertional tendinopathy of the pectoralis and rhomboid muscles 106

lnsertional tendinopathy of the triceps 108

Newer indications 109

Tendinopathy and myofascial trigger points involving

the spinal column 110
Cervicooccipital and cervicothoracic regions of the spinal column 111

Lumbar spine region and gluteal region 117

Erector trunci muscles (multifidus and rotator muscles;

longissimus thoracis muscle, iliocostalis thoracis muscle) 117

Piriformis syndrome 125

Carpal tunnel syndrome (CTS) 129

Trigger finger (stenosing tenosynovitis) 133

De Quervain's tenosynovitis 134

Morton's neuroma 134
Frozen shoulder 137

Dupuytren's contracture 139

ESWT and fibrosis 140
Closing remarks and outlook
Acknowledgements
List of abbreviations
List of references
THE EDITOR AND AUTHOR
Ulrich Dreisilker, a specialist in orthopae­
dics, sports medicine and chirotherapy,
has been a shock wave therapy
practitioner for more than 25 years.
He has, in numerous presentations and
courses, widely shared his knowledge and
experience gained within the field
of ESWT.
Dreisilker is a co-founder of DIGEST, the
German-language International Society
for Extracorporeal Shock Wave Therapy,
having served this organization over
many years in roles including board
member and president. He is currently
an instructor for DIGEST and was appoin­
ted an honorary member (senator) four
years ago.
Dr. med. Ulrich Dreisilker
Orthopaedic specialist, chiropractic
medicine, naturopathic medicine, and
sports medicine
Private practice Dr. med. U. Dreisi/ker,
Mettmann, Germany
1968 Licence and doctorate
Specialist orthopaedic training:
Casualty hospitals run by .,Berufs­
genossenschaften" (Employers' Liability
Insurance Associations)
Duisburg-Buchholz, Ludwigshafen­
Oggersheim, Orthopaedic University
Clinic Essen.
Consultants' practice in Mettmann,
initially group practice, then individual
practice.
1992 Practice transferred to Velbert.
1995 Foundation of IGESTO (Interna­
tionale Gesel/schaft fiir StoBwellen­
therapie in der Orthopadie / International
Society for Orthopaedic Shock Wave
Therapy), which merged with the DGST
(Deutsche Gesellschaft fiir StoBwellen­
therapie / German Society for Shock
Wave Therapy) and became today's
DIGEST. President and board member of
DIGEST for many years.
2002 DIGEST lecturer, honorary president
of DIGEST since 2005
2001 End of Statutory Health Insurance
work, then private practice in Mettmann.
FOREWORD
Shock wave therapy has made rapid strides since it was first used for musculo­
skeletal pathologies in the early 1990s. The unravelling of mechanotransduc­
tion mechanisms enabled shock wave therapy to be understood as a regene­
rative method, thus paving the way for ever more new applications. Practi­
tioners who routinely employ shock wave therapy need to upskill themselves
continuously to stay abreast of the latest developments.

With this new and updated monograph, my colleague Ulrich Dreisilker has
once again succeeded in clearly and comprehensively describing the state
of the art in shock wave therapy. Dreisilker is not only a pioneer of the Ger­
man shock wave scene. From an early stage, his publications have contri­
buted to the development and increasingly widespread use of this method.
As a founder member of DIGEST e.V. (the German-language International
Society for Extracorporeal Shock Wave Therapy), Ulrich Dreisilker is recog­
nized as a key figure and information disseminator in the field of ESWT.

It is all the more gratifying that, with this new book "Enthesopathies - Know­
ledge Update", we now have a revised edition of his reference work entitled
"Enthesopathies", now considered a classic in its field. This book can be seen
as a contribution that updates our knowledge and practice of shock wave the­
rapy - one that provides valuable tips for both newcomers to the field and
advanced users.

May I congratulate Ulrich Dreisilker on this very fine textbook, and wish all
those who read it the best of success and satisfaction in your work applying
shock wave therapy.

Augsburg, Germany; April 2020

Dr. med. Martin Ringeisen

Secretary-General, DIGEST e.V.
 ..
PREFACE
A growing evidence base concerning the mechanisms of action of shock wave
therapy resulted, about two years ago, in the decision to revise and expand
the reference work "Enthesopathies" (published by Leveho Buchverlag, 2010).

German and international literature produced on ESWT over the last decade
could fill a great many bookshelves. Animal studies and evidence-based
trials have contributed substantially to our understanding of how this therapy
works and helps. ESWT is now well established as a treatment for many muscu­
loskeletal disorders and diseases, even replacing certain surgical interventions.

Mechanical stimuli provided by ESWT open up signal transduction pathways

at cellular and molecular-biological level between the extracellular matrix
(ECM) and the cell interior. Growth factors are released. The activation of stem
cells by ESWT is generally what sets in motion the accelerated regeneration of
pathological tissue - as is the case with enthesopathies and tendinopathies,
the subject of this book.

Shock waves and pressure waves release trigger points by means of enhanced
blood circulation. They improve lymphatic drainage and offset the energy
deficiency of cellular mitochondria.

In a review article, K. Knobloch reports on positive observations made in

animal studies. Even low doses of shock wave energy stimulate growth of
lymphatic capillaries. Could this be a way of improving lymphatic drainage
and initiating the "recycling" of molecular protein fragments? Does it reduce,
or even eliminate altogether, the potential for fibrosis?

In K. Knobloch's view, ESWT appears to have an antifibrotic effect in patients

with Dupuytren's contracture, Ledderhose's disease, Peyronie's disease and
fibrotic scarring. Depending on dosage, shock waves block signal pathways,
including that for growth factor TGF-beta 1.
This new edition presents technological innovations and new treatment indi­
cations. A brief account is given of Extracorporeal Magnetotransduction The­
rapy (EMTT®), which evidently shows strong systemic action at depth and, in
conjunction with ESWT, promises to expand the spectrum of musculoskeletal
disorders that can be treated.

This new edition includes little of Pavel Novak's excellent, detailed chapter
headed 'Physical basics' in the first edition of this book. (Those who wish to
read it should refer to the original 2010 work.) Only a few physical aspects that
are relevant in a practitioner's day-to-day work are addressed in this edition.
Physics distinguishes, of course, between shock and pressure waves. In dif­
ferent ways, both techniques generate mechanical energy that biologically
influences tissue cells.

The fascial tissues include not only joint capsules and joint ligaments, but
also the tendons with their high collagen content. Without fascia, we could
neither move as we do, nor maintain our upright posture. We can do both
these things because - between the fixed points and stable elements that
bone constitutes - there exists an elastic network, held under tension, that
is made of chains of muscles and fascia. If the equilibrium of this system
(involving the tensegrity principle described by R. Buckminster Fuller) is
disturbed by internal or external factors, the system reacts - in the form of
muscle strain, myofascial trigger points and insertional tendinopathy.

Different indications call for different treatments. When are shock waves
used, when are pressure waves preferred, and when is a combination of both
desirable? These questions are addressed in a dedicated chapter.

The instructions given here on patient positioning during treatment are

proven practice. Low-energy doses are recommended as these are known to
be more effective. Most ESWT therapists have personally found this to be the
case in recent years.
The aim of this new edition is to refresh readers on, and augment, specialist
knowledge relating to ESWT.

Patients must be informed about the regenerative effect and the recovery
period needed. It is thus important they are aware that ESWT helps treat
chronic degenerative conditions only, and not acute pathologies.

By using clear, patient-friendly language to explain how ESWT works, we are

relating to the sufferer on an equal footing and creating trust. For example,
"A 50/50 chance" is the honest answer to a patient's question about the like­
lihood that their medial epicondylitis can be healed. This is because, if ESWT
does not succeed, the patient will recall this pre-treatment consultation and
understand that the chance of improvement was always limited. In this way,
the trust placed in the practitioner is not compromised.

That ESWT is performed by a competent physician (and not an assistant) is a

key factor in therapeutic success; this should, therefore, be standard practice.
This service is not one that can be delegated.

A question frequently asked by patients, namely how the shock waves used to
break up kidney stones can help with tendon problems or even wound healing
disorders, can be answered very straightforwardly. The skill lies in using low
levels of mechanical energy to open up biomolecular signal pathways, acti­
vate stem cells and stimulate new cell growth.

When a practitioner properly applies a therapy form that has proven effective
for many years, working in cooperation with well-informed patients, the out­
come is bound to be lasting success.

Mettmann, Germany; spring 2020

Ulrich Dreisilker
 ESWT - an updated overview

Despite evidence-based medicine (EBM) being brought to bear in this area,

and the existence of level I and II randomized, controlled trials (RCTs), many
health insurance companies - both statutory and, in some cases, private in­
surers - consider scientific evidence to be lacking with regard to the effective­
ness of ESWT in treating enthesopathies and tendinopathies. In the USA, how­
ever, the FDA, on the strength of scientific studies then available, approved
this therapy for the treatment of plantar fasciitis (as long ago as 2000) and
lateral epicondylitis (in 2002).

In its meeting of 19 April 2018, Germany's Federal Joint Committee (G-BA)

approved ESWT for plantar fasciitis as a treatment covered by health insu­
rance, but only if certain requirements are met.

Generally speaking, in comparison with other conservative treatments, no

other procedure that replaces surgery has been as closely scrutinized in scien­
tific research as ESWT has. This is the case not only for plantar fasciitis, but also
for other indications. The many excellent publications both in Germany and
elsewhere are a source of ongoing gratification to us as shock wave therapists.

Mechanistic explanations of the effect of ESWT, derived from urinary stone

fragmentation, are now obsolete and should be consigned to the 'stone age'
of orthopaedic ESWT, when the impact of shock waves was explained by refe­
rence to urological nephrolithiasis. False notions persist concerning 'fragmen­
tation' in cases of calcific tendinitis of the shoulder or, worse still, heel spur.

In his presentation on behalf of DIGEST at the 2017/2018 German Congress of

Orthopaedics and Traumatology (DKOU) held in Berlin, and again at the 2019
Annual Conference of the Association of Orthopaedists and Trauma Surge­
ons in South Germany (VSOU) held in Baden-Baden, one of the leading pio­
neers of ESWT, W. Schaden, neatly summed up the view now held concerning
this procedure's mode of action. Schaden explained that mechanical stimuli
from shock and pressure waves are transduced into biochemical signals in the
tissue's mechanosensory receptors and then transmitted to the cell nucleus
via cellular signal pathways and diverse cell structures (i.e. mechanotrans-

19
 duction). The process ends with the cellular response, namely the formation
of growth factors (including VEGF, which promotes angiogenesis and vascu­
logenesis) and the activation of stem cells that proliferate, differentiate and
mature. Cell migration and homing lead to tissue regeneration in damaged
areas.

ONGOING TRAINING IN ESWT

Two organizations aimed at the ESWT community - the ISMST (International
Society for Medical Shockwave Treatment) and DIGEST e.V. (German-language
International Society for Extracorporeal Shock Wave Therapy) - are cons­
tantly improving their offering of high-quality continuing medical education
(CME) seminars and courses that include final examinations, organized in
conjunction with medical associations and professional bodies. Experienced
instructors involved in research into ESWT talk about the latest findings and
practices.

The forerunner here is DIGEST e.V., which offers training leading to a certi­
ficate of professional competence in orthopaedic shock wave therapy. Doc­
tors and patients should look for this credential to help them choose the right
ESWT practitioner. DIGEST certification comes up for renewal after a certain
length of time, conditional on holders proving up-to-date knowledge and
skills. Ongoing training in ESWT, including regular upgrading courses, is also
already available. In this way, a non-invasive treatment option that has long
been embraced by patients is continuously future-proofed and kept up to
date.

NEWER INDICATIONS
As recently as 10 to 15 years ago, the spectrum of indications for ESWT was
restricted to calcific tendinitis of the shoulder, epicondylitis, heel spur and de­
layed healing of bone fractures / pseudarthrosis. It was about 15 years ago, at
a meeting of experts, that representatives of DIGEST and ISMST proposed ex­
tending the list of indications for ESWT to include trochanteric bursitis, patel­
lar tendinitis and achillodynia, despite a relative lack of positive studies. As the
evidence base back then was fairly insubstantial compared with today, this

20
 ESWT - an updated overview

prevented the range of indications from being expanded. The body of robust
scientific evidence today leaves no room for doubt. Clinical successes are an
argument in favour of ESWT application for achillodynia, and for tendinopa­
thies affecting the apex of the patella and greater trochanter.

Chronic tendinopathies, overstrained muscles and muscle imbalance, liga­

ment problems of considerable duration, and haematomas are increasingly
being treated with ESWT at clinical sessions for sports injuries. Fatigue frac­
tures or delayed fracture healing / pseudarthrosis of, for example, a metatar­
sal are not directly indicative of surgical intervention and are indicated only if
and when non-invasive ESWT proves unsuccessful.

Burns and scars, diabetic wounds and varicose ulcers can be successfully
treated using ESWT.

PRESSURE WAVE SYSTEMS, IMPROVED TRANSMITTERS, EXTRACORPOREAL

MAGNETOTRANSDUCTION THERAPY (EMTT®)
Shock waves have been used in orthopaedic pain therapy for more than 20
years now. Some 15 years ago, pressure wave systems were developed and
flooded the market, their simple production technology making them high­
ly affordable. Treatment outcomes achieved using pressure waves were also
successful and lasting. Advancements took place that improved the equip­
ment. The new "FALCON" handpiece for pressure wave application, used in
conjunction with the concave Ro 40 transmitter, both from STORZ MEDICAL
AG, allows trigger points to be localized - even in deep layers more than 3 cm
below the surface - when additional manual pressure is applied. Also benefi­
cial here is the "Deep Impact" (DI 15) transmitter made of titanium which, at
comparable penetration depth and with the same energy input, generates an
up to 50% higher acoustic output (ultrasound).

Rapid and reliable pinpoint localization of trigger points can be achieved with
the improved ergonomic shock wave handpiece "SEPIA", which has various
exchangeable stand-offs allowing therapeutic depths of up to 12.5-15 cm to
be reached. Therapists treating trigger points and fascia can now use not only

21
 the familiar oscillating transmitters but also the recently developed "PERI­
ACTOR" and "SPINE-ACTOR" models, with special, replaceable attachments
(all handpieces and transmitters mentioned are manufactured by STORZ
MEDICAL AG).

Future use of pulsed electromagnetic fields should be of great interest in the

treatment of musculoskeletal pathologies. It would appear that ESWT and
Extracorporeal Magnetotransduction Therapy (EMTT®) are mutually comple­
mentary, and not competing, procedures. Localization and local treatment
will remain associated with shock waves, and regional, systemic effects with
pulsed magnetic field therapy. Combining ESWT with EMTT® will augment
the range of indications treatable. Gerdesmeyer et al. report that EMTT® is
an additional means of treating musculoskeletal disorders, this having been
evidenced in a previous report (dated September 2017) drawing on findings
from 53 patients diagnosed with achillodynia.1 Comparative studies involving
extracorporeal shock waves and pressure waves, or these approaches in com­
bination with EMTT®, are not yet available. 2

The EMTT® system makes use of the high-energy range. This is the case both
for the strength of the magnetic fields and, primarily, for their frequency cha­
racteristics. The theoretical model posited is that, by means of as yet unex­
plored signal pathways and changes in transmembrane permeability, high­
energy waves are (following their biochemical conversion) introduced into
the cell interior where they stimulate the mitochondria.

22
SHOCK WAVE
THERAPY VS.
PRESSURE WAVE
THERAPY
 PHYSICAL AND TECHNICAL DIFFERENTIATION
Dr Pavel Novak

Electrohydraulic (EH), electromagnetic (EM) and piezoelectric (PE) systems

have one thing in common: the waves they produce are generated in the
water contained in the handpiece. This enables utilization of the acoustic im­
pedance of water, which is comparable to the impedance of biological tissue.
Since the energy loss inside the handpiece is limited, the convergent waves
can be introduced into the body with almost no loss at all.

Pressure waves are generated by means of a projectile located within a tube

and accelerated by compressed air, causing it to strike an impact plate that
acts as a transmitter. This transmitter introduces the pressure waves into
the body tissue. Unlike extracorporeal shock waves, pressure waves are not
generated in water.
Physically speaking, there is only one type of shock wave, namely the type that
can be focused. In strict physical terms, radial shock waves are actually pres­
sure waves. Hence, they should in fact be referred to as radial pressure waves.

The term "radial" describes the divergent pressure field generated by pres­
sure wave systems. Radial pressure waves develop their maximum energy
flux density at the point of entry into the body rather than at depth. From
the point of entry of the pressure waves, the energy flux density decreases
rapidly with increasing distance. In fact, the decrease in energy flux density
is proportional to the square of the distance, i.e. 1/r2• The term "radial shock
wave", though not correct, is commonly used for marketing purposes. In the
past, this caused a lot of confusion, and still does to this day. Even in some
clinical publications, it is often unclear whether shock waves or pressure
waves are being referred to.

Pressure waves achieve penetration depths of 2 to 2.5 cm, meaning they have
a more superficial effect than shock waves. By contrast, shock waves reach
their maximum energy at the focus deep in the tissue. The generated pressure
field converges into a focus located in deep tissue regions.

24
 Shock wave therapy vs. pressure wave therapy

Evidence has shown that radial pressure waves generate a pressure field with
a range of 40-60 mm, depending on the transmitter employed. By contrast,
the therapeutic depth reached during extracorporeal shock wave treatments
is about two to three times greater.4 We do not yet know whether the thera­
peutic action of shock waves and pressure waves is based on identical biolo­
gical effects. Moreover, the biological effects are assumed to depend also on
the type of system employed (EH, EM, PE) and on the selected energy set­
tings. Generally speaking, the following major differences apply: shock waves
achieve greater penetration depths than pressure waves and a higher energy
density in deep tissue layers.

Shock waves and pressure waves differ in terms of their physical properties
and the technology employed to generate them. Shock waves reach signi­
ficantly higher pressure values. The physical characteristics of shock waves
include: short and fast rise time, high peak pressure and non-linear propaga­
tion.5 The pulse duration of shock waves is in the microsecond region, that of
pressure waves in the millisecond range. The wavelength of shock waves in
water is about 2 mm at a sound velocity of approximately 1,500 m/s. By con­
trast, pressure waves have wavelengths of 2-20 cm. This difference explains
why pressure waves cannot be focused.6

In experiments with two different electrohydraulic systems, the measured

rise times of the generated waves ranged between 25 and 40 nanoseconds.
Investigators identified typical shock wave properties from the plotted
curves. Using a pressure wave system, the measured rise time was 2.5 micro­
seconds. The plotted curve did not reveal any further typical shock wave pro­
perties.7 Based on these physical findings, the correct term to use would be
"radial pressure wave", "ballistic pressure wave" or simply "pressure wave".

Tests have been conducted, in the past and again more recently, to examine
the feasibility of focusing pressure waves by installing a concave focusing
transmitter into a pressure wave system. In these tests, the plotted pressure
wave curve did not reveal any characteristics of a genuine shock wave.5

25
 PRESSURE FIELD OF A SHOCK WAVE AND PRESSURE WAVE SYSTEM I Fig. 1

Shock wave
Coupling cushion Effect in deep tissue
pressure field in the focal zone

Electromagnetic shock wave Body

source with cylindrical coil

Superficial
Pressure wave effect
pressure field
energy • 1 / r•

compressed
air /
1))
I

projectile impact body body

26
 Shock wave therapy vs. pressure wave therapy

Defocused or planar shock wave generators generally have a larger focus,

which means that the mechanical energy spreads over larger areas. The phy­
sical characteristics of acoustic waves remain uncompromised, and the waves
penetrate into deep body regions. This therapeutic procedure is frequently
adopted in the treatment of wound healing disorders and skin burns as well
as in aesthetic medicine. These issues are discussed in extensive detail by
K. Knobloch and his co-authors in a dedicated volume entitled "ESWT IN
HAND SURGERY", recently published by Leveho in the SHOCK WAVE THERA­
PY IN PRACTICE series.8

TYPICAL PARAMETERS OF SHOCK WAVES AND PRESSURE WAVES I Fig. 2

Pressure waves Shock waves

0 .1 - 1 MPa 10 - 100 MPa

(1:100)

� 0.2 - 5 ms � 0 . 2 µs
(1000:1)

Time Time

27
 S h o c k waves: m e c h a n i s m of a c t i o n

ESWT - FROM MECHANISTIC HYPOTHESIS TO BIOLOGICAL

RESPONSE - ANGIOGENESIS, NO, ENOS, GROWTH FACTORS
(VEGF ETC.)

Following the treatment approach adopted in urinary lithotripsy where high

amounts of energy are required to achieve fragmentation of urinary stones, a
high energy dosage was also used in the early days of orthopaedic shock wave
therapy of calcific tendinitis of the shoulder, heel spur and epicondylopathy.
The general assumption was that a high energy dosage with its mechanistic
effects was also required in the treatment of enthesopathies in order to cause
microlesions by the application of shock waves and thus induce repair and
regeneration processes.

Hence, the successful treatment of calcific tendinitis of the shoulder by

means of ESWT was attributed to the mechanistic disintegrating effect of
shock waves. Minute calcium fragments were said to result from cavitation
effects and could thus easily be resorbed from the bursa and intra- or para­
tendinous tissue.9 • 1 0

However, the healing of venous or arterial ulcers and tendinopathies achieved

even at a low shock wave dosage led to growing doubts about the validity
of the mechanistic hypothesis. Today, the mechanistic theory is considered
obsolete, whereas angiogenesis is increasingly assumed to play a crucial role
in the healing process.

