TENS (Manual Book Endomed 484) Van Der Esch

TENS treatment using the Endomed 484:
multi-channel application
Editor:
M. van der Esch
Published by Enraf-Nonius B.V.,

in conjunction with the Jan van Breemen Instituut,
Centre for Rheumatology and Rehabilitation, Amsterdam.
We would like to thank the authors, M. Vanderthommen, F. in 't Groen, J. Cloostermans, M. van
der Esch and J. Oechies, the editor M. van der Esch and editorial assistant M. van Velzen, for
their respective contributions to the production of this therapy guidebook.
Enraf-Nonius B.V.
Copyright:
Enraf
Nonius
Enraf-Nonius B.V.
Postbus 810
2600 AV Delft
Nederland
Tel: 015-26 98 400
Fax: 015-25 61 686
Ordernummer 1497.766-40
1st print
January 2000
2
Contents
Page
Foreword 5
Introduction 6
Chapter 1. Neuro-Muscular Electrical Stimulation (NMES) in the treatment of sports 8

injuries
by M. Vanderthommen, PT
1.Theoretical background 8
1.1. Introduction 8
1.2. What types of muscle fibre are there ? 8
1.3. The influence of NMES on muscle fibre typology 9
1.4. Influence of NMES intensity 9
1.5. Metabolic effect of NMES-induced contractions 10
1.6. Single-channel or multi-channel treatment ? 12
2. Treatment examples 13
Chapter 2. Neuro-Muscular Electrical Stimulation (NMES) following a CVA 18

by F. in ‘t Groen, PT Revalidatiecentrum Het Roessingh
Introduction 18
1. Tonus normalization 18
1.1. Introduction 18
1.2. Electrical stimulation 18
1.3. Tonus normalization in hypertonic musculature 21
2. Contracture prevention 23
3. Trophic improvement and pain relief 24
Chapter 3. Neuro-Muscular Electrical Stimulation (NMES) following a transverse lesion 26

by J. Cloostermans, PT Revalidatiecentrum Het Roessingh
Introduction 26
1. The stimulation of functionality (associated with standing) 26
1.1. Introduction 26
1.2. Facilitation of standing by stimulation of mm. Quadriceps and mm. Gluteus maximus 27
1.2.1. Selection criteria 27
1.2.2. Preparatory training for standing 28
2. Cardiovascular training 30
3. Spasticity reduction 31
4. Trophic stimulation 33
Chapter 4. Use of electrical stimulation (ES) for pain modulation 35