Initial explanations of the mechanism of action of ESWT that caused previ­

ous theories to be revised were obtained from studies in rabbits conducted
by a group of researchers led by C.J. Wang. In these animal experiments, the
tendon-bone junction of the Achilles tendon in the right hind leg was treated
with shock waves (0.18 mj/mm2 ) . The left hind leg (control side) did not re­
ceive any treatment. Biopsies were then performed 1, 4, 8 and 12 weeks after
shock wave application. Microscopic examinations confirmed neovasculari­
zation in the treated leg compared to the control side (Figure 3, Figure 4).
The angiogenetic markers VEGF (vascular endothelial growth factor), eNOS

29
 (endothelial nitric oxide synthase) and PCNA (proliferating cell nuclear anti­
gen) identified by immunohistochemical analysis were found to have signifi­
cantly increased after only one week. Levels of these markers remained high
for eight weeks before dropping, with the exception of PCNA (Figure 4). The
PCNA increase that occurred concurrently with neovascularization is a clear
indication of enhanced endothelial cell proliferation (Figure 5). 1 1 • 12

MICROSCOPIC FEATURES OF eNOS EXPRESSION I Fig. 3

Figure J :
ESWT promotes eNOS --- Control
expression and its signal ---0--- Shock wave
transmission; h ighest 450
number of eNOS cells
4 weeks ofter ESWT''
(U
..D
E::, 300
C

�
l/)
0
zQJ 150
QJ
.:':
-"'=
:g
CL 0

0 4 8 12

Weeks after shock wave therapy

ESWT promotes the expression of eNOS signal transduction.

The effects of shock waves appear to be time-dependent.

30
 S h o c k waves: m e c h a n i s m of a c t i o n

MICROSCOPIC FEATURES OF VEGF EXPRESSION I Fig. 4

_._ Control Figure 4 :

---0--- Shock wave Histological evidence of
50 angiogenesis (VEGF) after ESWT
...
QJ
compared to the con trol prep a ­
ration; Co ns idera b ly e n h anced
.D 40
E:::J neovascularization compared to
C: u n treated s ide; highest n u mber
a:; 30 of vessels after 4 weeks"
Q)
>
u... 20

Q)
> 10
"vi
0
Cl.. 0

0 4 8 12

Weeks after shock wave therapy

ESWT promotes VEGF induction for angiogenesis.

The effects of shock waves appear to be time-dependent.

MICROSCOPIC FEATURES OF PCNA EXPRESSION I Fig . s

- Control
-0- shock wave Fig u re 5:
PCNA increase after 1 week,
400
s till positive after 12 weeks:
... indication of e n h a n ced
endothelial cell p ro lifera tion "
E
QJ
300
:::J
C:

a:;
u
200

z
<(

u
Cl..
100
·-,=;
"vi
0
Cl..

0 4 8 12

Weeks after shock wave therapy

ESWT promotes cell proliferation at the tendon-bone junction.

The effects of shock waves appear to be time-dependent.

31
 O t h e r i nvesti g ators p e rfo rm i n g a n i m a l experi m e nts ( i n rats) i d e ntified
e n h a n ced a rteri a l m icrocircu lation i n m uscles after shock wave a p p l icati o n ,
with a n add itio n a l i n crease b e i n g achieved after repeated s h o c k wave treat­
ments. The effects on m icroci rcu lation observed d u ri n g a n i m a l experi ments
fu rther the u n d ersta n d i n g of a n g iogenetic p rocesses a n d the reg enerative
mecha nism of ESWT_,3-,s with the beneficial effects of n itric oxid e ( N 0 ) 1 6• 17 a n d
a n g iogenetic sprouti n g , t h e regeneration o f path olog ica l tendons a p pea rs
h i g h ly co n ceiva ble. Recent resea rch demonstrates that the effects of mecha­
n ica l sti m u l i go beyo nd a n g iogenesis a n d vascu logenesis. 8 I n vitro exa m i n a ­
1

tions have revealed t h e molecu l a r a n d cel l u l a r effects o f shock waves on lym­

phatic endoth e l i a l tissue.1 8 · 9 I n creased endoth e l i a l m i g ration res u lts i n g reater
1

fo rmation of lym phatic ca p i l l a ries .

Rea ders may rem e m ber the case report of a dia betic fa cing a m p utation of
both g a n g renous big toes d i scussed i n the fi rst edition of this book. Severa l
months of rigorous ESWT at a low dosage resu lted i n both toes being saved
(Fig u re 6 ) . This positive cl i n ica l outco me was attri buted to loca l a n d reg ional
a n g iogenesis i n d u ced by shock wave a p p l icati o n . 2 0
•
21

DIABETIC GANGRENE OF BOTH BIG TOES BEFORE AND AFTER SEVERAL MONTHS
OF SHOCK WAVE TREATMENT I Fig. 6

As l o n g a g o as 2 0 0 8 , a n other i m p ressive case was re ported i n a perso n a l

co m m u n i cation fro m R. Thiele, Berl i n . The patient's d i a betic leg u l cer h a d
fu l ly h e a l e d afte r five m o nths o f ESWT.

32
 Shock waves: mechanism of action

DIABETIC LEG ULCER AT THE BEG I N N I N G OF ESWT ANO AFTER 5 MONTHS

OF TREATMENT. I Fig. 7

ESWT AND BIOLOGICAL RESPONSE: ANALGESIA

A hypothesis discussed among experts in the field stipulates that repeated

shock wave application prevents non-myelinated C-fibres (nociceptors)
from releasing the pain-producing neuropeptides substance P or CGRP
(calcitonin gene-related peptide). This results in fast pain relief. - 4 The
22 2

analgesic effect is further enhanced by additional repeated shock wave

application in order to prevent recurrent neuropeptide release in the region
treated following spontaneous recovery of nociceptors.2 5-27

Repeated ESWT ensures continuous washout of pain-producing neu­

ro-peptides such as substance P. Pain is gradually alleviated and even­
tually relieved permanently if ESWT is continued to completely elimi­
nate substance P. 22 Some authors think it likely that this analgesic effect is
achieved via neural hyperstimulation as a result of shock wave application;
however, they do not provide any details to substantiate their assumption. 8 2

Still, there is clear and convincing evidence of the continuously diminishing

concentration of substance P in the paratendinous tissue and of a reduction
in non-myelinated C fibres. , 8 , 9
22 2 2

33
 ESWT AND BIOLOGICAL
' RESPONSE:
GROWTH FACTOR TGF-BETA 1 , COLLAGEN I AND Il l

Experimental and clinical investigations have shown that tendon cells respond
to mechanical stimulation from shock waves by increased gene expression of
the transforming growth factor beta 1 (TGF-beta 1), a member of the super­
family of growth factors. The greater release of TGF-beta 1 translates into
stronger proliferation, i.e. cell formation, to induce regeneration processes in
tendons.3°-32

Another study found that proliferation of normal fibroblasts had increased af­
ter ESWT. The study revealed greater gene expression (mRNA) of TGF-beta 1
and collagen type I and 1 1 1, which is a clear indication of the factors primarily
involved in the regeneration of tendinopathies}J, 34

The energy flux density (EFD) and number of shock wave pulses determine
the effects of ESWT. Low energy levels and small numbers of shock wave pul­
ses enhance the effect of shock waves, whereas a high dosage reduces it,34 -3 7
The low energy input triggers upregulation of growth factors, among them
TGF-beta 1, and collagen I and Ill gene expression. Highly active vasodilating
nitric oxide (NO) produced by fibroblasts contributes to TGF-beta 1 release
and collagen synthesis.38 • 3 9

The low mechanical forces associated with shock waves induce biochemical
signals that lead to interaction between cells and the extracellular matrix
(ECM). Complex intracellular signal transduction pathways enable fast cell and
tissue proliferation, differentiation, increased gene expression and transcrip­
tion of stem cells, TGF-beta 1 release and synthesis of the gluey substances
that are collagen I and Ill.

The cited studies show that shock waves stimulate tenocyte proliferation and
collagen synthesis.1 6 · 3 8 · 3 9

34
 Shock waves: mechanism of action

ESWT AND BIOLOGICAL RESPONSE:

MECHANOTRANSDUCTION

Cellular a nd active biochemical/ molecular links exist between the intracel­

lular structures a nd the extracellular matrix ( ECM ) . The outer a nd inner cell
membra nes have a multitude of receptors, a mong which are integrins that
act as mecha noreceptors. Tensile stress or mecha nical pressure originating
from the cell environ ment or acting on adhesive protein fi bres of the ECM trig ­
ger sig nals that are tra n smitted to the cell n ucleus via integrins a nd intracellu­
lar sig nal pathways of the cytoplas m. The ECM a nd the interior of the cell are
linked with each other within a commu nication system via sig nal tra n sdu c­
tion pathways . 4 0 As a result of mecha nical stimulation , extracellular, intracel­
lular a nd tra nsmembra ne receptors ena ble the opening u p of specific sig nal
tra nsduction pathways for mechanotra nsduction thera py.

The mechanical energy of shock waves induces acute reaction s in da maged

cells, leading to the gradual recovery of the affected tissue. Extracellular me­
diators react indirectly when mechanical stimuli are tra n smitted, whereas the
sensors a nchored in the cell membra ne or interior of the cell produce direct
actio ns. Both systems are closely linked a nd interdependent, characterized by
complex interactions. Tissue fu nction a nd structure depend strongly on whe­
ther the mediators a nd sensors are stimulated directly or indirectly. 41

The indirect reaction of growth factors outside the cells - s u bsta nces bou nd
within the ECM - tra nslates into cellular response a nd perma nent cellular
ada ptatio n . Acting as tra nsmitters of mecha nical stimuli, growth factors are
released into the extracellular space a nd released from their associations in
the cell membra ne. 42 As free molecules they bond with tra n s membra ne re­
ceptors . The compou nds formed in this ma nner induce molecular sig nals in
the cytoplasm. Their primary task is to activate different sig nal cascades to
reg ulate fast cellular response a nd perma nent cellular ada ptatio n .

I n direct mechanotra nsduction , no molecular portions are released from

the cell environ ment. Similarly to the recently detected tunnelling nano-

35
tubes (TNTs), gap junctions - i.e. channel-like connections between intercel­
lular communication pathways - act as signal mediators over long distances.
They enable bidirectional and unidirectional transfer of cellular micro- and
nanocomponents, acting as bridges between cells. The role they play in cell
migration is the subject of ongoing discussion. They might be able to trans­
fer curative "freight", though this is still pure speculation.4M4 Different mole­
cules can pass through these channels, including nucleotides, which are im­
portant for the regulation of gene expression (via RNA), as well as amino acids
for protein synthesis, adenosine triphosphate (ATP) for energy supply (gene­
rated by mitochondria), cell organelles, glucose, ions and water. 41

Experimental and clinical studies are instrumental in our understanding of the

biological mechanism of action involved in mechanotransduction.
R. Mittermayr et al. describe investigated cellular and molecular biological
processes.19 According to their findings, the mechanical impulse of shock
waves is absorbed by mechanosensitive elements in the ECM, by ion channels,
the glycocalyx ( outer layer of the cell membrane) and by the cell-cell adhesion
molecules of the cytoskeleton, which then convert the mechanical stimulus
into a biochemical signal, activate intracellular signal transduction and even­
tually enable cellular reaction.

In vivo studies have shown that the cytoskeleton, Ca and K ion channels, cell
adhesion molecules and integrins (transmembrane proteins), when acting
in conjunction with kinases (specifically focal adhesion kinase), ensure the
transfer of ESWT stimuli between the cell and the ECM.

lntegrins primarily mediate cell adhesion and migration, but they are also in­
volved in cell proliferation, differentiation and apoptosis.

At a molecular level, three different MAPK signal transduction pathways

( MAPK = mitogen-activated protein kinase) have been decoded, consisting
of a multi-stage cascade of sequenced kinases. The first of these pathways
impacts cell growth (proliferation) and differentiation.
 Shock waves: m echanism of action

The second pathway involves cytokines that have a n influence on infla mm­
atory processes a nd cell apoptosis.

Stress, including UV light, activates the third kinase sig nal tra nsduction
pathway. Tissue infla mmatio n is modulated. In addition to this, cell prolifera ­
tio n , differentiation a nd a poptosis are activated.1 9

Decoding of specific sig nal tra nsduction pathways for endothelial cells, a nd
especially eNOS, was achieved after stimulation with low-energy ESWT via a
mecha nosensitive complex. Special mention should be made of the increase
in endothelial cell migration , resulting in enhanced formation of lymphatic
vessels as well as enha nced a n giogenesis a nd vasculogenesis.12 · 18 19
· · 45-47

When citing the sig nal tra nsductio n pathways known to be involved in ten ­
dinopathies a nd other conditions'S, reference should be made to the decoding
of toll-like receptor 3 (TLR 3) a nd its mechanism of action . This receptor, which
is part of the innate immu ne system, was identified in a n attempt to modify
the regenerative effects of ESWT in the ma nagement of musculoskeletal
disorders in order to use them for cardiac treatments. Shock wave induced
activatio n of TLR 3 via its sig nal tra nsduction pathway stimulates all effects of
ESWT, including a ngiogenesis, vasculogenesis a nd infl a mmatory modulation ,
both in ischaemic muscles a nd in pathological conditions o f the musculoskel­
etal system. The proven effect of activated stem cells in ischaemic tissue is
pa rticu la rly noteworthy.1 s, 4 8

I n conclusion , ESWT ca n be referred to as mechanothera py. Acting through

mech a notra nsduction , it has a n impact on molecular a nd cellular systems
a nd results in the proliferatio n , differentiation a nd migration of different
effector cells, including immu ne cells a nd stem cells.

37
ESWT AND BIOLOGICAL RESPONSE: STEM CELLS

Animal tests have demonstrated that shock waves activate and mobilize stem
cells and progenitors. 49 - 52
Mesenchymal stem cells (MSCs) are progenitors of mature specified cell types
of the musculoskeletal system and can be isolated and cultured from almost
any tissue, including tendons53 and muscles54 · 55 . Their characteristic proper­
ty is their ability to proliferate and differentiate. 5 6 They activate or suppress
genes, thus contributing to the regeneration of pathological processes. Spe­
cific growth factors promote and control cell proliferation, differentiation and
division in order to recruit a constant pool of new MSCs with identical replica­
tion potential for physiological cell renewal and replacement of pathological
tissue.

In pathological processes, MSCs release a multitude of cytokines and growth

factors with immunomodulatory and trophic effects. A bioactive, protective
protein molecule prevents apoptosis and fibrosis. Angiogenesis is stimulated
by the release of VEGF. 5 6 - 5 8

If these functions are weakened or even lost and homeostatic tissue break­
down and tissue formation are not regulated, the mechanical energy of ESWT
and mechanotransduction can be utilized to activate multipotent resident
(endogenous) MSCs which have a curative effect on degenerative inflamm­
atory processes in the musculoskeletal system. 5 6 · 59· 60 ESWT has been shown
to result in an increase in levels of TGF-beta1 growth factor and in enhan­
ced proliferation, differentiation and migration of human MSCs from bone
tissue. 61 The ESWT procedure has been used for many years and has become
an integral part of regeneration medicine. As the body of scientific findings
grows, ESWT will play an even more important role in daily clinical practice in
the years to come. 45 · 5 5 . 6 2 - 64

In order to investigate the clinical benefit of shock waves in the treatment of

tendinopathies, Leone et al. took five samples of healthy semitendinosus tis­
sue and five samples of ruptured Achilles tendons and examined the tendon
 S h o c k waves: m e c h a n i s m of a c t i o n

samples for tendon stem/progenitor cells (TSPCs). The clonogenetic poten­

tial, i.e. the genetic material, was found to be intact only in the healthy tissue
samples.

The clinical advantage of shock wave-stimulated stem cells is likely to derive

from the more potent effects in inducing the healing of tendon defects.Gs
Human TSPCs treated with shock waves showed increased proliferation and
expression of tendon-specific markers (scleraxis * ) and collagen I. The produc­
tion of growth factors (VEGF, TGF-beta1) and anti-inflammatory cytokines
(IL-10) was also found to have increased. This resulted in the complete restora­
tion of damaged tendons, which exhibited regenerated microregions without
any signs of inflammation after treatment.GG

Stem cells/ MSCs evidently play a key role in ESWT-activated processes and
constitute the main target during the regenerative signal transduction
phase.Go

• Scleraxis (protein) is a transcription factor responsible for synchronizing

gene activity with the cell cycle and metabolism.

39
 Pres s u re waves: m e c h a n i s m of a c t i o n

PRESSURE WAVE ENERGY, MECHANOTRANSDUCTION

Biological tissue is capable of changing its properties in response to a vari­

ety of stimuli. The molecular or cel lular response to mechanical stimulation
eventually results in the adaptation and modification of tissue morphology
and physiology. This ability to adapt is characteristic of tendons, ligaments,
bones, muscles, skin and endothelial cel ls.41 • 1 -70
6

Similarly to the mechanism of action of shock waves (SW), the effects pro­
duced by the application of bal listic pressure waves (PW} are based on the
principles of mechanotransduction. Bloch and Suhr simply refer to mechani­
cal energy, irrespective of whether it is generated by pressure waves or shock
waves.41 Information on the impact of mechanical energy in the treatment
of enthesopathies/ tendinopathies has been gathered primarily from experi­
mental studies conducted with focused shock waves. However, various ran­
domized control led clinical trials - including one at evidence level 1 - have
also confirmed the sustained effect of pressure wave therapy in the treatment
of different types of enthesopathy.11 -1 8

A major physical difference between shock waves and pressure waves is that
the former penetrate more deeply into tissue, whereas pressure waves have
a more superficial effect. Consequently, they are used for different clinical ap­
plications and indications. Other properties that distinguish them are their
frequencies (shock waves being of high frequency and pressure waves of
low frequency) and pressure amplitudes. No conclusive evidence has been
gathered so far as to whether shock waves and pressure waves use the same
mechanobiological signal pathways.

In vivo trials with rats were conducted to confirm that pressure waves induce
osteogenetic processes. In these trials, fluorescence microscopy revealed that
pressure waves resulted in extensive periosteal and endosteal bone forma­
tion on the application side of a bone, whereas their osteogenetic effects in
the endosteal and contralateral area on the side opposite the pressure wave
transmitter were found to diminish continuously and eventual ly disappear

41
 completely. This experiment demonstrates that the energy of pressure waves
decreases with increasing distance, which explains why they have a superficial
effect.79 If one applies these findings to the treatment of tendinopathies, pres­
sure waves offer a clear benefit: the radially propagating pressure wave energy
with a penetration depth of about 2 cm can be utilized to provide maximum
impact in extensive superficial tissue regions spreading out from the point of
skin contact of the transmitter. When treating superficial, easy-to-reach ten­
don pathologies, pressure waves can be applied to large areas within a short
time and without any major technical input, whereas shock waves need to be
targeted at specific spots with maximum precision.

Tendons, ligaments and cartilage are tissues that are subjected to considera­
ble mechanical stresses. They consist primarily of fibrocytes or chondrocytes
that possess an almost complete set of mediators and sensors required for
the translation of mechanical stimuli into biochemical signals. After transmis­
sion of a mechanical stimulus, kinases mediate the signal pathways that need
to be activated or inhibited to regulate the transcription of different genes
such as collagen fibre or proteoglycan genes, the primary ECM stabilizers. 0 8

In tendons, even mechanical stimuli induced in the form of physical exercise

may increase their strength. Discussions are still going on as to whether me­
chanical stimulation (by shock waves) leads to a higher concentration of pro­
tein collagen in the cross-links of tendons and fibril morphology, and thus to
improved tendon stability. 1 -
8 82

.,
PRESSURE WAVE ENERGY, MYOFASC IAL TRI GGER POI NTS

Based on the theory developed by Janet Travell and David G. Simons, the root
cause of painful myofascial trigger points (MTrPs) is the energy crisis caused
by trauma or overuse, which has drastic consequences at muscular level: in­
creased release of acetylcholine, depolarization of motor end plates, conse­
cutive sarcomere contracture, vascular compression, hypoxia and ischaemia.
This leads to the release of painful nociceptive substances. As a result, actin-

42
 Pressure waves: mechanism of action

myosin bonds can no longer be broken due to the energy deficit. This, in turn,
causes painful trigger points.83 - 86

A theoretical explanation of the effects of mechanical pressure waves on

myofascial trigger points (MTrPs) is that pressure waves reduce, or ideal ly re­
verse, the energy crisis by their response to the factors that initiate it.

Speculations based on the biological mechanisms of action of mechanotrans­

duction stipulate that mechanosensitive receptors convert pressure wave
energy into biochemical signals, thus activating intracellular signal transduc­
tion pathways. The signal is transmitted to the cel l nucleus of the sarcomeres,
the smallest functional units of muscles. This process eventual ly activates the
respiratory chain. Intracel lular mitochondria are stimulated and ATP produc­
tion is increased to compensate for the cel lular energy deficit. Permanent con­
tractures of the actin-myosin filaments and the associated trigger point taut
bands are released.

The reflections of Bloch and Suhr on this issue are quite fascinating: "The
skeletal muscle is also sensitive to mechanical stimuli and can be functionally
and structural ly regulated by mechanotransduction. The myofibres and sa­
tel l ite cel ls are muscular cel l components of skeletal muscle tissue exposed
to mechanical loads in a manner comparable to tendon and cartilage tissue.
They produce skeletal muscle-specific proteins, e.g. actins and myosins. The
skeletal muscle tissue has developed different ways to react and adapt to me­
chanical stimul i at variable levels. Mechanical stresses activate different sig­
nal ling cascades in skeletal muscle components. It has been demonstrated
that intensive cycling exercise has a strong impact on the respiratory chain
in skeletal muscle mitochondria leading to the speculation that mechanical
stress can induce adaptation of the metabolic capacity in skeletal muscle. Me­
chanical stimuli are involved in this way in the regulation of skeletal muscle
regeneration after injuries."41 , 81

V ibrations of 35 Hz and above act as physiological muscle tremor and are the
most potent driver of microcirculation.88 The fine resonance ensures meta-

43
 bolic influx and efflux via minute blood vessels and lymphatic channels in the
ECM. This function is not performed by the cardiovascular system. In many
cases, physiological muscle vibrations are markedly reduced by overuse or
strain of poorly exercised muscles. The metabolic nutrient supply to the cells
is potentially compromised. This leads to painful myofascial trigger points
which may cause cramps and palpable muscle induration.

Nitric oxide synthesis and release, angiogenesis / vasculogenesis and genesis

of minute lymphatic capillaries are conceivable biological responses to me­
chanical vibrations with oscillating energy. These processes ensure overall im­
provement of microcirculation.1 5 · 18· 4 6· 4 8 The energy deficit is compensated for,
metabolic waste products are absorbed and removed by lymphatic capilla­
ries. Trigger points, muscular taut bands and indurations gradually disappear.

PRESSURE WAVE ENERGY, FASCIA

Fascia is soft connective tissue characterized by a high degree of elasticity

due to its substantial collagen content. There are three distinct layers of fascia
tissue: superficial, deep and visceral. Visceral fascia suspends and wraps the
organs. Superficial fascia is located primarily in the subcutaneous tissue and
is interconnected with deep fascia. Planar connective tissue layers envelop
bones, tendons, ligaments, retinacula, capsules, nerves, blood vessels and
muscles. Muscle fibres, bundles of muscle fibres and the muscle in its en­
tirety are all enclosed by a microscopically thin layer of fascia. Fibrocytes and
progenitors produce collagen, stabilizing the microscopically fine web of
fibres. They dissolve old fibres (autophagy) while at the same time rejuvena­
ting the fascia through proliferation of young cells. Depending on the density
and activity of the fibroblasts, contractures and stiffness may occur in cases
of excessive strain or where patients are getting insufficient exercise. These
tissue changes can be identified by the examiner as easily palpable adhe­
sions or densifications. In addition to nociceptors, proprioceptors and che­
mo-thermoreceptors, fascia has specific mechanoreceptors for the percep­
tion of pressure, tension and vibrations. 81 · 8 9 When subcutaneous mechano-

44
 Press u re waves: m e c h a n i s m of a c t i o n

receptors receive pressure wave or tension stimuli, these are, in turn, transmit­
ted via neurally linked sensors to mechanoreceptors in deeper tissue layers,
thus influencing fasciaI and myofascial adhesions. The multitude of sensitive,
interconnected sensors provide continuous information on the condition of
fascia I structures to the relevant brain centres. In this manner, they contribute
significantly to strong body awareness.9 0 • 9'

WHAT IS EMTT® (EXTRACORPOREAL MAGNETOTRANSDUCTION

THERAPY}?

EMTT® is a recently developed procedure which - similarly to pulsed electro­

magnetic field therapy (PEMF therapy) - can be used in the treatment of mu­
sculoskeletal disorders. Physically, EMTT® and PEMF systems differ in terms of
magnetic flux density and frequency.

The characteristic features of pulsed electromagnetic field (PEMF) therapy

are low frequencies (1 to 50 Hz), low magnetic flux densities and superficial
penetration depths. PEMF therapy was first approved by the FDA in the 1980s
as a treatment option for delayed bone union and pseudarthrosis. A number
of scientific investigations have been conducted to study the mechanism of
action of pulsed electromagnetic fields. In vitro trials have shown that the
activity of osteoblasts is stimulated while that of osteoclasts is inhibited.92 · 93

The use of pulsed electromagnetic fields in the treatment of mesenchymal

stem cells (MSCs) of different origin has demonstrated their ability to change
the cell cycle. The differentiation spectrum has been extended. MSCs from
bone marrow exhibited an increase in cell proliferation.94- 9 7 Osteogenetic9s ,
9 7 - 99 and chondrogenetic100 · 101 differentiation was markedly higher. PEMF treat­

ment of MSCs derived from tendon tissue was found to induce the expression
of collagen, scleraxis, VEGF, TGF-beta 1 and tissue-specific markers. The expe­
riment also revealed a slight increase in cell proliferation.66 · 10 2 A higher num­
ber of anti-inflammatory mediators was found along with trophic mediators.
In an in vitro study, different dosages of PEMF treatment on isolated human

45
semitendinosus and gracilis tendons were tested. None of the tests revealed
any apoptosis. Increased proliferation of human tenocytes occurred with dif­
ferent dosages. Treatments performed with 3 millitesla (mT) improved cellu­
lar vitality. The 1.5 mT treatment induced strong formation of scleraxis, VEGF
and collagen I expression. Overall, the best results in human tendon cell cultu­
res were achieved with 1.5 mT PEMF treatments. 10
2

The cited studies show that pulsed electromagnetic field therapy (PEMF the­
rapy) is capable of stimulating stem cells (MSCs) in an experimental approach.
In the near future, Extracorporeal Magnetotransduction Therapy (EMTT®),
which has now undergone clinical testing, may represent a viable option for
the treatment of musculoskeletal disorders. Observational studies led by
Professor Dr Ludger Gerdesmeyer were conducted at the Kiel-based
Department of Orthopaedics and Trauma Surgery of the University Hospital
Schleswig-Holstein (UKSH), Germany, to determine the effectiveness of high­
energy pulse therapy (pulsed magnetic field therapy) in the treatment of
degenerative joint disorders and enthesopathies.

In an EBM Level 2a randomized controlled trial, patients suffering from ten­

dinopathy of the rotator cuff and long bicipital tendon were divided into two
groups. Subjects in the first group were treated with ESWT alone. Patients in
the second group received a combination of ESWT and EMTT® . The results
were assessed on the basis of the Constant-Murley Shoulder Outcome Score
(CMS) and a visual analogue scale (VAS). Patients in both groups experienced
significant improvements in their condition, with the ESWT / EMTT® combina­
tion therapy providing still better outcomes than ESWT alone. 2

In an observational study, a total of 168 patients suffering from the fol­

lowing disorders were treated: shoulder impingement, spondylarthrosis
of the lumbar spine, gonarthrosis, coxarthrosis, heel spur, pseudarthrosis,
wound healing disorders, radiculopathy from disc herniation and trigeminal
neuralgia.
 Pressure waves: mechanism of action

In s u m m a ry, it ca n be said that, so fa r, h i g h -energy mag netic field thera py has

provi ded exce l l ent treatment res u lts without a ny side effects . Further obser­
vational stud ies to be co n d u cted at the U KSH i n Kiel a n d scientific p u b l i ca ­
tions b y Professor Gerdesmeyer a re expected with g reat i nterest.

PHYSICAL FUNDAMENTALS OF EMTT®

Dr M a rkus Belau a n d Dr Rafael Sto rz

Extracorporeal M a g n etotra nsd uctio n Thera py ( EMTT® ) util izes p u l sed elec­
tromagnetic fi elds. By d efi n iti o n , EMTT® uses a decayi ng s i n usoidal field with
an osci l lation frequ ency of between 1 0 0 kHz and 300 kHz and a field strength
of > 1 0 mT i n the therapeutic vo l u me. Wea k d a m p i n g of the reso n a nt circuit is
a typica l featu re of EMTT® systems. This n ecessitates the tra n s m itter havi n g a
relatively h i g h i n d u cta nce ( L) a n d fa i rly l ow resista nce (R), achieved by m ea n s
o f a coi l . With a s u ita b l e tra n s m itter, these fi e l d properties can be i m p lemen­
ted by using powerfu l vo ltage sou rces, similar to those that have been used in
shock wave thera py fo r decades.

MAG N ETI C F I ELD PRO F I LE OVER TIME O F AN EMTT® SYSTEM WITH WEAKLY
DAMPED OSC I LLAT I O N AT A FREQUENCY O F 1 30 KHZ, TYP I CAL P R O F I LE O F EMTT®
PULSE OSC I LLAT I O N I Fig. B

So

60

;:::"
40

20

-20

-40

-60

0 20 40 60 So 100 120 140

Time [µs]

47
From the EMTT® definition cited above it follows that the magnetic field, and
in particular its time derivative, are strong enough to produce clinical relevant
health effects. The absolute field amplitude is required to generate forces of
sufficient strength (e.g. Lorentz force acting on charged moving particles/mo­
lecules). Rapid changes in the magnetic field result in high induction voltage,
which may affect the permeability of membranes103 and the activation of ion
channels, as well as the mechanical activation resulting from the piezoelectric
effect in, for example, bones and collagen.1 04 . 10 s

In EMTT® , the magnetic field is typically generated by a weakly damped reso­

nant circuit comprising a coil and a capacitor. The capacitor is charged with
several kilovolts (kV) by a high voltage source. It is discharged by means of
a switch, which closes the circuit to the coil. Electric current reaching seve­
ral kiloamps (kA) in magnitude passes through the coil, generating a magne­
tic field whose amplitude and spatial distribution can be calculated by apply­
ing the Biot-Savart Law1 0 6 • 107 • Owing to their high frequency and strong mag­
netic field, EMTT® systems typically have magnetic field gradients of between
60,000 T/s and 150,000 T/s. Pulse repetition rates may reach several Hz.

Figure g shows the magnetic field distribution across the coil cross-section.
The therapeutic volume is typically located at a depth of 2 to 7 cm, with a
typical maximum field strength of 30 to 70 mT. It is important to note that
only the magnetic field sited at the depth of the therapeutic volume is rele­
vant for the therapeutic effect, whereas the higher field values that may be
achieved at the coil wire surface are insignificant in terms of the treatment
outcome. This part of the coil cannot be used due to the necessary coil
insulation. Since the magnetic field is capable of penetrating biological tissue
almost unhindered, its strength is exclusively determined by the geometrical
distance from the coil wires. Typical geometries of EMTT® transmitters exhi­
bit a highly uniform magnetic field at typical treatment depths. Absorption is
almost zero and pulse oscillations decay after about 100 to 200 µs. As a conse­
quence, no tissue heating occurs.
 Press u re waves: m e c h a n i s m of a c t i o n

TWO-DIMENSIONAL MAGNETIC FIELD DISTRIBUTION ACROSS THE COIL CROSS­

SECTION OF AN EMTT® SYSTEM I Fig. g

1omT

Fig ure 9 :
10
At a typica l treatment depth
E s:
� "'"' of 4 cm, the magnetic field
s trength is h o m ogenous at a b o u t
·x,.,
::,
�;;·
'" �
60 mT over the en tire coil dia-
m e ter. Magn etic field amplitudes
� 5 0::
exceeding 10 m T can be measured
a t a distance of a b o u t 13 cm from
the coil cen tre.

0 10
-10 -s 0 5 10
Lateral axis [cm]

49
G EN ERAL TREATMENT
I N FO RMATI O N
AN D TREATMENT
FU N DAMENTALS
 G e n e r a l treatment i nfo r m a t i o n a n d treatment fu n d a m e n t a l s

PATIENT POSITIONING

Getting patients into a stable and relaxed position facilitates localization of

painful tendinopathies or myofascial trigger points (MTrPs) and their treat­
ment with extracorporeal shock waves (ESWs).

Treatment of the shoulder girdle is generally performed with the patient in

side-lying position. Trigger points and insertional tendinopathies can be
rapidly scanned both ventrally and dorsally.

Fig ure 1 0 :
Stable side-lying position

The supine position is ideal for enthesopathies and myofascial trigger points
in the upper arm or forearm. Treatment of lateral epicondylitis is performed
with the elbow lying flat on the patient table and flexed to about 100 ° .

Fig ure 1 1 (left) :

Supine position

Fig u re 12 (rig h t) :
Fo rearm position w i t h the patient
supine (medial epicondylitis)

51
 Arm external rotation with flexed elbow enables ESWT of medial epicondylitis
with the patient in a relaxed position.

The prone position is a stable alternative for the treatment of lateral epicon­
dylopathy with ESWT.

Fig ure 1J :
Pro n e position

Paravertebral trigger points in the cervicothoracic junction, at the supe­

rior margin of the trapezius muscle and in the levator scapulae muscle at the
superior angle of the scapula can best be localized with the patient seated
and their arm placed as for the adduction and internal rotation test; this also
applies to tendinopathies (affecting the rhomboid muscles) at the medial
margin of the scapula.

Fig ure 14 :
Patient s e a te d with a rm
placed as for the adduction
and i n tern a l rotation test

Sensitive patients should be treated in prone position with the head rest of
the patient table tilted downwards.

52
 Genera l treatment information and treatment fundam entals

lnsertional tendinopathies and myofascial trigger points associated with myo­

fascial thoracolumbar pain syndrome should also be treated in prone position.

A wedge pillow can be placed under the patient's stomach to compensate for
pronounced lumbar lordosis.

A stable side-lying position is recommended for the treatment of trochanteric

tendinopathy and trigger points in the gluteal muscles and deep external ro­
tators of the hip (piriformis syndrome, gluteus minimus muscle). Relaxed, but
secure patient positioning is achieved with the affected hip flexed to 70 ° , the
thigh adducted to 20-30 ° and internal hip joint rotation to about 30 ° .

In the rare cases of bilateral trigger points in the gluteal muscles, the patient
needs to be repositioned from one side to the other. In many instances, glute­
al trigger points are difficult to identify, especially in obese patients.

Trigger points and insertional tendinopathies in the iliotibial band can best be
localized with the patient in side-lying position, with the knee and hip joints
slightly flexed.

Trigger points in the ischiocrural muscles (hamstrings) can be reached with

the patient in prone position.

Attachment trigger points at the ischial tuberosity cannot be localized by pal­

pation, nor by means of the shock wave handpiece, when the patient lies pro­
ne on the table. This is easier in supine position, with the hip flexed to about
100-120 ° . This position should be maintained throughout the examination
and treatment. Attachment trigger points in this region can be localized by
palpation as the ischial tuberosity causes local tenderness.

53
Fig u re 15:
Loca liza tion of the isch iol
tuberosity with the shock
wave h a n dp iece

lnsertional tendinopathy of the pes anserinus and in the lateral aspect of the
tibial plateau (Gerdy's tubercle) can be localized by means of shock waves or
pressure waves, with the patient in supine position with their knees slightly
flexed.

Fig u re 1 6 (left) :
Supine position for trea tment
of p a tellar ten dinitis

Fig u re 1 7 (rig h t) :
Shock wa ve application
to pes a nserinus

lnsertional tendinopathy in the knee region is treated in supine position, with

knees slightly flexed. Tender spots at the superior and inferior patellar margin
and at the tibial plateau can be palpated and localized with the shock wave or
pressure wave handpiece.

Fig u re 18:
Treatment of inferior
p a te/far pole (insertio n a l
tendinopathy)

54
 General treatment information and treatment funda mental s

Treatment of attachment trigger points and myofascial trigger points in the

hip adductors should be performed with the patient in a supine position, with
the hip abducted to about 30-40 ° , the leg placed into a figure-4 position and
the heel resting on the opposite knee.

Fig ure 1 9 :
Fig ure-4 position

Plantar fasciitis and Achilles tendon pathologies should be treated with the
patient in prone position. The foot joints should extend beyond the end of
the patient table. The therapist should be seated at a suitable height in order
to immobilize the patient's foot with the therapist's near knee, keeping the
foot in a right-angled position and subjecting the plantar fascia and Achilles
tendon to slight tensile stress. This leaves the therapist's hands free for the
actual treatment.

Fig u re 2 0 (left) :
Fee t extending b eyo n d
the end of the ta ble

Fig u re 21 (rig h t) :
Foo t i m m o bilized by
therapis t 's knee

55
 SHOCK WAVE AND PRESSURE WAVE DOSAGE,
SHOCK WAVE NAVIGATION BY PATIENT FEEDBACK

Mechanical energy supports a nd induces healing processes in tendons, carti­

lage, bones, muscles a nd skin. The extent to which mechanotra nsduction is
infl uenced by different energy fl ux densities, freq uency, n u mber of pulses a nd
type of system used as the energy source is still u n known. 68 · 7 0

Experiments conducted with h u ma n mesenchymal stem cells ( M SCs) revealed

that even minimal variation s in the energy flux den sity of focused shock waves
have a s u bsta ntial impact on cell proliferation . An increase in shock wave
intensity fro m 0 . 2 to 0 .3 mJ/mm2 did not lead to a ny major reaction in adi­
pose stem cells . H owever, the osteogenetic differentiation resulting from this
minor increase was fou nd to be much stronger. A dosage of 0 . 2 mJ/ mm2
proved to have a more favoura ble effect on cho ndrogenetic differentiation
tha n the 0 .3 mJ/ mm2 dose. Even in a n u ntreated control preparation , the
0.2 mJ/ mm2 dosage improved chondrogenetic differentiation of h u ma n
MSCs t o a much greater extent tha n the 0 .3 mJ/ mm2 energy level. 6 This de­ 1

monstrates that a n additional increase in dosage cou nteracts the positive ef­
fects .

These investigations show h o w difficult i t i s t o determine the ideal settings

a nd achieve optimu m treatment res ults with mecha n ical energy sources in
order to meet the req uirements for low-intensity extracorporeal shock a nd
pressure waves. The general assu mption is that mechanical stimulation in­
duces a biological response even at very low energy flux densities. I n experi­
ments conducted at a relatively early stage, A. Aicher was a ble to prove that
low levels of shock wave energy induce the recruitment of circulating endo­
thelial progenitor cells both in non-ischaemic a nd in chronically ischaemic tis­
sue by improving the expression of biochemically attractant factors. 45

The difficult issue of selecting the optimu m ESW dosage had already been
addressed by H. Neula nd68 at several ISMST conventions.41, 10 8- 1 09

56
 General treatment information and treatment funda m entals

Neuland had already emphasized the pluripotency of stem cells and their spe­
cial ability to differentiate nearly two decades ago in personal discussions held
with the author of this book and other colleagues.

Mechanotransduction is only possible if cell functions and stem cells are not
damaged and remain intact after the input of mechanical energy. The Arndt­
Schulz Law, which states that weak stimuli induce vital activity, moderate
stimuli promote it, strong stimuli inhibit it and excessively strong stimuli sup­
press it, can also be applied to ESWT. The fact that some indications for extra­
corporeal shock wave therapy failed to respond to the treatment in the early
days of ESWT may be due to excessive (i.e. an "overdose" of) energy input and
resulting cell apoptosis.

PROCEDURAL GUIDANCE FOR ESWT

Painful attachment trigger points and even central myofascial trigger points
can be localized spontaneously at low energy levels following the patient's
feedback without requiring any time-consuming navigation.

The penetration depth (focal depth) is dependent on the pulse frequency and
can be varied by using different stand-offs.

If localization of painful spots proves more complicated, the energy level

should be increased gradually (e.g. starting at 0.05 mj/mm2 ) while continuing
to navigate until pain recognition occurs. After successful localization, treat­
ment can be started using the same energy level. Along with the low energy
input, this approach enables gentle activation of stem cells and induces the
desired cellular/molecular response.

Energy levels above 0.25 mj/mm2 or between 1.2 and 2.8 bar should only be
used in exceptional cases.

57
 A high number of pulses and frequent treatment sessions add up to a high
total energy input. This results in a negative impact on the healing process.
Treatment should be limited to three sessions at intervals of 8 to 10 days,
applying between 1,500 and 1,800 pulses per session. Experience has shown
that this treatment regimen should be followed by a planned interruption in
therapy lasting about three weeks, at the end of which the regeneration pro­
cess and additional treatment requirements are assessed. The visual analogue
scale (VAS) and sonography (power Doppler imaging (POI), exclusion of pa­
thological capillaries) can help the therapist weigh the pros and cons of con­
tinuing treatment.

The VAS is a valuable and reliable tool for measuring subjective pain associ­
ated with isolated myofascial trig ger points (before and after the therapy).
Treatment of specific trig ger points is generally continued if the patient re­
ports persistent pain. Pain relief is achieved when the muscular energy deficit
is compensated for and permanent contractures are eliminated.

Pressure waves and vibrations (V-ACTOR® vibration therapy handpiece from

STORZ MEDICAL AG) are applied to release adhesions of muscular fascia and
the criss-cross array of fascia I bands by improving blood circulation and by
mechanically shifting the tissue layers. The ultimate objective is structural re­
organization of collagen fibres.

58
 G e n e r a l treat m e n t i nfo r m a t i o n a n d treat m e n t fu n d a m enta l s

CRITERIA FOR SELECTING SHOCK WAVE OR

PRESSURE WAVE TECHNOLOGY

Shock wave and pressure wave technology provide a variety of benefits. What
are the criteria for selecting one or the other?

ADVANTAGES OF SHOCK WAVE TECHNOLOGY

I Precise pinpoint localization of a tendon insertion or trigger point even in
deep tissue layers. Targeted energy input into the centre of the trigger point.
Precise energy application to the spot requiring treatment.
Therapeutic effectiveness up to 15 cm depth.
Local shock wave pressure results in effective and sustained release of
deep-sited trigger points.
Shock waves induce proliferation, differentiation, migration and collagen
synthesis in endogenous stem cells.

ADVANTAGES OF PRESSURE WAVE TECHNOLOGY

I Variety of transmitters for local application or treatment of larger areas.
Target areas located at a depth of up to 3 cm can be reached without exer­
ting additional manual pressure. It is not necessary for pressure waves to
penetrate into deeper tissue layers because many free nerve endings and
sensors - part of a neural network - transmit information directly from
subcutaneous to deep mechanoreceptors of the myofascial tissue via di­
rect signal pathways.

ADDITIONAL BENEFITS OF PRESSURE WAVES

I Trigger points along muscle chains can be treated with pressure waves.
Pressure waves mobilize tissue layers to release trigger points and fascial
adhesions. The intent is to restore the equilibrium or homeostasis of myo­
fascial structures following the principles of tensegrity.
Blood circulation is increased and the metabolic exchange between cells
and the extracellular matrix (ECM) is enhanced.
The so-called myofascial release - an essential requirement for fascia I and
trigger point therapy - is achieved by mechanically moving the tissue
layers.
59
 COMBINATION OF SHOCK WAVE AND
PRESSURE WAVE TECHNOLOGY

Shock wave and pressure wave technology can be combined in order to fully
exploit the benefits of both. Target regions sited at different depths can be
treated directly with shock waves after precise localization. However, treating
individual spots in superficial areas with shock waves is very time-consuming
and provides unsatisfactory results.

Myofascial release is about releasing and loosening fascial adhesions. This

cannot be achieved with focused shock waves. Deep adhesions and trigger
points can be treated by applying superficial pressure waves because the sti­
muli they induce are received by the neural network of fascia and transmitted
to deeper fascia I regions.

In many cases, patients suffer from complex pathologies such as thoracolum­

bar or gluteal pain syndrome or piriformis syndrome in which no sustained
treatment effects can be achieved with shock wave or pressure wave therapy
alone. A combination of both technologies provides a significantly enhanced
clinical outcome.

60
 Genera l treatment information and treatment funda menta ls

SUG GESTED ESWT PROCEDURE - REGIMEN A: COMBINED

SHOCK WAVE {SW) AND PRESSURE WAVE {PW) TREATMENT
(for thera pists using shock waves plus pressu re waves)

Clinical palpation , localization of painful tendon insertions a nd myofascial

trigger points (MTrPs) with low-energy shock waves. G radual increase in
intensity (depending on patient's feedback) .