by M. v.d. Esch, PT
1. Introduction 35
2. Equipment for the modulation of pain 37
3. Treatment example 38
3
Chapter 5. Electrical stimulation for the promotion of tissue recovery 42
by J. Oechies, PT
1. Introduction 42
2. Complex Regional Pain Syndrome, Type 1 42
2.1. General 42
2.2. Therapy implications 43
3. Claudicatio Intermittens 44
4. Oedema 45
Index 47
References 48
Chapter 1 48
Chapter 2 50
Chapter 3 51
Chapter 4 53
Chapter 5 54
Protocol Reference List for Endomed 481, 482 and 484 55
Illustrations 56
4
FOREWORD
Enraf-Nonius B.V. has for some years been publishing therapy guidebooks to provide physiotherapists with
concise and practical information on new developments within the profession. A new guidebook usually
follows each time a new item of electrotherapy equipment is developed and introduced. While the books are
intended to help practitioners use the new equipment, that is not their sole purpose. Recognizing the
responsibility that goes with its publishing activities, Enraf-Nonius also seeks to make a positive contribution
to the theory and practice of contemporary physiotherapy.
When producing this publication, Enraf-Nonius has, as usual, sought to discharge this responsibility by
approaching several leading physiotherapists for contributions. However, it should be stressed that the
contributors did not set out to write a scientific textbook and that the product of their labours has no
pretensions to be a comprehensive reference work. Rather, the authors’ primary aim was to give readers a
concise introduction to recent developments in the field of electrotherapy. Anyone who wishes to study the
subject in more depth should refer to the recognized textbooks. The authors have also sought to stimulate
and, in the most positive sense, to provoke. It is hoped that the guidebook will suggest questions, possible
research topics and ideas about how individual patients are best treated. Thus, perhaps this publication can
emulate the stimulus-response pattern of electrotherapy itself. Ultimately, it is up to the individual
physiotherapist to decide how he or she will make use of the information presented.
For me, as editor, it has been a pleasure to work with texts produced by authors who recognize the way the
discipline is changing. Interest in the use of various types of electrical current for neuro-muscular stimulation
goes back a long way. However, not all the research conducted in this field has been of the highest quality
and insufficient attention has perhaps been given to the subject within the profession. Nevertheless, the
stimulation of motor efferent nerve fibres is well established in physiotherapy. Furthermore, technological
advances and increasing scope for the application of electrical techniques are creating new opportunities for
the treatment of patients with neuro-muscular conditions. It should be noted that the specimen cases
included in the various chapters are intended not to prescribe what can be done, but as examples of how
electrotherapy may be used.
A great deal of important research into pain has been carried out in recent years. This has in no small part
been due to the excellent work of the IASP (International Association for the Study of Pain). Accordingly, the
chapter on pain draws heavily upon information published by the IASP. It is up to practising physiotherapists
to look into this matter more closely, and the chapter provides a starting point for doing so. The chapter on
pain also explains briefly how TENS (Transcutaneous Electrical Nerve Stimulation) can be used to influence
pain.
The therapy guidebook for the Endomed 484 has been written by a team of dedicated authors, all of whom
are practising physiotherapists, fully aware of the practical importance of what they write. The Jan van
Breemen Instituut (JBI), Centre for Rheumatology and Rehabilitation, took on the task of editing the
contributions and bringing them together to form a cohesive text. As an expertise centre for posture and
movement, the JBI naturally follows developments within the discipline closely. Many of the centre’s patients
suffer from chronic mobility-impairing conditions. With a view to reducing the limitations imposed by these
conditions, physiotherapy makes use of various resources. Many patients also suffer from chronic pain, which
can itself be completely immobilizing and can severely restrict day-to-day activity. Chronic pain is complex
and needs to be tackled on a multidisciplinary basis where possible. Physiotherapy makes use of the
available resources to increase the activity level of patients afflicted by such pain. In this context,
electrotherapy is a useful tool. Given its experience and expertise in this field, it made sense for the JBI to
take on the job of editing this guidebook. By doing so, the centre hopes to contribute to the dissemination and
application of valuable knowledge.
M. van der Esch