I
STEP 1 STEP 2 STEP 3
SW therapy of PW therapy Vibration therapy of
tendon attachment of MTrPs the affected muscles,
trigger points muscle smoothing
(V-ACTOR® up to
2 . 0 bar, approx. 30 Hz)

ENERGY 0 . 0 8 - 0 .25 mj/mm2 1 . 2 -2 bar

NUMBER OF PULSES 1 ,5 0 0 -1 , 8 0 0 2 , 0 0 0 -3 , 0 0 0

I
FREQUENCY 4- 6 Hz 1 2 -3 0 Hz

SESSIONS 3 3
INTERVAL approx. 8 days approx. 8 days
BREAK IN THERAPY approx. 3 weeks for regeneration

Resu mption of extracorporeal shock wave/ pressu re wave thera py after the
brea k from treatment if symptoms persist (criteria: clinical symptoms, VAS or
PDI ). If treatment is continued, the regimen outlined above should be adopted.

There have been repeated suggestions that the steps outlined above should
be performed in inverse order; i.e. to sta rt with muscle smoothing a nd vibra­
tion thera py, followed by the treatment of myofascial trigger points a nd,
fi nally, of insertional tendinopathy. This procedu re aims at decreasing muscle­
induced tensile stress in tendons in o rder to eliminate o r at least reduce local
tendinopathy pain in the region of the tendon insertion . This is a via ble option .
H owever, based on the experience gathered b y the a uthor o f this book, the
treatment outcome is the sa me as with the regimen detailed a bove.

61
 SUG GESTED ESWT PROCEDURE - REGIMEN 8: PRESSURE
WAVE (PW) TREATMENT
(for thera pists using radial pressure wave thera py)

Localizatio n of i nsertional tendi nopathy a nd myofascial trigger poi nts ( M TrPs)

with low-energy pressure waves. Gradual i ncrease in i ntensity (dependi ng on
patient's feedback).

STEP 1 STEP 2 STEP 3

Muscular vibration PW therapy PW therapy
therapy, muscle of tendon insertions of myofascial
smoothing trigger points
(V-ACTOR ® up to
2.0 bar, approx. 30 Hz)

ENERGY 1. 2-2. 5 bar 2. 5-2. 8 bar

NUMBER OF PULSES 1,200-2,000 3, 000-6,000
FREQUENCY 12-15 Hz 12-15 Hz
SESSIONS 8-10 8-10
, INTERVAL approx. 8 days approx. 8 days

BREAK IN THERAPY approx. 3 weeks for regeneration

Res u mptio n of press u re wave thera py after the brea k fro m treatment if
symp-toms persist (criteria : cli n ical symptoms, VAS or PDI ) . If PW thera py is
conti n u ed, the reg i men outli ned a bove should be adopted.

62
Sonography allows anatomical imaging that is beneficial in diagnosing ten­
dinopathy and has an advantage over X-ray and MRI procedures, namely dy­
namic representation. Ultrasound findings should be documented prior to
ESWT, partly as evidence in the event of litigation (claims occasionally being
made that shock waves have caused damage to a tendon). Moreover, accu­
rate imaging of a tendon pathology is a key factor favouring a positive treat­
ment outcome.

Grey sonographic images provide relevant information about the echoge­

nicity and texture of soft tissues and tendinopathies. This dynamic method
of examination reveals complete or partial ruptures, retractions, intramural
thinning, flattening or swelling. It has proven effective for typical ESWT in­
dications such as rotator cuff syndrome (RCS), achillodynia, plantar fasciitis,
patellar tendon pathology and enthesopathy of the elbow, but also for new
indications such as enthesopathy of the lower extremity or for myofascial pain
syndrome.

When dynamic examination techniques are applied, a calcific deposit within

the rotator cuff m oves with the practitioner's handpiece. By contrast, a well­
delimited Gartner type 1 calcium deposit (Gartner's classification scale) cau­
ses marked shadowing in the adjacent cortical bone of the humeral head. This
is not the case where calcium accumulates in the subacromial bursa. A bone­
tendon rupture at the greater tuberosity of the humerus may erroneously
be thought to be a calcific deposit. Multiple deposits can be topographically
assigned to tendons of the rotator cuff in various sectional planes. Inho­
mogeneities caused by calcium deposits can be imaged without ultrasonic
attenuation. The paste-like calcium deposit (Gartner type 2 or 3) lacks the
acoustic shadowing.
 Son ography

Fig ure 22 (left) :

Mu ltiple small calcific deposits in
the RC; no acous tic shadowing

Fig ure 23 (rig h t) :

Major calcific deposit in the R C
with sh adowing in the cortical
bone; moves with the probe
during functional exam in a tion

Sonography plays an important role in patients with myofascial pain syn­

drome. Penetration depth in ESWT is determined using an appropriate stand­
off. Following sonographic measurement of soft-tissue and muscle thickness,
subsequent treatment is risk free. It was long the case that this recommenda­
tion applied, in particular, to ESWT applied directly above lung tissue, neuro­
vascular bundles and internal organs. Today, the view is held that pulmonary
and neurovascular structures should no longer be regarded as tissues vulne­
rable to shock wave damage, because doses now used are far lower and hence
safe. This was discussed at sessions held by the German-language Interna­
tional Society for Extracorporeal Shock Wave Therapy (DIGEST) - as part
of the Annual Conference of the Association of O rthopaedists and Trauma
Surgeons in South Germany (VSO U) in 2019 - and was formally and unani­
mously adopted. Tumours and foetal tissue remain the sole contraindications
for shock waves.

Sonographic calculations of thickness and area prior to ESWT indicate the

extent of degeneration of the tendon. For example, at the origin of the ten­
don of the extensor digitorum communis muscle, thickenings may be found
that, if they exceed 4.2 mm in width and constitute an enlargement of over
32 mm2 in area, are deemed pathognomonic.11 0 • 111 Measurements of thickness
are useful in assessing pathological plantar fascia (threshold size 8 mm), the
typical spindle-shaped thickening in cases of achillodynia (10 mm) and inser­
tional tendinopathy of the patellar ligament Uumper's knee, 5 mm) before
and at the end of treatment. They are the crucial factor in the success or fai­
lure of ESWT.

65
 I n power Doppler i m a g i n g ( P O I ) , w e have a s u ita b l e proced u re for vasc u l a r
d i a g n ostics. I rreg u l a r i ntratendinous microvasc u l a rization i n pathologica l ly
altered reg ions of the tendon ca n be made visi b l e i n this way. 1 2 -1 4
1 1

M . Beck has proposed a g ra d u ated sca l e fo r i rreg u l a r new vessels that a re de­
tecta b l e i n POI i mages. Absen ce of vasc u l a rity is assigned a score of o . Where
there a re more tha n t h ree vessels, the score g iven is 3 . This g ra d u ated sca l e
is h e l pfu l i n docum entation for diag nostic p u rposes a n d fo r m o n itori n g p ro­
g ress i n treatment.1 01

At the site where tendons a re attached to a n epicondyle, POI reveals patho­

log ica l n eovascula rizati o n , as is a l so the case with degenerative Ach i l les a n d
pate l l a r ten dons. These n ew blood vessels a re t h e m a n ifestation a n d "co n ­
d u it" o f n u merous nociceptive fi bres t h a t have s i m u ltaneously g rown i nto t h e
tissue fro m adjacent tiss ue (e.g. i nfra pate l l a r fat pad). The n u m ber o f these
vessels co rrelates with the n u m ber of pa i n fi bres. H istological exa m i nation
of pate l l a r ten d i n o pathies co nfirms this a n g iogenesis (wh ich ca n be seen by
m ea n s of P O I ) a n d the n ociceptive fi bres in the vascu l a r wa l l s . The more pro­
n o u n ced this neovascu la rity, the g reater the extent to which pa i n med iators
a re rel eased . This was fi rst d iscovered fo r epico ndyl itis by a resea rch tea m led
by E. Zeisig in 2006, using P D l . 1 2 -
1 11
4

The l evel of i rreg u l a r n eovascu la rization as revea led by P O I , i n terms of the

n u m ber of vessels vis u a l ized , is a crucia l fa cto r i n recovery. If n ew vessels
conti n u e to be evident, these fo rm the point of o ri g i n fo r the sprouti n g of
u n desirable, path ological vessels. In such cases, recu rrence is poss i b l e a n d
treatment must be conti n u e d . If n ew vessels a re not evident i n post-ESWT
sonogra p hy or i n fol low- u p exa m i nations, this sugg ests that a l l pa i n fi b res i n
t h e treatment a rea have been fu lly e l i m i nated . Persistence o f sym pto ms of
latera l epicondyl itis, or a recu rrence of this co n d ition, i n d i cate that n eovascu­
la rization and nociception have not been eradicated . 11 5 • 116

66
 S o n o g ra p hy

Figure 24:
Lateral epicondy/itis, neovoscu­
/arizotion in the ten don of the
extensor carpi radio/is brevis
muscle (POI}

Fig ure 25:

POI, neovascularization
of the Ach illes ten don
LO N G-ESTABLISH ED
AN D N EWER
ESWT I N D I CATI O NS
 Lon g -established and newer ESWT indications

INTRODUCTION

Chronic tendinopathies are mainly caused by abnormal, repetitive and uni­

form biomechanical stress over a long period of time. Today, the general
assumption is that they are due to structural damage resulting from changes
in tenocyte activity based on the continuum model from tendons that are
healthy to those that are painful and, ultimately, ruptured. This progression
of the pathology is typical of the Achilles tendon, patellar tendon and supra­
spinatus tendon, for example.11 4 - 117

Clinical manifestations include typical spindle-shaped or nodular thickening.

Microscopic examinations of surgical specimens have revealed immature
col lagen fibres (type 1 1 1), whereas the collagen found in healthy tissue is type I.
Another typical symptom is irregular vascularity as evidenced by power Dopp­
ler imaging (POI). The new blood vessels that sprout from the surrounding
tissue do so together with nociceptive fibres. These fibres are no indication
that healing is progressing and do not have any vascular function.11 8

Inflammation processes play a major role in chronic tendinopathies. Adap­

tive immunological activity against specific pathogens gradually decreases
as normal ageing progresses and as a result of prolonged uniform overuse.
On the other hand, the unspecific innate immune defence increases in
strength over time and releases proinflammatory messenger substances
such as prostaglandin E2, interleukin-6, interferon-gamma (IFNy) and tumour
necrosis factor alpha (TNF-a). In turn, this mix of messenger substances sti­
mulates the formation of free radicals, which act as aggressive oxygen com­
pounds and may damage any type of tissue, including tendons." 9

69
 Long -estab lished ESWT indicati o ns

SHOULDER IMPINGEMENT/TENDINOPATHY WITH OR WITHOUT

CALCIFICATIONS, ROTATOR CUFF SYNDROME

PATHOGENESIS
Shoulder motion is achieved by a combination of glenohumeral joint move­
ment and multidimensional scapular movement. The strong ligaments of the
joint capsule and the muscles of the rotator cuff (RC) stabilize the glenohume­
ral joint. By exerting cranial tensile forces, the shoulder girdle muscles secure
the humeral head in its position in the shoulder blade socket. The scapula is
attached to the thorax by muscles. Here, the adhesive suction forces between
the fasciaI layers of the subscapular muscle and the serratus anterior muscle
play a crucial role.

The latissimus dorsi and biceps brachii muscles act as antagonists to the
shoulder girdle muscles. The humeral head remains in its socket when the
tensile forces in the cranial and caudal direction are balanced. If there is no
such equilibrium, enthesopathies and myofascial trigger points will develop
in the shoulder girdle region.117

If the muscle force caudalizing the humeral head decreases, the humeral
head is slightly displaced in the cranial direction and may be decentralized
over time. As a result, the rotator cuff, specifically the supraspinal portion
of the tendon, is subjected to increased tensile stress. The long lever arm
effect of the supraspinatus tendon and the resulting biomechanical bene­
fits achieved when the humeral head is in normal position are gradually lost.
Increasing upward displacement of the humerus narrows the subacromial
space and so compresses the rotator cuff and subacromial bursa. Weakening
of the dorsal scapular muscles due to age or poor posture exacerbates the
constriction of the subacromial space. This may be accompanied by more
frequent bouts of acute subacromial bursitis. The constriction results in re­
duced microcirculation in the insertional region of the rotator cuff, which
leads to the degeneration of the supraspinatus tendon. Low-grade inflam­
matory processes, continuous bombardment by inflammatory messen­
ger substances and the formation of oxygen radicals attack the tenocytes,

71
 causing them to degenerate. lntratendinous deposition of calcium apatite
11 9

crystals represents a further complication affecting the rotator cuff tendons.

The clinical symptoms are those of subacromial pain syndrome. In the me­
dium and long term, destructive structural changes in the subacromial space
and osteoarthritic alterations of the acromioclavicular joint (AC joint) oc­
cur. Movements in the horizontal plane cause impingement. In many cases,
fissures and progressive tendon thinning in the region of the hypovascular
insertion of the supraspinatus tendon may occur in the long term, ultimately
resulting in tendon rupture (continuum).

HISTORY AND DIAGNOSIS

The incidence of shoulder impingement syndrome increases with age in peo­
ple over 30 years old. Answers to questions related to job-specific movements
or physical exercise, pain at rest or during activity, sleep disturbed by pain or
aching at night, tenderness, pain on exertion, and to acute or chronic symp­
toms provide valuable information for diagnosis.

During physical examination, the deltoid muscle, scapula position, shape of

the spinal column and the AC joint should be checked. Functional tests of the
range of motion and specific rotator cuff tests complete diagnostic proce­
dures for shoulder impingement. Examination, palpation and functional tests
of the shoulder girdle muscles and their tendon attachments (humerotho­
racic, scapulothoracic, scapulohumeral muscles) may reveal trigger points
which can be identified and instantly treated by means of pressure waves or
shock waves. 11 7

Extracorporeal shock waves (ESW) may induce typical referred pain as illustra­
ted below for the supraspinatus and infraspinatus muscles (examples).

72
Lon g -estab l ished ESWT indications

Fig u re 26:
Pain referral i n to the
proxim a l lateral upper
arm and into the radial
epicon dyle of the supra ­
spina tus m uscfe 7

Fig ure 2r
Referred pain from the
trigger points of the
infraspinotus muscle:
ventral upper o rm.
ulnar elbow o n d ulnar
forearm'

73
 DIAGNOSTIC IMAGING
I X-ray, including scapular Y-view, osseous pathologies
Sonography, functional examination, plus PDI (if required)
MRI of pathological morphologies

EXCLUSION CRITERIA
I Functional or secondary impingement
Vertebrogenic, vascular or neurovascular causes
Entrapment neuropathy of the spinal accessory nerve at the point where
it emerges dorsally from the sternocleidomastoid (SCM) muscle or where
it enters the trapezius muscle; adhesions after ENT surgery (e.g. neck dis­
section)
Traction/compression of the suprascapular nerve in the suprascapu­
lar notch, especially after RC rupture caused by medial displacement of
muscles1 20 . , 2,
Compression of the axillary nerve between the head of triceps and teres
major muscles in the lateral axillary foramen (overhead work)120
Neuralgic shoulder amyotrophy
Complete rotator cuff rupture
Acute subacromial bursitis with reactive effusion in the synovial sheath of
the long biceps tendon

TREATMENT
Suggestion: Regimen A, Regimen B for PW therapy (see chapter "Combination
of shock wave and pressure wave technology")

74
 Lon g -established ESWT indications

Patient positi o n i n g : sta b l e s i d e-lyi ng position

Fig ure 28:

Blue m arker: s upraspina tus
ten don attach ment to the
g reater tuberosity of the
h u merus. Other attach ment
trigger points ( n o t shown),
e. g. a t the rhomboid m uscles,
levator scapulae m uscle o r
latissimus dorsi m uscle, c a n
b e localized / R e d m arkers:
myofascial trigger points
in the suprasp i n a tus a n d
infrasp ino tus m uscles located
below the trapezius m uscle
layer

Figure 2 9 :
ESWT of the s uprasp i n a tus
insertion site and long b iceps
tendon after eliciting local
p a tient- recognized pain o r
referred pain (not consta n t)

Fig ure 3 0 :
PW treatment of myofascia/
trigger points in the s upra ­
spina tus tendon (example)

75
LATERAL AND MEDIAL HUMERAL EPICONDYLOPATHY

PATHOGENESIS
Prolonged overuse of the forearm extensor and flexor tendons attached to
the elbow or abnormal biomechanical stress lead to morphological (struc­
tural) pathologies at the tendon's osseous insertion site. Pronounced angio­
fibroblastic and degenerative changes occur in the collagen framework.
Moreover, a histological examination of surgical specimens revealed cal­
cifications in 20% of the investigated cases.1 22 On the extensor side, all four
extensors are affected, especially the extensor digitorum communis and
brachioradialis muscles. On the flexor side, the pronator teres and flexor car­
pi radialis muscles are involved, because these muscles are more strongly
activated when they are loaded than the palmaris, flexor digitorum und flexor
carpi ulnaris muscles located more medially.

Lateral and medial epicondylar tendinopathy, referred to as epicondylopa­

thy, results from long-term/repetitive overuse or abnormal biomechanical
stress, causing early ageing. Proinflammatory messenger substances develop
aggressive free radicals, which are responsible for degenerative tendon
damage. Deficiencies in the tendon strength of flexors and extensors com­
11 9

monly appear due to sporting activities (racket sports) or overuse associated

with manual work. However, even lower-strain repetitive activities, such as
working with a PC mouse or carrying serving trays, may cause lateral or me­
dial epicondylitis.

DIAGNOSIS
The clinical symptoms of lateral and medial epicondylitis include pain on
palpation at the tendon's osseous insertion. An important functional test to
check the range of motion in the diagnosis of epicondylitis is the Thomsen
test (overextending the wrist extensors), which also explains why holding a
cup of coffee with the elbow extended and the wrist overextended may cause
terrible pain. Patients suffering from medial epicondylopathy experience
stronger pain when they contract their forearm flexors. Any involvement of
the ulnar nerve must be ruled out. Irritation of the ulnar nerve manifests by
 Lon g -established ESWT indications

paraesthesia of fingers 4/5, which is exacerbated within 30 to 60 seconds after

maximum elbow flexion, marked forearm pronation and wrist overextension.
Epicondylopathy is frequently accompanied by myofascial trigger points,
which can be localized with shock waves. In the extensors, they primarily
occur in the extensor digitorum communis and brachioradialis muscles. In
the flexors, myofascial trigger points are localized in the pronator teres and
flexor carpi radialis muscles.

DIAGNOSTIC IMAGING
I X-ray: osseous alterations
I MRI: suspected irreversible pathological changes in structure
Attention: steroid injections up to 3 or 4 weeks before the MRI cause
higher signal in the MRI scan and lead to an erroneous diagnosis of tendon
pathologies.
Sonography: evaluation of tendon and muscular structures

EXCLUSION CRITERIA
I Cervical radiculopathy
I lnterscalene triangle compression
Posterior interosseous nerve syndrome, radial nerve compression
Osteoarthritis / cartilage damage
Synovial, rheumatic alterations, tumours, osteomyelitis
Adhesions of fascia I compartments
Acute lateral or medial epicondylitis

TREATMENT
Suggestion: Regimen A, Regimen B for PW therapy (see chapter "Combination
of shock wave and pressure wave technology")

77
 Patient positio n i n g : s u p i n e position

Figure 31:
With the elbow flexed, the
a rm rests on the patient table:
epicondylar tendon a ttach ­
ment (blue marker), examples
af myofascial trigger points in
extensors (red m arkers)

Figure 32:
Shock wa ve application to
treat local and referred pain
(if any); handpiece m us t be
in vertical position {!)

Figure 33:
Pressure wave application to
myofascial trigger points on
extensor side
 Lon g -established ESWT indications

Treatment of medial epicondylopathy is performed with the elbow flexed to

about 90° and with the externally rotated arm placed as flat as possible on the
patient table or on a foam wedge pillow.

Fig ure 34:

Tendon insertion a t m edial
epicondyle (blue marker),
examples of trigger points in
forearm flexors (red markers)

Fig ure 35:

SW treatment of
medial epicondyle

Fig ure 36:

PW treatment of
forearm flexors

79
 I NSERTIONAL TEN D I N O PATHY OF D ISTAL B I C EPS TEN D O N

lnsertional tendinopathy of the distal biceps tendon at the radial tuberosity

is a rather common condition. It is general ly caused by repetitive overexer­
tion of the distal biceps tendon, which is responsible for forearm supination.
Clinical symptoms are increased pain on resisted supination. After the resis­
ted supination test, the radial tuberosity region is characterized by marked
tenderness, which can also be elicited by extracorporeal shock wave applica­
tion. Myofascial trigger points in the supinator muscle and the resulting com­
pression of the radial nerve (posterior interosseous nerve) may contribute to
stress-induced pain.
Treatment should be performed as suggested on chapter "Combination of
shock wave and pressure wave technology"), fol lowing Regimen A or B.

Figure JT
MRI scan of elbow; sagittal
section: increased signal gain,
chronic insertional tendinopa­
thy of distal biceps tendon

ACH I LLODYN IA O R M I D-PORTI O N TEN D I N O PATHY, I NSERTIO­

NAL TEN D I NO PATHY OF AC H I LLES TEND O N

AETIOPATHOGENESIS
Every trauma surgeon wil l have seen advanced-age patients with Achil les ten­
don rupture experiencing delayed or even failed post-operative healing for
weeks or indeed months. These problems are frequently caused by hypoper­
fusion of the distal lower leg. Blood supply to the Achil les tendon is an issue
because the feet are the parts of the body that are farthest away from the

80
 L o n g - e s t a b l i s h e d ESWT i n d i c a t i o n s

heart. The descending branches of the posterior tibial artery and peroneal
artery do not provide sufficient arterial supply to the tendon and its surroun­
ding soft tissue.

The tendon is composed of longitudinal collagen fibre bundles. Thin fascia

envelops each fascicle to improve gliding. Other constituents of the tendon
include elastin fibres, tenocytes and tenoblasts, which are responsible for the
production of collagen fibres and for the remodelling process during tendon
healing. The tendon matrix is composed of mucopolysaccharides.

The physiological stress range of the Achilles tendon (500 to 1000 kg/cm2 )
decreases with age and with reduced exercise and mobilization. The meta­
bolism of the tendinous part of the muscle-tendon complex is much slower
than that of the contractile muscle element that produces the tendon's kine­
tic energy. Hypoperfusion and poor metabolism lead to structural changes
and reduced tendon stiffness. The gap between physiological stress resis­
tance and experienced stress widens.6 9 · 3
12

In mid-portion tendinopathy or calcaneal insertional tendinopathy, an in­

growth of irregular pathological capillaries and nociceptive fibres from the
peritendineum is observed. These fine capillaries have nothing in common
with the healing effects of inflammatory vessels. 4 • Mid-portion achillody­
11 118

nia can be easily diagnosed due to the spindle-shaped thickening about 4 cm

proximal to the tendon attachment to the calcaneus. Reduced tendon
strength and a sudden increase in tensile stress frequently cause tendon
rupture. 6 9 . 1 4 . ,,3
1

Overweight patients, men and athletes performing repetitive uniform move­

ments are at risk of developing Achilles tendinopathy. Uneven surfaces may
also be considered a risk factor.

DIAGNOSIS
The region of the tendo-osseous junction of the Achilles tendon and calcane­
us is found to be tender on palpation and exhibits a swelling. These are typi­
cal symptoms of a chronic inflammatory insertional tendinopathy. Along the

81
 tendon's path, a spindle-shaped thickening is observed about 2 to 6 cm pro­
ximal to the insertion site. This thickening may be accompanied by palpable
nodular indurations which often manifest in painful mid-portion achillodynia.

DIAGNOSTIC IMAG ING

I Sonography: texture, echogenicity
X-ray: exclusion of osseous lesions
MRI: rupture, degeneration

EXCLUSION CRITERIA, DIFFERENTIAL DIAGNOSIS

I Metabolic conditions (hyperuricaemia, familial hypercholesterolemia)
I Complete or partial rupture

TREATMENT
In treatment of insertional and non-insertional tendinopathy it is important
to reduce the tone of the shortened triceps surae muscles by means of the
V-ACTOR® vibration therapy system or by applying pressure waves (with the
Ro 40 transmitter).

Suggestion: Regimen A, Regimen B for PW therapy (see chapter "Combination

of shock wave and pressure wave technology")

Patient positioning (see p. 55)

Figure 38:
Foot joints extend beyond the
end of the patient table; thera­
pist immobilizes the patient 's
foot with h is/her knee

82
Lon g -esta b l ished ESWT indications

Fig ure 3 9 :
Blue m a rkers at tendon
attachment (insertion a l
ten dinopa thy) a n d three
fingers more p roxim a l
(mid-portion ach il/odynia/
n o n - insertio nal ten dinopa thy)

Fig ure 4 0 :
S W trea tment o f m id-portion
ach illodynia (blue m a rker)

Fig u re 4 1 :
Treatment of insertio n a l
ten dinopa thy

83
Fig ure 42:
PW treatment of calf m uscles
(red m a rkers)

The Sweden-based team led by H. Alfredson recommends eccentric strength

training to treat achillodynia. Muscle training results in increased sarcomere
elongation; it induces growth processes to add new sarcomeres and provi­
de enhanced strength. Inactivity, on the other hand, reduces the number of
sarcomeres and leads to muscle shortening.1 24 · 125 Eccentric stretching exer­
cises combined with ESWT has been shown to provide better results than
ESWT alone. This has been confirmed by long-term follow-up studies.74 • 75. 1 24
Treatment intensity is dependent on the size of the swelling and the degree
of neovascularization.

Eccentric stretching exercises can be easily done on any set of stairs. With the
balls of both feet on the stair (facing the stair as if going upstairs), the patient
raises and lowers the heel slowly and uniformly (two sets of 20 to 30 repeti­
tions, twice a day).
 Long -esta b l i s h e d ESWT i n d i ca t i o n s

PLANTAR FASCIITIS - HEEL SPUR

AETIOPATHOGENESIS
Pain when first getting out of bed in the morning is typical of plantar fasciitis,
also known as heel spur. It is caused by increased tensile stress on the three­
layer plantar fascia. Normal loading and heel-to-toe movement become
increasingly difficult over the day. The age-related loss of stability of the
foot skeleton, and foot deformities such as flat foot or hollow foot, lead to
an increase in tension that causes pain. This, in turn, results in micro-tears.
Sprouting pathological capillaries without the ability to induce repair are ac­
companied by nociceptive fibres. Continuous loading and overexertion of the
plantar fascia - which at this stage is already weakened by the reduced tear
resistance - lead to steadily increasing neovascularization and the formation
of additional nociceptors. As a consequence, the complete clinical picture of
plantar fasciitis develops. Common risk factors for developing plantar fasciitis
are excess weight, axial deviations in the lower extremity, standing for long
periods of time, reduced ankle joint mobility and running sports.

Biomechanical/functional considerations on the causes of plantar fasciitis

were discussed in Deutsches Arzteblatt (a weekly German-language medical
magazine). There, N.M. Hien writes: "Habitual inclination posture, highest
126

loading on the forefoot and reduced toe motor function, especially of the
long flexor muscles, lead to shortening of the calf, achillodynia and overloa­
ding of the plantar fascia and the metatarsal bone, which can be described as
a chain syndrome. The weakest link develops symptoms, while 'protecting'
the other chain links." Hien continues: "The load is spontaneously taken off
the painful side; consequently, the load increases on the opposite side, which
may then start to hurt." 1, 1 2 8
12

The slightly (physiological) valgus position of the calcaneus relative to the

tibial axis undergoes additional pronation due to the tensile force of the shor­
tened calf muscles. This condition, in combination with the acentric joint axis
of the subtalar joint, contributes to increased stress on the plantar fascia,
causing micro-tears on exertion. Over time, an osteogenetic reaction can
12 9

85
 be observed in the inflammation zone of the plantar fascia insertion. The
spur-like ossification of the plantar fascia is not the cause of pain. In fact, it is
often detected in X-rays as a secondary finding without causing any reported
symptoms. The heel spur represents the osseous repair of an insertional ten­
dinopathy.

DIAGNOSIS
Pain when first getting out of bed in the morning, which increases over the day.
Typical site tenderness at the media-plantar attachment of the plantar fascia.

EXCLUSION CRITERIA
I Metabolic conditions (hyperuricaemia, familial hypercholesterolemia)
Lumbar radicular symptoms
Local irritation of the tibial nerve whose medial branch innervates the
medial and plantar aspects of the heel, nerve entrapment
Bone tumours, fatigue fractures
Age-related shrinkage of fat pads protecting the calcaneus
Acute rupture of the plantar fascia

DIAGNOSTIC IMAGING
I X-ray: lateral soft X-ray exposures of the affected foot with the patient
lying on the table and standing (under load) to evaluate the fascia thickness
MRI: suspected rupture, diagnosis of a bone bruise
Sonography: examination of fascia thickness (normally 4 mm); however,
the findings have limited value because even asymptomatic patients
may exhibit a thickened fascia attachment. Echogenicity, texture com­
13 0

pared to healthy side, POI progress monitoring in case of pathological neo­

vascularization

TREATMENT
The effectiveness of ESWT has been demonstrated in a wealth of scientifically
robust studies. "There is no further need of discussion." This is how J. D. Rompe
repeatedly put it at the end of his articles on this subject as long as 10 to 12
years ago.

86
 Long-established ESWT indications

In the treatment of plantar fasciitis, special consideration must be given to po­

tentially shortened calf muscles. Clinical examination of calf muscle tightness
is possible with the Silfverskiold test. Reduced dorsiflexion of the ankle joint
of 0 ° , or even less, increases the risk of developing plantar pain by a factor of
23 compared to 10 ° dorsiflexion or above.43

Long-term muscle training over the entire range of motion improves sarco­
mere elasticity, induces the formation of growth factors so that new sarco­
meres are added, and maximizes strength development. By contrast, inacti­
vity results in permanent deterioration of the ankle range of motion and in
reduction of the number of sarcomeres, thus shortening the calf muscles. 1 2 5

Plantar fasciitis should be treated by a combination of ESWT and eccentric

stretching exercises (see p. 84, combination treatment of achillodynia).

As in the treatment of achillodynia, the muscle tone of the generally shor­

tened triceps surae muscles (long foot flexors) and quadratus plantae muscles
(short muscles of the foot) should be reduced with pressure waves or by
means of vibration therapy before starting to apply shock waves.

Suggestion: Regimen A, Regimen B for PW therapy (see chapter "Combination

of shock wave and pressure wave technology")
 Patient positio n i n g : p ro n e positio n (see p. 52)

Figure 43 :
Foot joints extend b eyond the
end of the patient table: thera­
pist immobilizes the patient 's
foot with his/her knee / Blue
marker iden tifies attachment
trigger point in the m edia ­
plantar region of the heel
/ Red marker: example of
trigger point in the m edial
gastrocnemius region; poten ­
tial trigger points in triceps
surae m uscles not shown

Figure 44 :
PW trea tment of calf muscles/
Red marker: example of
additional trigger points
(not shown)/PW treatment
of sole-side quadratus
plantae m uscle (not shown)

Figure 45:
SW treatment of the m edio­
plantar region of the heel with
strongest local pain (pain
recogn ition)

88
 Lon g -estab l ished ESWT indications

JUMPER'S OR RUNNER'S KNEE, PATELLAR INSERTIONAL

TENDINOPATHY

AETIOPATHOGENESIS
The lever arm effect of the thigh a nd lower leg ca uses tensile stress in the knee
extensor mecha nism, which may be exacerbated by j u mping sports a nd stop­
a nd-go movements. This ca n lead to the develop ment of insertional tendino­
pathy. Not only athletes are at risk, but also non -athletes, older or overweight
people demonstrating diminished muscle extensibility. Q uadriceps atrophy
a nd weakness of the contractile elements (sarcomeres) reduce the kinetic
energy in the tendons, ca using them to become ra pidly overexerted. As a
consequence, patellar tendinopathy - similarly to achillodynia - ma nifests
with micro-tears, irreg ular ca pillaries a nd nociceptive fi bres.

Besides impaired extensibility of the q uadriceps or innate liga ment weakness,

patella alta is a n other common risk factor for developing insertional tendino­
pathy.

Patellar enthesopathy occurs at the following sites: at the a pex of the patella
( 7 9 %), at the base of the patella (1 6%) a nd at site where the patellar liga ment
attaches to the tibial platea u (3%). Pathological cha n g es of the liga ment in its
entirety accou nt for only 2% of all cases of patellar tendinopathy.131 , ,3,

DIAGNOSIS
Typical symptoms are reddening , swelling a nd tenderness at the a pex a nd
base of the patella or at its tibial attach ment. Shortening of the tendons of the
knee extensor mecha nism ma nifests during the prone q uadriceps fl exibility
test ( measuring the dista nce from heel to buttock) . By extending the exten­
sor mechanism, a pulling pain is induced at the affected tendon attach ment
sites. The sa me pain is induced when the patient descends into a sq uat posi­
tion . Relia ble a nd precise localization of an attach ment trigger point is achie­
ved by mea ns of shock wave navigation a nd the patient's feedback.

89
 EXCLUS I O N C R ITERIA, D I FFERENTIAL D IAGNOSIS
I Femoral-patellar osteoarthritis
lnfrapatellar bursitis
Attention: growth disorders such as Sinding-Larsen and Johansson syndro­
me (patella) or Osgood-Schlatter disease (tibial plateau) are not conside­
red exclusion criteria.

D IAG NOSTI C I MAG I N G

I X-ray: osseous alterations, calcifications
Sonography: hypoechoic tendon insertion or increased echogenicity.
Thickened tendon distal to the apex of the patella (threshold size 7 mm),
hypoechoic texture, tears
Neovascularization in hypoechoic areas can be identified by colour Dopp­
ler imaging.
MRI: exclusion of tendon rupture, bone bruise at tendon insertion

TREATMENT
lsokinetic strength training on exercise machine combined with ESWT.1 33. ,34

Suggestion: Regimen A, Regimen B for PW therapy (see chapter "Combination

of shock wave and pressure wave technology")

go
 L o n g -esta b l i s h e d ESWT i n d i c a t i o n s

Patient positi o n i n g : s u pi n e positio n (see p. 5 1 )

Fig u re 4 6 :
Blue m a rkers: possible
attachment trigger points
at distal p a teffar m a rg in/
Red m a rkers: myofascial
trigger points in the vastus
• • m edia/is and fa tera lis m uscles

Fig ure 4 7:
Treatment of apex of p a tella
and myofascial trigger paints
in q u adriceps m uscle

91
 lnsertional tendinopathies of the quadriceps tendon at the superior patellar
pole and tibial plateau (exclusion criterion: Osgood-Schlatter disease) pose no
diagnostic challenge, especially if they are not preceded by an acute condi­
tion. The fairly rare cases of complete or incomplete superior rupture of the
quadriceps tendon are easily palpable in clinical examination. The extent of
the deficiency in extension reveals the width of the rupture. Slight inhibition
of extension and pain on compression of the superior patellar margin without
palpable indentation are indicative of patellar tendinopathy. The diagnosis is
verified by imaging. Treatment is performed following the procedure adop­
ted for distal patellar tendinopathy. Myofascial trigger points in the quadri­
ceps muscle, and in the ischiocrural flexors that act as antagonists, should be
treated with pressure waves (stamping and smoothing technique).

92
 HAMSTRING TENDINOPATHY (ISCHIOCRURAL MUSCLES)

AETIOPATHOGENESIS
Three tendons of the hamstrings originate from the ischial tuberosity. The
biceps femoris muscle runs laterally and converges dorsally with the short
head in the middle third of the femur, inserting at the fibula head with its ten­
don. The semitendinosus and semimembranosus run medially, along with the
gracilis muscle. Joined by the sartorius tendon, they terminate to form the pes
anserinus at the medial tibial plateau. The fibres of the strong semimembra­
nosus reach deep into the tendon ends of the pes anserinus. As their name
suggests, the ischiocrural muscles act upon two joints. They extend the hip
and flex the knee. Additional functions of the gracilis and sartorius muscles
are adduction and abduction, with the sartorius muscle also involved in inter­
nal rotation.

Sudden, massively impactful traumas generally result in strain or tears at the

muscle-tendon junction. Repetitive traumas cause chronic degenerative ten­
dinopathy. Tendons injured in this manner are prone to rupture. The normal
eccentric function of the ischiocrural muscles has a slowing or inhibitory effect
in terms of the speed of knee extension when placing the heel on the ground.
This braking effect is eliminated during extreme, repetitive sprinting or (in the
case of footballers) during shooting practice. In these types of sports, partial/
single bundle tears or complete rupture of a hamstring tendon - or even a
muscle fibre - are rather common. Hence, proximal tendinopathies are a war­
ning sign. lnsertional tendinopathy of the biceps femoris muscle at the site
of insertion into the fibula is the result of chronic overuse. Medial insertional
tendinopathy at the pes anserinus is more frequent in non-athletes. These
disorders occur after substantial breaks from training. The transition from an
acute injury to a chronic condition is a continuum.

94
 Other indications in sports medicine

DIAGNOSIS
I Tenderness in the lateral aspect of the head of the fibula proximal to
Gerdy's tubercle; tender trigger points in the lower third of the thigh along
the biceps femoris muscle
Medial tenderness two to three fingers distal to the knee joint cavity at the
pes anserinus
Tenderness in the region of the ischial tuberosity
Overextension pain during passive hip joint or thigh overextension

DIAGNOSTIC IMAGING
I X-ray: pelvis, knee joint
Sonography: muscle tendon tears
MRI: muscle tendon ruptures, differential diagnosis of bone bruise

EXCLUSION CRITERIA
I Meniscus disorders
Recent trauma, osseous alterations

TREATMENT
Suggestion: Regimen A, Regimen B for PW therapy (see chapter "Combination
of shock wave and pressure wave technology")

95
 Patient position i n g : s u pi n e positio n

Fig u re 4 8:
Hip flexed to 1 0 0 - 1 2 0 ° ;
SW h a n dp iece applied
to isch ial tuberasity

Fig ure 4 9 :
PW treatment af trigger
p o i n ts (exa mples) in the
h a m s trings a t the m uscle­
tendon jun ction

Fig u re 5 0 :
S W treatment of t h e
h a ms tring ten don insertion
(pes a n s erinus)

96
 Lon g -established ESWT indications

HIP ADDUCTOR TENDINOPATHY

AETIOPATHO G ENESIS
The pectineus muscle and the long adductor, short adductor and great ad­
ductor muscles can be chronically overloaded by sports activities such as
executing a sliding tackle in football, doing the splits in gymnastics or hor­
se riding (applying too much pressure on the horse's flanks with one's legs).
Tendinopathy may also develop from poor sitting habits with legs constantly
crossed or from an ergonomically poor sitting position in the workplace. The
adductor tendons shorten and may degenerate over time.

D IAGNOSIS
Pain when sitting cross-legged. Spreading the legs involving the hip joint
causes groin pain. Isolated tenderness at the ascending ramus of the pubis
manifests in cases of insertional tendinopathy of the long adductor and pec­
tineus muscles. Tenderness at the base of the femoral triangle presents due
to a myofascial trigger point in the pectineus muscle. Other painful trigger
points may be located along the long adductor muscle on the medial aspect
of the thigh. In this case, patients often report knee pain which, clinically, is
projected pain.

EXCLUSION C R ITERIA
I Soft groin
I Irritation or entrapment of the ilioinguinal nerve

D IAGNOSTIC IMAG ING

I X-ray: pelvis
I Sonography: soft groin
MRI: differential diagnosis, inguinal hernia

TREATMENT
Suggestion: Regimen A, Regimen B for PW therapy (see chapter "Combination
of shock wave and pressure wave technology")

97
Fig u re 5 1 :
S u p i n e position, l e g placed
into a fig u re-4 position/
Red m arkers: trigger p o i n ts
in adductors (co m m o n ly long
adducto r)/Blue m arker:
ten don insertion site a t
ascending r a m us of pubis

Fig ure 52:

S W treatm en t of ten don at
ascending ram u s of p u b is/
A tten tion: n e u rovascular
b u n dle

Fig u re 53 :
PW treatment of myofascia/
trigger points in adductors

98
 L o n g - e st a b l i s h e d ESWT i n d i c a t i o n s

ILIOTIBIAL BAND TENDINOPATHY

AETIOPATHOGENESIS
The iliotibial ba nd is formed by fusion of the tendon fi bres of the tensor fasciae
latae muscle a nd the gluteus maxi mus a nd medius muscles. On the lateral as­
pect of the trocha nter, the fi bres fuse to form an a poneurosis (a sta ble, mesh ­
like tendinous membra ne). The tensor fasciae latae muscle a nd iliotibial ba nd
exert a bala ncing force to cou nteract the bending stress on the thig h when
sta nding.

The iliotibial band inserts onto Gerdy's tubercle at the external tibial platea u .
Some fi bres project into the patellar retinaculu m.

Excessive run ning or cycling may ca use increased tensile stress at the inser­
tion site of the iliotibial ba nd. I n the long term, painful chronic tendinopathy
may develop at Gerdy's tu bercle.

I n the event of inj ury to, or wea kness of, the q uadriceps muscle (vastus la ­
teralis muscle) , knee extension is limited. This deficiency is compensated for
by the tensor fasciae latae a nd sartorius muscles, which are a ble to generate
increased tensile stress at the a nterior superior iliac spine via their tendinous
origin. This may lead to painful tendinopathy over time.

I nsufficiently developed hip sta bilizer muscles ca use the u nloaded hip to tilt
downwards with each step ( Duchen ne gait). The strong tensile stress of the
iliotibial band during short sta nding periods may lead to the develop ment of
insertional tendinopathy at the a nterior su perior iliac spine or at the lateral
tibial platea u .

I n the event o f pronou nced varus o f the thig h , co ntinual rubbing o f the ilioti­
bial ba nd over the lateral femoral epicondyle results in friction syndrome.
Leg length discrepa ncy, foot su pination a nd ru n ning on slo ping surfaces may
co ntribute to the develop ment of iliotibial ba nd tendinopathy at the origin or
insertion sites.

99
 DIAGNOSIS
Tenderness and pain on extension at the lateral tibial plateau (Gerdy's tuber­
cle); tenderness along the iliotibial band and at the anterior superior iliac spine

EXCLUSION CRITERIA
I Lateral meniscus injury
I lnsertional tendinopathy of the biceps femoris muscle

DIAGNOSTIC IMAGING
I X-ray: osseous alterations of the pelvis; genu varum
Sonography: iliotibial band, suspected fibrosis
MRI: soft-tissue changes after trauma

TREATMENT
Suggestion: Regimen A or B

Patient positioning: side-lying position

Figure 54:
Blue marker: Cerdy 's tubercle,
an terior superior iliac spine
/AS/5) and apaneurosis (about
4 inches distal to the greater
trochanter)

100
Long-esta b l i s h e d ESWT i n d i c a t i o n s

Figure 55:
ESWT of anterior superior
iliac spine (ASIS)

Figure 56:
PW treatment of iliotibia/
band (here oponeurosis)

Fig ure 57:

Treatment of Gerdy 's
tubercle, insertion site
of iliotibia/ band

1 01
 ANTERIOR TIBIAL SYNDROME

The tibialis anterior muscle is part of the anterior muscle compartment of the
lower leg, along with the extensor hallucis longus muscle and the extensor
digitorum longus muscle. Short-term eccentric loading of the muscle during
certain forms of exercise, such as when walking downhill, may lead to the de­
velopment of tenovaginitis, accompanied by crepitus, in the muscle tendon.
The syndrome disappears after a training break and local antiphlogistic treat­
ment.

Myofascial trigger points may remain in the upper and middle third of the ti­
bialis anterior muscle. These trigger points should preferably be treated with
pressure waves. Chronic tendinopathy at the mediodorsal attachment to the
first metatarsal is treated with shock waves. Attention: Pressure waves ap­
plied in osseous regions cause pain.