PT, MT
5
INTRODUCTION
Electrical stimulation has many potential therapeutic applications and is used in physiotherapy for the
treatment of various conditions. Within the discipline, electricity is used mainly to stimulate nerve fibres with a
view to generating certain responses in the central nervous system and the periphery. If one is to make the
most effective use of this technique, it is important to have a good understanding not only of the electrical
current itself, but also – indeed, crucially – of the (central) nervous system in which the responses are
induced. In clinical practice, one needs to be able to recognize these responses in order to determine
whether the treatment is having the desired effect.
An electrical current is capable of depolarizing a peripheral nerve and ultimately, if it is strong enough,
creating considerable action potential. Being thoroughly described in various textbooks, the mechanism of
depolarization is not considered in any detail here. Nevertheless, to follow the ideas put forward in this book,
it is important to have a basic understanding of peripheral nerves. Peripheral nerves link the spinal cord to
peripheral organs, such as muscles or joint capsules. Each nerve is made up of nerve fibres, called axons.
Nearly all peripheral nerves contain several types of fibre, and none consist entirely of motor fibres. Typically,
a peripheral nerve will contain sensory and motor fibres in combination with sympathetic and/or
parasympathetic fibres. The nature of a nerve’s make-up is important in relation to electrotherapy, which
tends to focus on particular types of fibre. In a particular case, the emphasis may, for example, be on
stimulation of motor efferent peripheral nerve fibres, or on sensory afferent fibres. The motor efferent fibres
originate from the alpha and gamma motor neurons and innervate the muscles and the muscle spindle. The
neurons of the sensory afferent nerve fibres are located in the dorsal root ganglion and the spinal cord. The
fibres lead from particular sensors, such as the pacinian corpuscles, Krause’s bulbs or Golgi’s corpuscles.
However, half of all afferents do not contain sensors and have little or no myelin sheathing. Such afferents
are known as free nerve endings. The nerve fibres of the sympathetic and parasympathetic nervous system
have neurons in the truncus sympaticus and lateral bundles of the spinal cord, particularly the thoracic
section. Under normal circumstances, the action potential of a motor or sympathetic efferent fibre is
transmitted to the periphery of the body, while the sensory afferent fibres conduct action potential to the
spinal cord. Afferent fibres may be divided into myelinized and non-myelinized fibres. The first group includes
the I/II and IIIa afferents and the second group the IIIb and IV afferents. For details of the various classes of
fibre, readers should refer to a textbook dealing with the Erlanger/Gasser and Lloyd/Hunt classification
systems. In the context of electrotherapy, it is important to understand the differences between the various
fibres in order to decide which should be stimulated. Stimulation of type IIIb/IV fibres involves noxious
stimulation, since these fibres only discharge in the event of (potential) damage. The myelinized fibres mainly
register action potential generated by tactile and pressure (i.e. non-noxious) stimuli.
Modern electrical stimulation equipment is designed to enable accurate differentiation of the various nerve
fibres. This makes it possible to generate differentiated responses. However, the central nervous system can
be disrupted to such an extent that when myelinized afferents are stimulated, responses which one would
normally associate with noxious stimulation occur. In this sense, the central nervous system remains
something of a mystery, despite the fact that sufficient research has now been conducted to make it possible
to predict with reasonable confidence where activity will occur during peripheral stimulation.
A number of levels may be distinguished in the intensity of electrical stimuli applied to peripheral nerves.
Under normal physiological circumstances, stimulation of a limited intensity (‘sensory level stimulation’) will
cause the myelinized afferents to discharge. If the intensity is increased to what is known as 'motor level
stimulation’, the motor efferent nerve fibres will also discharge. Finally, the non-myelinized afferent nerve
fibres will discharge to warn the nervous system of potential damage once the stimuli reach the so-called
‘noxious level’. Under patho-physiological circumstances, however, these levels can overlap, due to
sensitization of the fibres and neurons. Consequently, even mild stimulation can cause discharge of the IIIb
and IV afferents, which normally only respond to noxious stimulation.
Modern electrical stimulation equipment is designed to provide as much differentiation as possible in the
intensity of stimulation. The level one selects will always depend on the aim of the treatment in the individual
case. When electrical stimulation techniques were first introduced, galvanic current was normally used.
Subsequently, interrupted modulated galvanic current (diadynamic current) was introduced, following on from
the research of Träbert and Bernard. As time went by, it became more and more clear that differentiated
stimulation of the various afferents could also be achieved using other types of current. Technical advances
made it possible to employ alternating current with no galvanic component in the pulse form. Alternating
current of this kind was referred to as ‘interference’. In the sixties, portable electrical stimulation appliances
suitable for prolonged use came onto the market. Known as transcutaneous electrical nerve stimulators
(TENS), these appliances could generate numerous different pulse forms and wide frequency ranges. In-
depth explanations of the various pulse forms are given in the established electrotherapy textbooks. Here, we
shall confine ourselves to pointing out that the stimulators use a sufficiently wide variety of current types,
pulse lengths and frequencies to allow for development of this technique well into the future. The availability
6
of several channels and the ability to adjust these channels are particularly advantageous. In addition to the
classic types of current, the stimulators can deliver some very modern alternatives and therefore offer an
extensive range of options.
Various TENS forms and stimulus characteristics
Conventional TENS Burst TENS Brief intense TENS Low frequency TENS
phase duration phase duration phase duration phase duration
10-100 µs 50-250 µs 100-250 µ s 100-300 µs
frequency 40-200 Hz freq. 80-120 Hz freq. 60-120 Hz freq. 1-5 Hz
strength: mitis (just normalis/fortis fortis (tolerance limit) fortis (tolerance limit)
discernible)
treatment time: variable ± 15-60 min ± 15-20 min ±15-20 min

(hours)
non-noxious noxious
All forms of TENS are available via one, two, three or even four channels. The parameters one sets depend
entirely on the aim of treatment and the responses observed in the diagnostic phase.
This guidebook is intended to provide information about the various ways in which TENS can be used within
physiotherapy. The full range of possibilities is examined. Consideration is given not only to the stimulation of
motor efferent nerve fibres under physiological and patho-physiological conditions, but also to the stimulation
of sensory afferent nerve fibres in order to relieve pain and promote tissue recovery. In doing so, the intention
is not to create an alternative to the existing textbooks in this field, or to present a scientific research paper.
Rather, it is to briefly outline the clinical uses of TENS by reference to clear specimen cases, and thereby to
encourage the users of electrical stimulation equipment to consult appropriate reference literature, to widen
their experience of using the technique in the assistance of various patient groups and finally to consider
undertaking their own research.
The structure of this guide is as follows. Chapter 1 describes the use of electrical stimulation to aid recovery
from sports injuries. Chapter 2 goes on to look at the application of electrical techniques in the treatment of
conditions affecting the nervous system. In the latter context, particular attention is given to brain trauma,
such as cerebrovascular accidents (CVA) and transverse lesions of the spinal cord. The complex nature of
pain and how it may be influenced by electrical stimulation are covered in chapter 3. Finally, there is a chapter
devoted to promoting tissue recovery by the stimulation of blood circulation.
7
1. Neuro-Muscular Electrical Stimulation (NMES) in the treatment of
sports injuries
1. Theoretical background
1.1. Introduction
Various sport-related conditions can be influenced by electrical stimulation. Distinction should be made
between problems arising out of inactivity in the neuro-muscular system and problems caused directly by
disorders of the muscular system itself. As well as assisting recovery from sport-related musculoskeletal
conditions, electrical stimulation can benefit the physiological neuro-muscular systems, even if they are
undamaged. Generally speaking, sports injury treatment is concerned with therapies that influence tissues
affected by cellular damage and/or necrosis. The process of adapting the tissue during repair and
regeneration determines the intensity and the duration of the individual’s training. The principle of overloading
is often applied as well, in order to effect complete recovery in the shortest period of time. Hence, training
intensity and duration are used as variables in order to influence cell functions.
If the peripheral neuro-muscular system is intact, an electrical current can stimulate the nerve to generate
action potential, similar to the potential created under physiological circumstances. Although the origin of this
potential is not physiological, electrical stimulation results in a muscle contraction, albeit a different kind of
contraction from that induced by physiological means. Despite the differences between physiologically
generated and electrically generated potential and between the associated forms of contraction, similarities
do exist. In both cases, for example, the contraction will result in afference from the muscle to the central
nervous system and the communication of information regarding the contraction. Electrical stimulation has
the important advantage that a muscle contraction can be identified and motor output thereby improved.
In the treatment of sports injuries, it appears that the greatest benefits are obtained by stimulating adaptation
processes, so that intact nerve-muscle systems can be brought into use as quickly as possible during
training. The strength of the contraction, in relation to its duration, should be the maximum tolerable without
pain (the overload level).
In this context, the aims of electrical stimulation are:

• to increase strength;
• to reduce muscle fatigue;
• to increase co-ordination;
• to prevent muscle atrophy.
It is vital that the patient is as active as possible during and after NMES.
For the improvement of muscle strength during and after a period of immobilization, e.g. following an anterior
cruciate ligament injury, NMES generally seeks to promote the adaptation of muscle fibres. The technique
utilizes the plasticity of muscle fibres to achieve the desired effect.
1.2. What types of muscle fibre are there?