EXCLUSION CRITERIA
I Fatigue fractures
Compartment syndrome

TREATMENT
Patient positioning: supine position
Suggestion: Regimen A or B

Figure 58:
ESWT of m ediodorsa/ aspect
of foot; insertional tendino ­
pathy of tibia/is anterior
m uscle; example of myofascial
trigger point in tibia/is ante·
rior m uscle (red marker)

102
 Other indications in sports medicine

SHIN SPLINT (MEDIAL TIBIAL STRESS SYNDROME AND

TENDINOPATHY OF THE PERONEAL TENDONS)

The tibialis posterior muscle is part of the posterior compartment of the fe­
mur, along with the flexor hallucis longus muscle and the flexor muscle of the
toes, whereas the lateral compartment comprises the peroneus longus and
brevis muscles. The primary function of the tibialis posterior muscle is two­
fold: flexion and supination of the interior foot portion of the subtalar joint,
and stabilizing the transverse and longitudinal arch of the foot. When run­
ning, the peroneal tendons are subjected to antagonistic pronation-related
tensile stress in order to dampen impact forces and absorb shocks during
heel-to-toe movement. Insufficiently developed plantar muscles cause the
foot arch to flatten, increasing foot pronation. To counteract this process, the
tibialis posterior muscle tenses up and increases the tensile stress on its ten­
don. Pain on the medial side of the tibial crest, experienced during running
or ball sports, is an indication of this condition. Trigger points are located not
only in the tibialis posterior muscle, but also in the other two muscles of the
posterior muscle compartment. During passive foot pronation by the exami­
ner, tendinopathy manifests as pain along the course of the tibialis posterior
tendon below the medial malleolus and at the insertion site at the base of the
first metatarsal. This pain is also present during the single-heel rise test. If the
patient is unable to maintain this stance due to flattening of the longitudinal
arch and navicular subluxation presenting as flat foot, this may be an indica­
tion of tibialis posterior tendon rupture.

Trigger points in the posterior compartment are localized with shock waves.
The identified trigger points can then be treated with shock waves or by using
an alternating combination of shock waves and pressure waves.

Imbalance of the muscles forming the sling (also called the stirrup) may result
from strong pull of the peroneal tendon and/or - in the medial aspect - the
tibialis posterior tendon. If pronation is the dominant movement, the longi­
tudinal arch flattens. The tendinopathy manifests clinically with tenderness
at the base of the fifth metatarsal, which is the insertion site of the short pe-

1 03
 roneal tendon. In patients with long-term foot supination (as in genu varum,
for example) attachment trigger points may be present at the medial tendon
attachments of the long peroneal tendon and tibialis posterior muscle.

DIAGNOSTIC IMAGING
I X-ray: exclusion of osseous alterations
Sonography or MRI (if required): partial tears/ruptures, tendon split
syndrome of the peroneus brevis tendon

EXCLUSION CRITERIA
I Tears, partial ruptures of the tendon of the tibialis posterior muscle
Tendon split syndrome of the peroneus brevis tendon

TREATMENT
I Patient positioning: supine position
Regimen B: 1.0-2.5 bar; number of pulses 3,000-4,000;
frequency 10-14 Hz; 5-8 sessions at weekly intervals
Regimen A: energy 0.05-0.15 mJ/mm2 ; frequency 4-6 Hz;
number of pulses 1,000-1,800; 3-5 sessions at weekly intervals

Fig ure 59 (left):

Blue m arkers: insertion of •
tibia/is pos terior a n d peroneus
/ongus tendons a n m edial
aspect o f fo ot/Red m a rker:
exa mple of trigger p o i n t in
posterior m uscle compartment
of lower leg

Fig ure 6 0 (rig ht):

Red m arker: example of
trigger paint in calf m uscles/
Blue m arker: insertion of
peroneus brevis tendon at
fi fth m e ta tarsal base

1 04
Other indications in sports medicine

Fig ure 61 :
ESWT of m edial a n d
lateral ten don insertions

Fig u re 62:
Exa mple of PW treatment
of trigger points in posterior
m uscle compartment of
lower leg

105
 INSERTIONAL TENDINOPATHY OF THE PECTORALIS
AND RHOMBOID MUSCLES

Repetitive overuse from bench pressing or butterfly machine exercises may

cause insertional tendinopathy of the pectoral is muscles. In non-athletes, a
long-term forward inclined posture and drooping shoulders may lead to the
development of insertional tendinopathy in the thoracic muscles and the an­
tagonist rhomboid muscles at the medial margin of the scapula. The condi­
tion manifests clinically with ventral tenderness distal to the humeral head
along the anterior axillary line and at the coracoid process of the scapula.
Abduction, external rotation and anteversion are impaired. Referred pain
patterns caused by myofascial trigger points in the pectoralis major muscle
occasionally occur in the medial aspect of the upper arm/elbow region and
in fingers 3 to 5. If local pain manifests in the pectoralis major muscle, cardiac
causes must be ruled out. The adduction and internal rotation test allows the
examiner to localize and treat scapular insertional tendinopathy of the rhom­
boid muscles by means of palpation and/or additional shock waves.

EXCLUSION CRITERIA
I Cervical radiculopathy
Cubital tunnel syndrome
Angina pectoris
Tendon rupture

TREATMENT
I Patient positioning: side-lying position
Combined shock wave and pressure wave therapy of the pectoralis
and rhomboid muscles
SW: energy 0.05-0.15 mJ/mm2 ; number of pulses 300-600;
frequency 4-6 Hz; 4-6 sessions at weekly intervals
PW: 0.8-1.5 bar; number of pulses 1 ,000-2,000; frequency 12-14 Hz;
4-6 sessions at weekly intervals

106
Other indications in sports medicine

Fig u re 63 :
Adduction a n d intern a l
rotation test clea rly reveals
a ttach ment trigger points in
rh omboid m uscles at m edial
m a rg i n of scapula, a t a n terior
axillary line and at coracoid
process of scapula (insertions
of pectoralis m uscles)

Fig ure 64:

ESWT of rh o m b o id tendons
with a rm placed os fo r the
adduction a n d in tern a l rota­
tion test

1 07
 INSERTIONAL TENDINOPATHY OF THE TRICEPS

Acute symptoms frequently develop into chronic insertional tendinopathy at

the olecranon, especially when no breaks in training are taken for regenerati­
on purposes. The condition manifests clinically with pulling pain and tender­
ness at the tendon insertion site when flexing the elbow.

TREATMENT
I Patient positioning: supine position
SW: energy 0.05-0.15 mj/mm2 ; number of pulses 300-600;
frequency 4-6 Hz
Alternative PW treatment: 1-2 bar; frequency 15-20 Hz;
4-6 sessions at weekly intervals

Figure 65:
ESWT of attachment trigger
points a t olecranon/
PW therapy of myofoscia/
trigger points
(example; red markers)

108
 .
TENDINOPATHY AND MYOFASCIAL TRIGGER POINTS
INVOLVING THE SPINAL COLUMN

More than 80% of all neck, back and lumbar pain conditions result from over­
use or lack of exercise of postural muscles. The sedentary lifestyle associated
with modern civilization is a causal factor for disorders affecting the postural
muscles. This leads to muscular imbalance, tensed muscles, shortened ten­
dons and myofascial trigger points. In many cases, pressure waves or targeted
shock waves enable localization of myofascial trigger points and insertional
tendinopathy in the cervicothoracic and thoracolumbar junctions and gluteal
muscles, which are responsible for the development of typical pain patterns
and referred pain.

Myofascial trigger points and insertional tendinopathy can only be treated

successfully with ESWT if their causes and the factors responsible for their
formation and development are incorporated into therapy. Otherwise, ESWT
would merely address the symptoms, but not the underlying root causes.
Neuroplastic capabilities of the central nervous system would then lead to
the development of autonomous neural pain circuits, resulting in a chroni­
cally autonomous pathological process that is independent of the underlying
disease. Irreversible muscular damage may occur in the long term. Biopsies
taken from locations of contraction knots or trigger points have revealed loss
of myofibrils and an empty sarcolemma.6 · ,3 5

Morphological changes in the spinal column such as facet joint osteoarthritis

or osteoarthritis in the pelvic region are frequently accompanied by tendino­
pathy and myofascial trigger points. Along with regular physiotherapy, which
may also be necessary to prepare for surgical procedures, ESWT is an effective
and appropriate treatment approach.

110
 Newer indications

CERVICOOCCIPITAL AND CERVICOTHORACIC REGIONS

OF THE SPINAL COLUMN

Vertebral trigger points with local and regional referred pain are located prima­
rily at the cervicothoracic and thoracolumbar junctions of the spinal column.

Cervicocephalic occipital pain, a potential cause of migraine, cannot be trea­

ted successful ly with ESWT (suboccipital application, cranial to C3). Here,
ESWT may even involve certain risks due to the anatomical proximity to sensi­
tive vascular/neural structures (e.g. risk of vertebral aneurysm).

Shock wave or pressure wave treatment of the scalene muscles or sternoclei­

domastoid muscles causes coughing or a gag reflex even at a low dosage, thus
preventing correct treatment in most cases.

Occipital pain as a result of occipital insertional tendinopathy and shortened

and tensed cervical muscles has been shown to respond particularly well to
pressure wave therapy using the ATLAS »Soft Tip« transmitter. Application
of a small number of low-dose pressure wave pulses (0.5-0.8 bar, frequency
4-6 Hz, 8-10 pulses) to the fascio-muscular tender points (Co-C7) in the occi­
pital region (these points being known from manual therapy) and to the pro­
prioceptor-rich transverse processes of the atlas, which are responsible for the
tone and control of the postural muscles, may provide a successful outcome.

Fig ure 6 6 :
PW transm itter (ATLAS
"Soft Tip« transmitter from
S TORZ MEDICA L AG)
used with PW h a n dpiece
to tre a t trans verse processes
of a tlas

111
 In many cases, local and paravertebral pain is present at the cervicothoracic
junction C3 to Th10/12 (involving especially the semispinalis, splenius, rotator
and multifidus muscles). Such pain may even radiate into the occipital region.
Trigger points in this region of the spinal column may cause referred pain in
the neck/shoulder angle and even to contra lateral regions. The condition ma­
nifests clinically with tension in the descending part of the trapezius muscle
and with impaired cervical spine rotation due to shortening of this muscle.

The patient's history often includes back pain in the interscapular region,
along the scapular margin, in the dorsolateral thorax region and even in the
posterior region of the shoulder. Pain in the ventral and parasternal thoracic
region is less frequent. The pain experienced may be exacerbated if shock
waves or pressure waves stimulate corresponding local trigger points at the
superior margin of the descending part of the trapezius. This pain can be pre­
cisely localized by means of feedback provided by the patient.

Fig ure 67:

Pain referral from tropezius
m u s cle. L eft: ln terscapular
region (1), dorsolateral
thoracic reg ion (2), dorsolate­
ral upper arm (4) , from there
m o re dista lly towards the
elbow and forearm .

Rig h t: Pain orig inating in the

a n terior m uscle portion and
radiating into the la teral (2)
a n d ventral thoracic region (3)
(ascending pain p a tterns n o t
shown)'

To identify trigger points, the shock wave or pressure wave handpiece is ap­
plied to the neck angle at the C7 vertebra and then moved along the superior
margin of the trapezius muscle and laterally towards the acromioclavicular
joint. Upon localization of a corresponding trigger point, the patient will re­
cognize the typical pain described during history-taking. In this manner, the
examiner is able to proceed directly with treatment.

112
 Newer indicati ons

Fig ure 68:

Application of the ESW
h a n dpiece to the neck/s h o u l­
der a ngle, fo llowed by latera l
movement. Prompting of pain
recogn ition by ESW stimula­
tion of correspo n ding trigger
points.

Below: (4 examples of trigger

points at superior m a rgin of
descending p art, red m a rkers).
Trigger points in trapezius
m uscle (sch e m a tic), red
m arkers (ascending part Th 6
to Th B/9 ; descending part
of the region of the neck/
s h o u lder a n g le, C7 region;
h o rizo n ta l part p a ra vertebral
C5 to Th3; localiza tion by pain
recognition. Tendon origin
and insertion sites of levator
scapulae m uscle. Blue m a rkers
as examples of C2 to C4 ;
superior medial angle of
scapula

The trigger points and their referral patterns mapped by Travell and Simons
using manual techniques provide valuable guidance.'3 6 • '3 7 When localizing
trigger points, the induced referred pain hardly ever coincides fully with the
mapped information. The incomplete pain pattern is, however, sufficient to
enable treatment of trigger points. Moreover, the pain patterns identified
in detail by M. Gleitz by means of focused shock waves, and the systematic
treatment strategies he developed for myofascial trigger point syndrome, are
a helpful guide to facilitate treatment.'33

Based on his animal studies, S. Mense explains the mechanism involved in the
origin/development of referred pain and the resulting clinical pictures. 3 6 , 38
1 1

113
 Normal route of
Figure 69: � nociception (local pain)
The m echanism of generation
of referred m uscle pain . Nor­
mally, the L4 and L5 segments
Route in the presence
are the main area in which the of a chronic lesion
GS n erve exerts its effects in (referred pain)
the rat (GS, gastrocnemius­
sa/eus m uscle), characterized I neffective
by effective synapses (blue (dormant)
triangles) that reliably excite synapse
the postsynaptic n eurons.

Local pain arising in these

segments is felt a t the site of t>-------._
the lesion (black a rrows). In Ineffective synapse
animals with an inflamed GS
m uscle, the area of influence
�
of the GS nerve was found to
Effective synapse
h a ve expanded into the L3 Fibular ( peronea l ) nerve
segment, which contains only
ineffective synapses (white
triangles) of GS afferent fib ers.

These synapses do not nor­

Nociceptive stimuli are transmitted to spinal cord segments via afferent
mally induce any action po­ nerves and synaptic connections and then passed on to post-synaptic neu­
tentials in the L3 n eurons. In
the presence of a lesion in the rons. The pain produced in this segment is perceived instead of that from the
m uscle, the m uscle afferen ts
in the L4 and L5 segments original myofascial trigger point. However, afferent stimuli are not confined
secrete substances (e. g.
SP - substa n ce P, black dots) to one specific segment; in fact, they propagate to a wider area via ineffective
that diffuse to the L3 segmen t
and convert the ineffective
dormant synapses, which means they are unable to induce any action in the
synapses there into effective post-synaptic neurons.
ones.

Thus, it was n ewly possible for

impulses from GS nociceptors Afference from the painful trigger point results in increased release of noci­
(blue a rrows) to excite the
L3 neurons, ultimately giving
ceptive substances (substance P and others) in the associated primary seg­
rise to referred pain that was ment, which diffuse into adjacent segments and awaken dormant (ineffective)
felt in the distribu tion of the
fibular n erve (lateral calf and synapses. This opens up new afferent pathways, which explains the mecha­
foot). '''
nism of development of referred pain and pseudoradicular pain.

Dorsalgia is primarily the result of interscapular referred pain caused by a trig­

ger point in the ascending part of the trapezius muscle and a trigger point in
the descending part of the trapezius in the neck/shoulder angle. The trigger
point in the ascending part of the trapezius is located in the region of Th6 to
Th8 next to the medial margin of the scapula. It is very painful during ESWT
and refers pain as far as the superior margin of the descending part. Pain can
also be referred in the other direction, i.e. towards the ascending part. Addi-

114
 Newer indications

tional ascending pain referral in the ascending part of the trapezius muscle
frequently manifests in the paravertebral muscles of the cervical spine and at
the aponeurosis of the trapezius (see second image in Figure 68).

Chronic cervicothoracic referred pain (local and paravertebral) is always re­

lated to a trigger point in the horizontal part of the trapezius muscle. This
trigger point is located lateral to the spinous processes Cs to Th3 (see second
image in Figure 68).

The levator scapulae muscle, similarly to the trapezius muscle, is also involved
in the development of myofascial pain at the cervicothoracic junction. Its pain
referral pattern is shown in Figure 70.

Fig u re 7 0 :
Referred, local a n d in terscapu ­
lar pain res ulting from trigger
points in the levator scapulae
m uscle. the descending part
of the trapezius m uscle. a n d
the p a ra vertebral m uscles.
Pain referral to the medial and
lateral elbow and fo rea rm is
less frequent. '

Strong local pain and reduced rotation of the cervical spine to the opposite
side are typical symptoms of the condition. In many cases, paravertebral, local
and interscapular pain also manifests in weakened form on the opposite side.
If this occurs, the relevant trigger points are incorporated into treatment.

The levator scapulae muscle, which is always involved in myofascial pain

within the cervical spine region, is covered dorsally by the descending part
of the trapezius muscle in the neck/shoulder angle. During the pinch grip

115
 test, the condition ma n ifests cli n ically with marked a nd pai nful bulg i n g of the
th ickened su perior marg i n of the tra pezius muscle a nd with tenderness at the
tendon i nsertion of the levator sca pulae muscle. The sca pular attach ment
trigger poi nt of the levator sca pulae muscle a nd the myofascial trigger point
of the descendi ng part of the tra pezius muscle ca n be con sidered the 'ch ief
trou blema kers' i n the neck a nd shoulder reg i o n .

Duri ng ESWT, t h e a bove-mentioned trigger poi nts i n t h e tra pezi us muscle

a nd the attach ment trigger point of the levator sca pulae muscle aro u nd the
medial s u perior a ngle of the sca pula are localized with shock waves a nd then
treated with pressure waves. This should prefera bly be done with the patient
seated a nd their arm placed as for the adduction a nd i nternal rotation test.

Fig ure 71 :
ESW localiza tion a n d treat­
ment of ten don insertion sites
at C2 to C4 of levator scapulae
m uscle

Below: Alternative PW
loca liza tion a n d treatment af
scapular attachment of leva­
tor m uscle at superior angle
of scapula

11 6
 Newer indications

I n ma ny cases, tender attach ment trigger poi nts a re fou nd i n the sca pulotho­
racic rhomboid muscles, wh ich must not be confused with i ntersca pula r refer­
red pai n (see section headed " l nsertional tendi n opathy of the pectoralis a nd
rhomboid muscles" ) .

The cra n ial o ri g i n o f the levator sca pulae muscle tendon i s at the transverse
processes C2 to C4 . Trigger poi nts i n the levator muscle ca used by contrac­
tu res a nd strai n may contri bute to the develo pment of cervical headache.
This may result, for exa mple, from entra p ment of the sensory b ra nches of the
g reater occi pital nerve as they pass th rough the tensed semispi nalis ca pitis
muscle a nd the aponeu rosis of the trapezius.1 21

The serratus posterior su perior muscle is situated between the sca pula a nd
the thoracic wall a nd i nserts di rectly i nto the second to fifth ribs - fa r below
the levator sca pulae a nd rho mboid muscles. A trigger point in the serratus
posterior su perior muscle may ca use local sta bbing pai n in association with
respi ratory movements. Referred pa i n va ries, but generally ma nifests at the
medial ma rg i n of the sca pula , in the dorsal aspect of the sca pula or even in the
u p per a rm a nd forea rm up to fi ngers 4 a nd 5 . ESWT of the relevant myofascial
trigger poi nt should be performed with the patient in prone position a nd thei r
a rm placed as for the adduction a nd i nternal rotation test.

LUMBAR SPINE REGION AND GLUTEAL REGION

ERECTOR TRUNCI MUSCLES (MULTIFIDUS AND ROTATOR MUSCLES;

LONGISSIMUS THORACIS MUSCLE, ILIOCOSTALIS THORACIS MUSCLE)

All pa ravertebral trigger poi nts in the lu mba r spi ne reg ion may i nduce refer­
red pa i n distally. Si mila rly to the cervicothoracic j u nction , local trigger poi nts
at the thoracolu mba r j u nction (Th12/ L2) di rectly adjacent to the spi n o us pro­
cesses, the deep portions of the erector tru nci muscles ( multifidus a nd rota­
tor muscles) , ca n be localized with shock waves / pressu re waves. 6

11 7
Fig ure 72:
Red m arkers identify examples
of myofascial trigger points at
Th12 to L 2 (two each) in deep
and superficial erector trunci
m uscles

Second: PW o r S W treatment
of trigger points in deep erec­
tor trunci m uscles

Th ird: By way o f example.

treatment o f attach m e n t
trigger point in iliocostalis
lumborum m uscle a t costal
arch. Blue m a rker iden tifies
insertion site at iliac cres t

118
 N ewer i n d i c a ti o n s

In patients with tendinopathy, trigger points in the superficial portions of the

erector trunci muscles (longissimus thoracis and iliocostalis thoracis muscles)
can be induced two to three fingers lateral to the spinous processes. This ex­
plains local pain at the paravertebral thoracolumbar junction.

Myofascial trigger points, especially those located in the deep internal portion
of the erector trunci muscles at the thoracolumbar junction, refer pain direct­
ly and distally to the sacroiliac joint and gluteal muscles. Irritation of the ex­
ternal portion of the erector trunci muscles (ilioocostalis lumborum muscle)
and of the quadratus lumborum muscle situated deep under the erector trun­
ci, accompanied by insertional tendinopathy at the iliac crest and costal arch,
can cause referred pain which may be more or less intense or manifest only
occasionally and vary from patient to patient. Sufferers generally report dif­
ferent patterns of pain at the lateral abdominal wall, below the costal arch, at
the anterior iliac crest, at the sacroiliac joint, in the buttocks, in the lateral hip
region, in the groin and in the ischial region.6 Hence, examiners often find it
difficult to evaluate and identify the origin of the reported referred pain.

Chronic referred pain from the lumbar, pelvic and hip regions is mostly ex­
perienced in the gluteal muscles. Myofascial trigger points may be caused
by structural pathologies such as facet joint osteoarthritis, coxarthrosis and
leg length discrepancy or by non-orthopaedic internal, urological or gynae­
cological conditions. They may also result from functional disorders such as
overuse or lack of exercise of muscles and from psychological stress. Chronic
referred pain from the thoracolumbar junction of the erector trunci or quad­
ratus lumborum muscles frequently causes satellite trigger points to form in
the gluteal muscles.

Chronic progression of the condition causes tendon shortening and inserti­

onal tendinopathy in the gluteal muscles at the greater trochanter and iliac
crest. Many pain patterns in the lumbar/pelvis/hip region are associated with
attachment trigger points at the trochanter.

119
 As with cervicothoracic syndrome (see p. 111), the application of shock waves
will not always evoke the complete typical pain pattern. The relevant criterion
is recognition of the referred pain, even if attenuated. Treatment can then be
started straight away.

In many cases, trigger points in the gluteal region are located next to or on
top of each other. Mapping is more difficult where satellite trigger points are
present.