There are numerous different types of muscle fibre, distinguished by various biochemical, histological,
enzymological and physiological characteristics.
Type I fibres (also known as red or slow-twitch fibres) are characterized by high levels of myoglobin. They are
also rich in glycogen and triglycerides, contain numerous mitochondria and are surrounded by dense capillary
networks. The metabolism of type I fibres is essentially oxidative (aerobic). Muscle fibres of this kind tire
slowly; in other words, they are capable of responding to repeated stimulation for long periods.
Type II fibres (also known as white or fast-twitch fibres) contain few mitochondria and are surrounded by a
relatively light capillary network. On the other hand, they exhibit high concentrations of myosin ATPase and
phosphorylase. The metabolism of these fibres is basically glycolytic (anaerobic). Activation of type II fibres
results in rapid and strong contractions, but they tire easily. This class of fibre is subdivided into types IIa, IIb,
IIab and IIc.
8
1.3. The influence of NMES on muscle fibre typology
Snyder-Mackler, Delitto et al very recently published the results of research into the effect of NMES on
patients recovering from anterior cruciate ligament (ACL) operations. After four weeks of m. Quadriceps
stimulation, NMES patients were able to develop a contraction force 70 per cent higher than patients in a
control group. Those receiving NMES also showed a corresponding improvement in the functionality of the
affected leg. The extent to which these effects are attributable to particular changes in the nature of the fibres
in the muscle tissues is still the subject of debate. However, animal experiments suggest that NMES does
lead to fibre type adaptation. In this context, the intensity and duration of the contractions induced are
important variables.
Present hypotheses suggest the following explanation. The motor units in the type I muscle fibres begin to
fuse when the frequency reaches 10 Hz and complete tetanus follows at about 30 Hz. At this frequency,
summation of type IIb motor units is also initiated. The latter cause complete tetanus at approximately 65 Hz,
an effect that depends on the speed and strength of the contraction. In short, an increase in strength is
associated with NMES when the stimulation frequency is raised from 10 Hz to 70 Hz, given constant intensity.
As the frequency is raised, the temporary summation is clearly discernible. Frequencies higher than 70 Hz do
not produce stronger contractions, since full summation of the fastest motor units (IIb) occurs at 70 Hz
(figure 1).
Figure 1:
Relationship between the moment of electrical excitation (MEE)
of quadriceps strength, expressed as the percentage of the maximum
moment (% MEEmax) and the impulse frequency (Hz).
Average values + ET (n = 40).
1.4. Influence of NMES intensity

Muscle tension increases as new motor units are recruited (spatial summation). The electrical current brings
about specific spatial summation: the surface motor units closest to the electrodes are activated first and
recruitment extends deeper into the tissue as the intensity of the current increases (figure 2). This is followed
by random recruitment of type I and type II motor units, depending on their topographic location within the
muscle. It would therefore appear that NMES is not able to select a certain type of muscle fibre.
Where NMES is used to increase strength, the intensity of the stimulation needs to be as high as the patient
can tolerate without pain (the overload level), in order to ensure that motor unit recruitment penetrates as
deep as possible. The greater the level of penetration, the greater the effect on the treated muscle will be.
9
Figure 2:
Spatial summation induced by electrical stimulation
1.5. Metabolic effect of NMES-induced contractions