Division of the gluteal region - namely, into a ventral and a dorsal area by
means of an imaginary connecting line between the posterior superior iliac
spine (PSIS) and the greater trochanter - facilitates systematic scanning of the
region for trigger points. Trigger point density is higher in the ventral portion.

Figure 73'
Yellow m arkers: end points
of connecting line between
g reater trochan ter and PSIS

•
Red markers: examples of
ventral and dorsal myofascial
trigger points

••

To scan the gluteal region for trigger points, the examiner starts below the
iliac crest and then moves the shock wave handpiece along the imaginary
connecting line and, finally, to the dorsal zone.

120
 Newer indications

Fig ure 74 :
Red m a rkers: examples of
myofascial trigger p o i n ts
loca lized by ESW stimulation
in the ven tra l a rea

Trigger points in the gluteus minimus muscle (focal depth 15 cm) are located
ventral to the imaginary connecting line. These trigg!;r points, along with a
trigger point in the gluteus medius muscle in the centre of the connecting
line, cause referred pain primarily in the lateral aspect of the leg.

Fig ure 75 (left) :

Referred pain from trigger
points in the gluteus minimus
a n d m edius m uscles'

Fig ure 76 (rig h t) :

Typical pseudoradicular
pain ; imita tion pain,
pseudo -scia tica'

From the region located dorsal to the line (gluteus medius and maximus
muscles), pseudoradicular pain referral occurs in the posterior aspect of the
thigh.

1 21
 ESW-induced referred pain from trigger points in the gluteus maximus musc­
le dorsal to the imaginary connecting line, and in the ventral aspect from trig­
ger points in the gluteus medius muscle, radiate regionally into the sacroiliac
joint, inferior lumbar spine and ischium.

Figure 77:
Referred pain from trigger
points in gluteus maximus
and m edius m uscles;
frequent cause of chronic
lumbago/lumbar pain 6

Referred pain from trigger points in the gluteus maximus muscle in the dorsal
and ventral aspects below the iliac crest manifests regionally in the ischium
and pubic bone and in the dorsal aspect of the cranial thigh.

Figure 78:
Pseudoradicular pain
when seated'

122
 Newer indications

EXCLUSION CRITERIA FOR TREATMENT OF CERVICAL,

THORACIC AND LUMBAR PAIN SYNDROMES
I Cervical, thoracic and lumbar radiculopathy
Chronic, internal, cardiac and abdominal diseases (affecting the liver,
gallbladder, pancreas; frequent pain in the interscapular region)
Spinal osteopathology
Fibromyalgia
Polymyalgia rheumatica
lntercostal neuralgia
Urological and gynaecological diseases

DIAGNOSTIC IMAGING
I X-ray: cervical, thoracic, lumbar spine, overall pelvic region
when standing
MRI
Sonography

Fig ure 79:

Sonographic m easurement of
s kin-ple u ra distance in cervico ­
thoracic region of very slim
pa tients
Cross-sectio n a l image: ln ter­
costal lung position 3 cm lateral
to spinous process {OF) a t a depth
of 20 mm, la teral to tra n s verse
process (QF)

Diagnosis and treatment with ESWT passing over pulmonary tissue, as would
be the case when treating the descending part of the trapezius muscle, for ex­
ample, have long been considered risky due to the possibility of pneumotho­
rax. However, sonographic imaging allows precise measurement of the dis­
tance between the skin su rface and pleu ra. Using a 20 mm stand-off, shock
wave treatment will not involve any risks, all the more so because the shock
wave dosage generally used today is much lower than was the case a few years
ago, so that pulmonary tissue damage is avoided.

1 23
 The reg ions of the n e u ra l fora m i n a and the vertebra l a rtery at Co to C3 s h o u l d
not be treated with ESWT ( neither s h o c k waves n o r press u re waves) . Potentia l
co m p l ications a ri s i n g fro m the risk of a n e u rysm of the vertebra l a rtery s h o u l d
be ta ken i nto co nsid eration . I n theory, m icroembolism i n the fl ow reg ion of
the ca rotid a rteries ca used by ESWT ca n n ot be ruled out.

Figure 80 :
Sonography of interscalene
triangle; image shows
proximity to lung

TREATMENT
I Patient positi o n i n g : seated fo r cervicothoracic reg ion; prone positi o n o r
sid e-lyi n g position for l u m ba r a n d g l utea l reg ions
Reg i m e n A fo r users of co m bi n ed shock wave/pressu re wave thera py
Reg i m e n B for users of p ressu re wave thera py

Co mbined ESWT offeri n g p recise loca l ization a n d treatment of trigger poi nts
a n d tend i n o pathy, even in deep reg ions, ca n be used for a l l s p i n a l syndromes,
provided that the a bove-mentioned risks a re ta ken i nto co nsiderati o n . Myo­
fasci a l release even of deep-sited tissue i s enabled by the neu rofascia l web.

The release of fascia I a d h esions by mea ns of pressu re waves genera l ly req u i res
a co nsidera b l e n u m be r of treatment sessions.

124
 N ewer i n d i c a t i o n s

PIRIFORMIS SYNDROME

AETIOPATHOGENESIS
The piriformis muscle originates from the anterior surface of the sacrum bet­
ween the first and fourth sacral foramen. It runs almost transversally through
the sciatic foramen and inserts into the superior margin of the greater tro­
chanter. The functions of the piriformis muscle are external rotation of the
extended thigh and abduction of the hip joint flexed to 90 ° . The gemellus
superior, obturator internus, gemellus inferior and quadratus muscles are all
deep external rotators and may contribute to the symptoms associated with
piriformis syndrome. This applies especially to the obturator internus which
is situated partly within the pelvis and whose functions include that of an
external hip rotator. All of these muscles are located distal to the piriformis
muscle.1 39

The piriformis syndrome results from contractures and trigger points in the
piriformis muscle and the associated synergists. Trigger points frequently ma­
nifest in the adjacent gluteus minimus and maximus muscles and in the leva­
tor ani and coccygeal muscles.

Many aetiological factors involved in the development of piriformis syndro­

me have been described by D. Jankovic in his comprehensive reference work
on pain therapy published in 2015.140 Previous traumas may be responsible for
the sciatica-like pain. Indirect, abnormal overextension in the lumbosacral
and hip regions during sports activities or from overexertion may result in pi­
riformis syndrome. Pain typical of piriformis syndrome has also been found to
occur after hip replacement surgery.

The above-mentioned book provides a full description of the neuropathologi­

cal component of sciatic nerve entrapment.1 40 It also includes detailed images
showing six different variant courses taken by the sciatic nerve as it passes
through or over the piriformis muscle. If fibres of the peroneus muscle are
partly affected due to muscular strain, paraesthesia manifests on the posteri­
or aspect of the thigh or in individual regions of the lower leg.

125
 Dysfunction of the sacroiliac joint is considered to cause trigger points and
myofascial pain.

CLINICAL MANIFESTATIONS
In many patients, a sedentary job and lack of exercise result in chronic blo­
ckage of the sacroiliac joint, which can be diagnosed by means of functional
tests that use manual techniques. Lumbosacral ligamentous connections are
found to be tight and irritated. Trigger points in the piriformis muscle and the
adjacent deep external rotators cause different types of referred pain, which,
in turn, are masked by pain from additional trigger points in the superficial
gluteal muscles. The concept developed by S. Mense explains the spreading
of additional pain patterns after ineffective (dormant) synapses have been
opened.13 8
Typical referred pain originating from parasacral trigger points of the pirifor­
mis muscle manifests in the upper third of the posterior thigh. Dorsolateral
trigger points around the trochanter refer pain into the groin and distally into
the adductors.

Figure 81:
Trigger points a n d pain
referral associated with
p iriformis syn drom e•

Permanent blockage of the sacroiliac joint may cause interaction with myo­
fascial trigger points and ultimately result in chronification. Sacroiliac joint blo­
ckage is maintained due to persistent, long-term muscle tension. Joint dysfunc­
tion continues or evidently perpetuates the development of trigger points.

126
 Newer i n d i c a t i o n s

Sonogra phy a nd M RI do not provide a ny rel iable fi ndings i n the dia g n osis of
piriformis syndrome. As a conseq uence, the pathology ca n o n ly be dia g nosed
by cl i n ica l exa m i nation. The h i p joint presents slightly pa i nfu l l i m itatio n of the
near-term i n a l ra nge of motion in externa l rotatio n . H i p a bduction in the 9 0 °
positio n ca uses marked pai n .

With the patient i n side-lyi ng o r prone position (the latter bei ng more dif­
ficu lt) a nd with the g l utea l m u scles relaxed, external pal pation near the s u pe­
rior border of the sacroil iac joint wi l l revea l a parasacra l tender trigger poi nt i n
the piriform is m u scle. Loca l ization with ESWT is m uch easier a nd, i n fact, very
stra ightforward. To identify th is trigger poi nt, a n i m a g i nary connecting l i ne
between the trocha nter a nd the second sacra l fora men is divided i nto three
eq u a l sections. The pa in-produci ng myofascia l trigger poi nt is located at the
imagi nary border between the centra l a nd s u perior sections.

A large n u m ber of procedures a i med at testi ng for piriform i s syndrome are

discussed i n the literature'3 8 , i ncl udi n g dig ita l vag i n a l or recta l pal pati o n , i n
order to identify o r rule o u t a pa i nfu l , tender a nd thickened piriform is m u scle
at the i nterna l latera l wa l l of the pelvis.

The cl i n ica l diag nosis of trigger poi nts, wh ich is essentia l to ena ble safe and
stra ightforward u ltrasou nd-g u ided i njection thera py i n pa i n management,
req uires extensive experience on the part of the pa i n thera pist. I njections may
be com p licated a nd are i nvasive. By contrast, diag nosis using shock waves is
simple a nd ra pid; even deep trigger poi nts ca n be l oca l ized in very l ittle ti me.
The thera pist i s a ble to pass directly from loca l izatio n to treatment.

EXCLUSION CRITERIA
I Sym ptoms of l u m bar radicu lopathy
Non -orthopaedic patholog ies in the pelvic reg ion

DIAGNOSTIC IMAGING
I X-ray of overa l l pelvic reg ion
I M RI / sonogra phy of h i p structures

1 27
Figure 82:
Yellow circle with blue marker:
greater trochanter/ Yellow
marker: secon d sacral
foramen/Red marker:
myofascial trigger point
(border between central/
superior third of imaginary
connecting line)

Figure 83:
SW treatment of a ttachment
trigger point a t greater
trochanter

Fig ure 84:

PW tre a tmen t of
myofasciol trigger point

128
 Newer i n d i c a t i o n s

DIAGNOSIS AND TREATMENT (SUGGESTION)

SHOCK WAVES PRESSURE WAVES

ENERGY 0.07-0.20 mj / m m 2 1. 5 -2.5 bar
NUMBER OF PULSES 800-1 ,000 2,000-2,500

FREQUENCY 4- 6 Hz 20-30 Hz

SESSIONS 3-5 3-5

INTERVAL approx. 8 days approx. 8 days
BREAK I N THERAPY approx. 3 weeks for regeneration

Resumption of extracorporeal shock wave / pressure wave therapy after the

break from treatment if symptoms persist (criteria: clinical symptoms, VAS).
If treatment is continued, the regimen outlined above should be adopted.

CARPAL TUNNEL SYNDROME {CTS)

CLINICAL MANIFESTATIONS AND AETIOPATHOGENESIS
Compression of the median nerve in the carpal tunnel causes nocturnal pain,
numbness and paraesthesia, which may even manifest as shoulder pain. Clini­
cal manifestations include dysesthesia of fingers 1-3 and of the radial aspect
of finger 4; one way of inducing this is by the hyperflexion test (Phalen's test).
A more frequent symptom is tingling or 'pins and needles' above the median
nerve during the percussion test (Tinel's sign). In most patients with these
symptoms, the outcome of neurological electrodiagnostic testing is no diffe­
rent from the results in symptom-free patients, i.e. the underlying pathology
is not flagged up by these tests. Patients at an advanced stage of carpal tunnel
syndrome suffer from thenar atrophy and partial paralysis. Thumb opposition
is impaired or even impossible.

The median nerve shares the carpal tunnel with nine tendons and tendon
sheaths that run from the forearm flexor muscles to the finger joints. Exces-

129
 sive repetitive wrist flexion and extension - especially of the tendons of the
flexor carpi radialis and fl exor pollicis longus muscles and of the radial tendons
-
of the flexor digitorum superficialis and profundus muscles - lead to increased
accumulation of intra- and peritendinous synovial fluid. This results in conges­
tion of lymphatic capillaries and in lack of space for tendons and Schwann cells
of the m edian nerve due to reduced lymphatic circulation and oedematous
swelling. In the long term, fibrosis of the tendon sheaths occurs, resulting in
chronic narrowing of the carpal tunnel. Contrary to earlier assumptions, the
transverse carpal ligam ent - the stabilizing roof of the carpal tunnel - is not
thickened and, therefore, definitely not responsible for the lack of space in the
carpal tunnel, which can only be treated successfully by surgical release of the
transverse carpal ligam ent.

Besides non-physiological wrist overuse, mild to moderate carpal tunnel syn­

drome in climacteric wom en may be caused by the hormonally induced mo­
difications in the tendon sheath structure.

Animal studies have demonstrated the effects of ESWT in lymphology. In his

contribution about the lymphangiogenetic effects of focused shock waves on
secondary lymphoedema (see p. 141), K. Knobloch refers to the studies con­
ducted by a Japan-based research group and the rabbit ear model used by
M. Kubo_,4, , ,42

ESWT has proved effective in the treatm ent of chronic pain after surgery to
split the carpal ligam ent ('carpal roof').143

In 2016, two studies were published demonstrating the successful shock wave
treatm ent of mild to moderate carpal tunnel syndrom e. In one of these stu­
dies, shock wave treatm ent (0.05-0.15 mJ/ m m 2 , 800- 1,100 pulses) was per­
formed at weekly intervals. The other prospective randomized single-blind
and placebo-controlled study was conducted using pressure waves at weekly
intervals. The outcomes obtained in the verum group were significantly bet­
ter than in the control group receiving sham treatment.'44, ,4s

13 0
 Newer i n d i c a t i o n s

A low level of mechanical energy in the form of shock waves or pressure waves
has a positive effect not only on the formation of blood capillaries, but - to
an even greater extent - also on the growth of lymphatic endothelial cells
and lymphatic capillaries. This enhances lymphatic drainage and prevents
fibrosis.1 s. 45 , 4 6 . 1 41 , 1 4 6

Repetitive application of shock waves to cel l cultures has demonstrated the

multipotency of adipose stem cells. It has been shown to increase the expres­
sion and persistence of mesenchymal markers and to strengthen the differen­
tiation capacity not only of osteogenic and adipogenic cell lines, but also of
cel ls that are similar to Schwann cel ls 52 · 66 and are known to contribute to axon
coating and the formation of myelin sheaths. These effects, along with the
release of anti-inflammatory cytokines and the drainage through new lym­
phatic vessels4 6 · 66 · may explain the healing of moderate carpal tunnel syndro­
me and persistent symptoms after surgical cleavage of the transverse carpal
ligament.

EXCLUSI O N C R ITERIA
I Advanced CTS (functional weakness of thumb, thenar atrophy)

DIAGNOSTI C IMAG I N G
I X-ray: osseous stenosing
I Sonography: examination of tendons and median nerve

TREATMENT
With the patient in supine position and the wrist overextended by placing it
on a suitable roller during therapy, the handpiece is applied preferably to the
palmar/radial aspect of the wrist (flexor tendons).

131
Figure 85:
Lateral ESWT ta
f/exor tendons

SHOCK WAVES PRESSURE WAVES

ENERGY 0 . 03 - 0 .1 0 mJ / m m 2 1 . 0 -1 -3 bar
NUMBER OF PULSES 8 0 0 -1 , 0 0 0 1 , 2 0 0 -1 , 5 0 0

FREQUENCY 4- 6 Hz 2 0 -3 0 H z

SESSIONS 3-5 3-5

INTERVAL approx. 8 days approx. 8 days

BREAK IN THERAPY approx. 3 weeks for regeneration

Resumption of extracorporeal shock wave / pressure wave therapy after the

break from treatment if symptoms persist (criteria: clinical symptoms, VAS).
If treatment is continued, the regimen outlined above should be adopted.

132
 Newer indications

TRIG GER FINGER (STENOSING TENOSYNOVITIS)

AETIOPATHOGENESIS
As with the tendons affected by carpal tunnel syndrome, repetitive overuse of
a finger flexor tendon may cause increased secretion of synovial fluid, chronic
synovitis and concomitant oedema. As well as overuse, aetiopathological fac­
tors involved in the development of trigger finger also include inflammatory
degenerative or rheumatic diseases. Tendinopathy or tenosynovitis manifests
between the deep finger flexor tendons and their synovial sheaths at the level
of the metacarpal heads. Thickening and swelling of the tendons and accu­
mulation of synovial fluid reduce lymphatic drainage. The proximal A1 pulley
undergoes relative stenosis. All fingers may be affected, either individually or
in pairs. The flexor pollicis longus tendon is responsible for the thumb, whe­
reas the flexor digitorum tendons are involved in tenosynovitis of fingers 2 to
5. Clinical manifestations include impaired flexion and extension, accompa­
nied by pain when attempting to flex the affected finger. Finger stiffness in
the morning, which improves on movement, is another typical symptom. In
some cases, a pea-sized, palpable nodular thickening is found proximal to the
metacarpophalangeal joints which may restrain tendon gliding and compro­
mise extension of the flexed finger. If extension is still achieved, it is accompa­
nied by the typical snapping and popping of the affected finger.

The objective of ESWT is to improve lymphatic drainage and regeneration

of the thickened and inflamed tendon tissue.18 · 4 6 • 1 41 · 142 In a cohort study con­
ducted in 2016, N. Malliaropoulos treated trigger finger patients with pressu­
re waves, using a relatively low energy dose. Both total energy input and the
number of sessions were unusually low. Overall, the study revealed a positive
correlation between the duration of symptoms before therapy and the num­
ber of treatment sessions required.1 47

1 33
 DIAGNOSTI C IMAG ING
I Sonography: examination o f soft tissue and tendon function

TREATMENT
I Patient positioning: supine position
Suggestion for pressure wave therapy: 1-4-2 bar, frequency 10-12 Hz,
2,000 pulses, weekly intervals, 6-8 sessions, Ro 40 transmitter
Shock waves: 0.07-0.15 mJ/mm2 , frequency 4-6 Hz, 1,500-1,800 pulses,
3-5 sessions, stand-off II

DE QUERVAIN'S TENOSYNOVITIS

The pathology known as de Quervain's tenosynovitis is characterized by in­

flammatory degenerative processes and thickened scarring in the first exten­
sor tendon compartment, most likely as a result of overuse, ageing or rheuma­
tic conditions. This leads to narrowing of the tendon sheaths of the abductor
pollicis longus and extensor pollicis brevis muscles. Clinical manifestations
include pain on thumb and wrist loading. Local swelling and tenderness are
also typical symptoms. Ulnar abduction and extension with maximum thumb
flexion cause pain due to additional narrowing and tensile stress on the exten­
sor pollicis brevis tendon.

Shock wave or pressure wave therapy is performed to stimulate regeneration

of degenerative tendons and to improve lymphatic drainage.Treatment and
patient positioning: as for trigger finger (stenosing tenosynovitis)

MORTON'S NEUROMA

AETIOPATHOGENESIS
Morton's neuroma, also referred to as Morton's metatarsalgia, is more of a
symptom than a diagnosis. The typical pain on weight-bearing is not due to
any distinctive anatomical feature. Clinical examination and diagnostic ima-

134
 Newer indications

ging do not provide any aetiological explanation. The symptoms are treated
with physical therapy, orthopaedic aids, shoe modifications and injections.1 48

The interdigital nerves are the terminal branches of the medial and lateral
plantar nerves which fuse in the third intermetatarsal space. Splay foot or
halux valgus deformity may cause mechanical nerve compression (entrap­
ment), especially in the interdigital space between the third and fourth toe.
At the site of the restriction, occasional nerve thickening distal and plantar
to the deep intermetatarsal ligament occurs (evidenced by targeted MRI),
which, hypothetically, can be interpreted as resulting from perineural and en­
doneural fibrosis caused by demyelination of the compressed nerve.

Morton's neuroma (a misleading name; it is actually a form of neuralgia) is

the primary cause of metatarsalgia. The condition has received little research
attention so far. It is still being diagnosed on the basis of its clinical symptoms,
and there are still no dependable technical procedures for its diagnosis. As
a consequence, studies conducted without specific diagnosis and treatment
seem to be lacking in scientific rigour. Conservative therapies merely help to
postpone or avoid surgery. And surgical intervention often fails because of
diagnostic errors, treatment of the wrong interdigital space or failed release
of the deep transverse ligament.1 4 9

In theory, a variety of aetiological factors may be responsible for the develop­

ment of Morton's neuroma, including chronic, repetitive trauma, ischaemia,
entrapment and intermetatarsal bursitis. Reference to Morton's neuroma as
a nerve tumour is fundamentally incorrect, despite the fact that histological
examinations have revealed inflammatory tissue changes in the form of peri­
neural fibrosis. In general, the condition involves nerve branches in the third
interdigital space. In most cases, it is diagnosed on the basis of the patient's
history and clinical examination, augmented by sonography and MRl.1 s0

A randomized placebo-controlled study has been conducted to demon­

strate the effectiveness of ESWT in the treatment of Morton's neuroma. The
researchers' focus was on examining the pain level, functional impairment

1 35
 and diameter of the neuroma. Follow-up examinations were performed one
week and four weeks after the last treatment session. The results revealed si­
gnificant improvements in the VAS and AOFAS scores (American Orthopedic
Foot and Ankle Society, assessment of treatment from a clinical and patient
perspective). Measurement of the neuroma and nerves did not show any dif­
ference between groups. s1 1

Morton's neuroma cannot be classified as a typical form of tendinopathy. In

patients with fibrosis of the flexor tendons of the toes or of the ligamentous
or capsular tissue, a potential cause of the pain associated with this condition
may be perineural entrapment.

TREATMENT
Dorsal and especially plantar application of shock waves
Energy: 0.10-0.20 mj/mm2
Number of pulses: 1,500-1,800
Frequency: 4-6 Hz
Sessions: 3-5 at weekly intervals
Therapy break for regeneration, then resumption of above regimen

Pressure waves for plantar foot muscles

Number of pulses: 2,000
I Energy: 1.2-1.8 bar

Fig u re 8 6:
Morton 's m e tatarsa/gia,
plantar treatment
 Newer indicatio n s

FROZEN SHOULDER
AETIOPATHOGENESIS
Functional disorders and imbalance of the shoulder girdle region are fre­
quently caused by trauma or surgery accompanied by psychological issues.
The term 'frozen shoulder' generally refers to three different categories of the
condition: the idiopathic frozen shoulde r, adhesive capsulitis and subacromial
fibrosis.' 40
lnsertional tendinopathy and trigger points of the scapular muscles with their
medial, lateral, cranial and caudal attachments result in a gradually decrea­
sing range of motion. The scapulocostal gliding movements resulting from
harmonious interaction between the concave scapula and the convex thorax
- essentially between the fasciae of the subscapularis and serratus anterior
muscles - are increasingly restricted. Fascial adhesions ultimately result in a
global loss of motion between the scapula and thorax. This, in turn, leads to
a decreasing range of motion of the glenohumeral joint, accompanied by in­
creasing capsular immobilization. Adhesions and fibrosis cause capsulitis and
stiffening of the glenohumeral joint.

TREATMENT
I Physiotherapy combined with pain therapy and subscapular injections
(using the technique developed by D. Jankovic) plus ESWT are required in
the medium to long term to treat frozen shoulder conditions.

Fig u re 87:
Infiltra tion of the s u bscapu •
loris m uscle, starting at the
central th ird of the m edial
m a rgin of the scapula towa rds
the acromion; superficia l
needle position for illustration
p u rposes

1 37
 Patient positi o n i n g : supine position

Pressu re waves a re used to treat the shou lder g i rdle muscles (attach ment
trigger poi nts a nd myofascial trigger poi nts; rhomboid muscles, levator sca ­
pu lae muscle).

Combined shock wave/ p ressu re wave thera py is used for the su bsca p u l a ris
muscle. After ma n u a l latera l ization of the sca p u l a using the tech n ique deve­
loped by M . Gleitz, the thera pist, using thei r free ha nd, appl ies the h a ndpiece
to the ma rg i n of the latera l ized sca p u l a . 6
H ig h -energy focused shock waves a re req u i red to avoid activation of fi b ro­
blasts a nd g rowth factors.3°-3,. 34 , 3 5

Figure 88:
Lateralization of subscapu­
laris m uscle; lateral margin
of scapula accessible to
handpiece

138
 Newer i n d i c a t i o n s

SHOCK WAVES PRESSURE WAVES

ENERGY 0 .1 0 - 0 -3 0 mj / m m 2 1 . 5-2.5 b a r

NUMBER OF PULSES 1 , 0 0 0 -2, 0 0 0 1 ,200-1 ,5 0 0

FREQUENCY 4-6 H z 12-1 5 H z

SESSIONS 8 -1 0 8 -1 0

INTERVAL weekly weekly

DUPUYTREN'S CONTRACTURE
Palmar fibromatosis of the hand (Dupuytren's contracture) can be effectively
treated at an early stage, when painful nodules have formed, using high-ener­
gy shock waves. The aim is to inhibit proliferative growth factors (see below).

If hard, cord-like contractures of the joints (stage 3 or 4 in Meyerding's clas­

sification) are present concomitantly with other joint contractures, generally
affecting fingers IV and V, these contractures cannot be released using ESWT
alone. In such cases, the procedures indicated are fasciectomy (including per­
cutaneous needle fasciectomy at early stages) and fasciotomy by means of
collagenase injections. After the site has been exposed to this enzyme for se­
veral hours, the contractures are manually stretched, 'broken' and subjected
to ESWT treatment (shock wave dosage 0 . 25- 0 .40 mj/mm2 , 2, 0 0 0 pulses,
5-8 sessions at weekly intervals). This is associated with significant improve­
ment in hand function. 8

In patients with fibrotic conditions such as Dupuytren's contracture,

Ledderhose's disease, Peyronie's disease, capsular contracture and fibrotic
scarring, application of focused shock waves not only blocks signalling casca­
des for growth factor TG F-beta 1, but also reduces expression of alpha-smooth
muscle actin (alpha-SMA). collagen I and fibronectin. Cellular proliferation can
be interrupted by inhibition of individual signalling cascades, with tissue res­
ponse dependent on shock wave dosage. In the case of tendinopathy, growth

139
factors such as TGF-beta 1 are desirable as they promote regeneration. Low­
level shock wave energy is sufficient here. By contrast, focused shock waves at
high doses lead to inhibitory (and hence antifibrotic) effects.3o-3,. 34 , 3s

The comprehensive account by K. Knobloch provides an in-depth explanation

of the effect of ESWT in cases of fibromatosis (see below).

TREATMENT
see section headed ' Frozen shoulder' (supine position).

ESWT AND FIBROSIS

Professor Dr Karsten Knobloch, FACS

Fibrosis refers to the proliferation of connective tissue fibres within an organ.

Where it occurs without a known cause, it is known as primary fibrosis, as in
cases where retroperitoneal fibrosis (Ormond's disease) involves displace­
ment of the urinary tract. Secondary fibrosis is the result of endogenous or
exogenous damage caused by factors such as inflammation, oligaemia or to­
xic agents. In alcoholic cirrhosis of the liver, alcohol acts as a toxin causing liver
tissue remodel ling with fibrosis and resultant liver dysfunction. Essentially,
any tissue can be affected by fibrosis.

There is now evidence for the benefit of ESWT in a range of fibrotic condi­
tions: fibrosis of the hand (specifical ly, Dupuytren's contracture), fibrosis of
the sole of the foot (Ledderhose's disease), fibrosis of the penis (Peyronie's
disease, also known as induratio penis plastica (IPP)), capsular contracture of
the breast fol lowing breast augmentation with implants, and fibrotic scarring
of the skin (Figure 89).
 N ewer i n d i c a t i o n s

Fig ure 89 :
Dupuytren 's Ledderhose's Fibrosis indications to dote
where ESWT has p roved
contracture disease beneficial

Capsular
contracture

CAPSULAR CONTRACTURE FOLLOWING AUGMENTATION MAMMOPLASTY

The development of capsular fibrosis (capsular contracture) subsequent to
augmentation mammoplasty, whether chiefly for aesthetic reasons or in
breast reconstruction following mammary carcinoma, involves the formation
of capsules - which are often highly painful - around the implant. Relevant
factors here include the choice of surface texture for a given mammary im­
plant, as well as surgical technique and (potentially) superinfection affecting
the implant.

Animal studies have shown that ESWT is able to reduce capsular contracture
in mammary implants:
ESWT improves capsular contracture in breast implants by inducing chan­
ges in pro- and anti-inflammatory proteins.1 s2
ESWT has reduced capsular thickness (as indicated by MRI scans) in two
animal models: a rat model1 s3 and a rabbit model1 s4 •

Clinical research published to date includes a cohort study1 ss involving twelve

patients with capsular contracture affecting a total of 19 breasts following
augmentation mammoplasty. An average of eight ESWT sessions (range:
3-26) took place (using electromagnetically generated focused shock waves,
0 . 25- 0 .38 mJ/mm2 , 1, 0 0 0 -1,5 0 0 pulses per session), the outcome being a
reduction in both pain and capsular contracture. Complications such as rup­
tured or otherwise damaged implants were not observed in this study.
Figure 9 0 :
Focused ESWT for scar revi­
sion purposes and to prevent
capsular fibrosis following
augmen tation mastopexy

FINDINGS OF ANIMAL STUDIES ON ESWT IN LYMPHOLOGY

In 2010, a research group led by M. Kubo described the influence of low­
energy focused shock wave therapy on secondary lymphoedema in a rabbit
ear model141 Following surgical severing of lymphatic vessels in the ear, the
team studied the effect of low-energy shock waves (regimen: 0.09 mJ/mm2 ,
200 pulses, applied three times weekly over a four-week period beginning
14 days after surgery, making a total of 12 sessions). The design included a
control group without intervention for comparative purposes. Western blot
analysis revealed that expression of both vascular endothelial growth factor
(VEGF)-C and VEGF receptor 3 (VEGF R3) was significantly increased in the test
versus the control group. Furthermore, the thickness of lymphoedematous
ears subjected to shock wave treatment decreased significantly compared
with untreated animals. lmmunohistochemistry for VEGF R3 showed the den­
sity of lymphatic vessels was significantly increased by shock wave treatment.
In 2011, a research group based in Sendai, Japan'4 6 published an animal study
using a rat tail model. Tail lymphoedema was treated using low-energy fo­
cused shock wave therapy (o.25 mJ/mm2, 500 pulses) four times at two-day
intervals.

Tail volume was measured (Figure 91), as was the fluorescence intensity of
indocyanine green (ICG) in the distal portion. Expression of VEGF-C and ba­
sic fibroblast growth factor (bFGF) were evaluated by reverse transcription
 N ewer i n d i c a t i o n s

RAT TAIL VOLUME IN A LYMPHOEDEMA MODEL I Fig. 91

Figure 91 :
Rat tail volume in a lymphoe­
dema model; con trol group
(blue) compared with
Tail volume
group receiving focused
shock wave th erapy
1.8 (red, 0 . 25 m}/ mm', 5 0 0 pu lses
n = 1 5 per group
1 .7 on day s 3, 5. 7 & 9)
1.6

- - -- J- - - - l--- -- J- - - - -l - - - - -
"' 1 . 5
>,

J r -
-::,
1 -4 - Contro l
>< 1 .3
>,
rtl * ···O··· Shock wave
-::, 1 .2
1 .1 * P < o.05
1.0
day1 day4 daY7 day 1 0 day13 day 1 6 day 1 9 day 22 day 25

polymerase chain reaction (RT-PCR) before, finally, histochemical assessment

of lymphatic vessel density was performed. Analysis showed that tail volume
was significantly reduced in the group exposed to shock waves.

Pronounced reddening with extensive oedema was clinically observed in the

control group on day 7; this was not the case in the ESWT group. Fluorescence
testing, using ICG injected distally to the lesion, revealed markedly accelera­
ted drainage of this dye - indicating improved clearance - within the ESWT
group from day 7. RT-PCR revealed significant upregulation of VEGF-C and
bFGF in the shock wave group compared to the control group. From day 15
onwards, newly formed lymphatic vessels were detected in the ESWT group.

In 2013, I.G. Kim et al. published an animal study that combined focused
shock wave therapy (0.05 mJ/mm2, 500 pulses, eight sessions within a four­
week period) with application of VEGF-C hydrogel to stimulate lymphangio­
genesis1 42. Four weeks after this combined treatment, the decrease in oede­
ma and collagenous deposits was greatest in the combination test group. The
presence of LYVE-1-positive vessels showed that growth of new lymphatic ves­
sels had been induced. The authors concluded that a synergistic combination
of focused ESWT and a VEGF-C hydrogel is most effective in promoting lym­
phangiogenesis.

1 43
 MECHANISM INVOLVED IN ESWT OF FIBROSIS

Transforming growth factor beta (TGF-B), with its multiple isoenzymes

(TGF-B1, TGF-B2, TGF-B3), plays a profibrotic role. The higher the local con­
centration of TGF-B, the stronger is the activation of intracellular signalling
pathways, which in turn leads to proliferation of fibroblasts and ultimately to
an increase in fibrosis.

Fig ure 92:

Progenitor fibroblasts a re
activated by TGF-B, res ulting
in differentiation into
myofibroblosts and fibro cytes
which, in turn, leads ta
in creased synthesis a n d
deposition of the extra­
cellular m a trix (fCM)

ESWT appears to exert antifibrotic effects via mechanisms inclu­

ding the modulating of the TGF-B signalling pathway.

144
 Newer indications

This hypothesis, namely the antifibrotic influence of ESWT, is supported by

various publications as outlined below.

In January 2018 a research group based in South Korea, led by H.S. Cui1 56 , pu­
blished an experimental study on the effect of focused shock wave therapy
on hypertrophic scarring. This involved exposing primary dermal fibroblasts
to focused 1000 pulses with energy flux density of 0.03, 0.1 or 0.3 mJ/mm2 At •

24 and 72 hours after treatment, detailed molecular biological analysis was

carried out by means of real-time PCR and Western blotting. Expression of
TGF-151 was significantly reduced by electromagnetically generated focused
ESWT, as was that of alpha smooth muscle actin (alpha-SMA), collagen I and
fibronectin.

In a rabbit hypertrophic scar model, low-energy ESWT (up to 0.1 mJ/mm2) de­
creased scarring by means of reduced fibroblast density and suppression of
alpha-SMA1 57 • Clinically speaking, keloids are improved when collagen type I
and I l l are significantly reduced and the MMP-13 enzyme increased1 s8 • In a stu­
dy with randomized controlled design, burn scarring is significantly improved
by application of electromagnetically generated focused ESWT (0.05-0.15
mJ/mm2 4 Hz, 1,000 pulses, three sessions)•s9 _
,

145
 Closing remarks and outlook

It was more than a quarter of a century ago that orthopaedists hit on the idea
of using focused shock waves - detected by Chaussy and employed to frag­
ment kidney stones - for another application, namely to treat calcific tendini­
tis of the shoulder.

2020 marks the 25th anniversary of DIGEST. From the year of its inception - in­
deed, in its very statutes - this professional society called for scientific studies
exploring how ESWT works. And much has happened since then. The last 20
years have seen a wealth of publications and of new knowledge about ESWT.
DIGEST and its international counterpart, the ISMST, regularly update their
treatment guidelines on this basis, i.e. in line with the latest research findings.
This makes it all the more surprising that, despite the unambiguous evidence
base, the effectiveness of ESWT in treating enthesopathies has still not been
recognized. And yet this therapy has been acknowledged to work in the case
of plantar fasciitis - which, since it explicitly represents a typical enthesopathy,
is a somewhat baffling inconsistency. Could the influence of the pharmaceu­
ticals lobby be a factor in this negative general attitude, or might it indeed
have been economic-policy manoeuvring that made this decision inevitable?
The failure to respect these studies (some of them at evidence levels I and 1 1)
are an affront to scientists in Germany and the wider world who have been ad­
vocating a well-founded, objective assessment of ESWT for many years now.

Recoveries from calcific tendinitis of the shoulder after ESWT, and from dege­
nerative tendinopathies in general, mean that attempts to explain ESWT in me­
chanistic terms are increasingly giving way to other explanatory models. A pa­
radigm shift in favour of mechanotransduction has rapidly emerged because,
both in animal studies and biochemically, evidence has been obtained for the
effectiveness of this therapy at cellular and molecular levels. In this context, the
theoretical (and perhaps overly bold) question can be raised as to whether di­
rect mechanistic fragmentation does in fact explain the outcome in cases of
nephrolithiasis or ureteral calculus. Could, instead, the mechanical energy of
the shock waves positively influence the pathological metabolic conditions that
originally led to kidney stone formation, thus inducing these deposits to break
up and disintegrate, enabling future renal calculus to be avoided?

1 47
The mode of action of ESWT has been illustrated in this monograph with refe­
rence to degenerative changes of the tendons and by unravelling several key
signalling pathways. It should be clear to us that we are just starting to piece
together details of a complex, multidimensional jigsaw puzzle. It will probably
be decades before further mechanosignalling pathways have been identified
and understood.

Mechanical energy, and mechanical principles relating to pressure, promote

the formation of osteoblasts and osteoclasts in the osteosynthetic process,
and in distraction and bridging techniques with external clamps, as used in
cases of leg shortening. Expansion and extension techniques are applied in
obtaining skin grafts for plastic reconstruction. All of these procedures are
mechanotherapies. Even treatment of infant hip dysplasia with a hip spica
160

cast is a proven form of pressure therapy and should be regarded as such here.
These procedures activate osteogenic and myofascial stem cells. All of these
methods of treatment are a standard and recognized part of clinical practice.

For some time now, we have also applied the mechanical energy of extra­
corporeal shock waves in treatment of posttraumatic bone marrow oedema
(bone bruising). Furthermore, ESWT looks increasingly promising for wound
healing disorders due to surgery or diabetes, and even for second- and third­
degree burns.

And what is happening in other branches of medicine? W. Schaden has re­

ported multiple times on fascinating experiments in mice conducted at the
Ludwig Boltzmann Institute in Vienna. Cardiac performance (on an exercise
wheel) was considerably poorer in mice after ligation of a coronary artery
than in control animals. Following local treatment of the cardiac muscle using
a specially generated miniature shock wave system, after six weeks these ani­
mals' performance was restored to the level of the non-ligated mice. Angio­
genesis was histologically confirmed.

Another animal experiment may be of similar importance in terms of future

clinical practice. In this study, again on mice, some animals had their spinal
 Cl osin g remarks and o utl ook

cord transected at the L4/L5 level, after which they could move only using
their front legs. Fol lowing local ESWT, however, some six weeks later mice in
the test group were observed to move using their hind legs as wel l. These fin­
dings in animal studies have now resulted in all trauma centres in Austria, and
one in Germany (Berlin's BG-Unfallklinik), consistently using ESWT in human
paraplegics. Expectations are high regarding further advances.

Urological centres use shock waves to treat not only kidney and urinary tract
stones but also erectile dysfunction, the fibrosing disorder Peyronie's disease
and deep pelvic pain (including prostatitis and cystitis). This was the subject
of a paper given by Nuremberg-based investigator G. Hatzichristodoulou at
the 201 9 DIGEST ESWT Update held in Berlin. Deep pelvic pain, often of un­
clear pathogenesis, may be a future indication for Extracorporeal Magneto­
transduction Therapy (EMTT®).

Important neurological indications here include the compressive disorder

that is carpal tunnel syndrome, and Morton's neuroma. Clinician H. Lohse­
Busch treats spastic conditions.

Many unanswered questions remain concerning the use of ESWT to treat de­
mentia sufferers. Researchers using a special MRI colorimetric technique have
reported that 20% of the input shock wave energy is detectable at a depth of
about 2 to 3 cm beneath the calvaria (skul lcap). What effect is at work here,
if it can indeed be proved at all? Are angiogenesis/vasculogenesis involved?
How would cognitive changes be measured, and who would assess them?
These issues directly give rise to many other questions and reveal how com­
plex it would be to assess changes that do not constitute recovery. It would be
a major achievement if objective criteria could be found which show, at least
in part, that the onset of suffering has been delayed. Is there a glimmer of
hope, at least for the vascular form of dementia?

I wish to make one final concluding remark. Certain cytokines (including in­
terleukin-L6} are being discussed in terms of their rheumatological and pain
therapy benefits, since they neutralize the pain receptors of nociceptive fib-

149
res and thus have an analgesic effect.
1 61 • Readers will remember that shock
162

waves activate endogenous MSCs and release cytokines. It might be specula­

ted that this gives us a key to explaining how extracorporeal shock wave the­
rapy - and, in the future, EMTT® as well - relieves pain.
Cl osin g re marks and outlook

151
1 52
 Ackn ow ledgements

ACKNOWLEDGEMENTS
My sincere thanks go to a number of friends and to various colleagues in
the scientific community, without whose publications and whose wealth of
ideas this book would never have come about. In alphabetical order, they are:
W. Bloch, L. Gerdesmeyer, M. Gleitz, J . Holfeld, D. Jankovic, K. Knobloch,
R. Mittermayr, P. Novak, R.F. Radel, M. Ringeisen, J .D. Rompe, W. Schaden,
M. Vigano and CJ. Wang. There are others not mentioned here to whom I am
also very grateful.

I owe particular thanks to H . Backer and S. Schulz for doing an excellent job of
proofreading the text and the English translation. From my family, I would to
thank Antje und Bastian for their ongoing support during this project, and for
their infinite patience in response to my (at times) near-obsessive enthusiasm.

1 53
 A b b revi a t i o n s

AC JOINT Acromioclavicular joint

AS Achilles tendon
BMPS Bone Morphogenetic Proteins
CGRP Calcitonin Gene Related Peptide
DGST Deutsche Gesellschaft fur StoBwellentherapie
DIGEST Deutschsprachige Internationale Gesellschaft
fur Extrakorporale StoBwellentherapie
ECM Extracellular matrix
EFD Energy flux density
EMTT Extracorporeal Magnetotransduction Therapy
ENOS Endothelial Nitric-Oxide Synthase
EPAT Extracorporeal Pulse Activation Therapy
ESW Extracorporeal shock wave
ESWL Extracorporeal shock wave lithotripsy
ESWT Extracorporeal shock wave therapy
FSW Focused shock waves
IGESTO Internationale Gesellschaft fur extrakorporale
StoBwellentherapie
ISMST International Society for Medical Shockwave
Treatment
MRT Magnetic resonance imaging
MSC Mesenchymal stem cell
MTRP Myofascial trigger points
NO Nitric Oxide
OP Osteogenetic Proteins
PCNA proliferating cell nuclear antigen
PW Pressure wave
RCS Rotator cuff syndrome
RSW Radial shock waves
RSWT Radial shock wave therapy
SW Shock wave
TGF-BETA Transforming Growth Factor-beta
VEGF Vascular Endothelial Growth Factor

1 55
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References
Today, Extracorporea l Shock Wave Thera py ( ESWT) is wel l esta bl ished as a treatment for
many muscu loskeleta l d isorders and d i seases, even replacing certa i n s u rgical i nterven­
tions. Practitioners who routi nely employ shock wave thera py need to upski l l themselves
conti n uously to stay a b reast of the latest developments.

• E nthesopath ies• by U l rich Dreisl l ker Is a new edition of the a uthor's reference work
entitled • Enthesiopath ies" , now considered a classic i n the field of orthopaedic shock
wave thera py. A g rowi ng evidence base concern ing the mecha nisms of action of shock
wave therapy resu lted i n the decision to revise and expa nd the earlier book. The u pdated
and fu l ly i l l ustrated edition presents tech nological innovations and new treatment ind ica­
tions. It offers va l uable advice for both newcomers to the field and adva nced users.

U l rich Drei s i l ker, a specia l i st i n orthopaedics, sports medicine and chl rothera py, has
been a shock wave thera py practitioner for more tha n 2 5 yea rs. He i s a co-founder of
DIG EST, the German-language I nternational Society for Extracorporea l Shock Wave
Thera py, a n d has served as Its president a n d as a boa rd mem ber.