A NMES-induced contraction results in powerful general energetic stimulation, substantially greater than that
induced by a physiological contraction of comparable force. The magnifying effect of electrical stimulation can
be explained as follows:
• Electrical stimulation brings about continuous recruitment within a fixed population of motor units
throughout the contraction, whereas the population of motor units involved in a contraction initiated by the
central nervous system is always changing.
• The stimulation frequency used is generally related to the maximum frequency of the auto discharge of
the fastest motor units (type IIb fibres).
• Skeletal muscle is activated on an asynchronous basis by a physiological contraction, while electrical
stimulation produces synchronous recruitment in the motoneural branches.
Consequently, electrical stimulation results in levels of energetic demand in certain areas of the muscle,
which are abnormally high in relation to the strength of the contraction. This in turn brings about a substantial
increase in the metabolism of the aerobic and anaerobic fibres. The enhanced level of metabolic stimulation
associated with NMES is reflected in the effectiveness of the technique for assisting muscular recovery.
Metabolic effects of the kind described are most pronounced where there has been no damage to the muscle
tissue. If, however, cell necrosis has taken place, it is not certain that NMES-induced overloading can bring
about such metabolic effects. Empirical considerations suggest erring on the side of caution under such
circumstances and the use of low-intensity stimulation.
NMES can therefore be used in two basic ways:

1. to treat muscle tissue atrophy;
2. to increase the strength of a muscle or muscle group.
Both of these uses involve the stimulation of muscles in which the neuromuscular transfer of action potential
has not been impaired.
Ad 1) Electrical stimulation for the treatment of muscle tissue atrophy
Treatment to prevent atrophy is used mainly during periods of complete immobility. When a muscle is
immobilized, the simultaneous cessation of tonic and phasic muscular activity results initially in general
atrophy of the muscle fibres, particularly type I fibres. To compensate for the loss of low-intensity tonic
muscular activity, which is normally induced by type I motor units with a low discharge frequency, non-tetanic
stimulation with a frequency of 8 Hz is provided. Phasic muscular activity can be effectively replaced by
tetanic stimulation at 50 Hz. Treatment will typically involve alternate periods of five-second tetanic
contractions at 50 Hz and twenty-five-second non-tetanic contractions at 8 Hz. Patients are treated for one
hour at a time (see figure 3). The basic object is to maintain prolonged electrical stimulation of the muscle
cells at different frequencies. Where possible, the patient should also be encouraged to actively contract the
muscle.
10
Figure 3:
The use of NMES to prevent muscle atrophy
Ad 2) Electrical stimulation for the development of muscular strength
In the treatment of sports injuries, NMES can be used to increase muscle strength not only following
immobilization, but also to remedy co-ordination defects – where muscle group contraction is not in line with
the theoretical agonistic pattern for a particular action. Alternate periods of five-second tetanic contractions at
50 Hz and equal periods of complete rest are used to stimulate the discharge of fast-twitch fibres. Patients
are treated for twenty minutes at a time (see figure 4), with the emphasis on overloading, which greatly
promotes the growth and conversion of muscle fibres. The hypertrophy induced may be expected to result in
an increase in muscle strength. In this context, NMES should be regarded as a supplement to active training.
Figure 4:
Schematic reproduction of the stimulation to increase muscle strength
(phase I)
Figure 5:
Schematic reproduction of the stimulation to increase muscle strength
(phase II)
As treatment progresses, the parameters are typically modified by increasing stimulus frequency and
intensity, while leaving greater intervals between the contractions and reducing the length of each treatment
session (see figure 5).
11
1.6. Single-channel or multi-channel treatment?
For the treatment to be really effective, the contractions induced must be powerful. Where NMES is used to
promote motor recovery, the target is a single muscle or muscle group. The greatest effect may therefore be
expected if a single channel is used, with electrodes of different sizes. The smaller electrode is known as the
stimulus electrode. The larger electrode – which should ideally be twice or three times as big as the stimulus
electrode – is called the scatter or indifferent electrode. Multi-channel treatment is more appropriate for the
stimulation of several muscles or muscle groups to increase co-ordination during physical effort. Improved
co-ordination can be beneficial in terms of strength.
Treatment involves placing the smaller stimulus electrode on the motor point of the muscle, i.e. on the skin
immediately above the motor nerve branch point in the muscle. This zone is characterized by a concentration
of axonal branches and may therefore be identified by the high level of response to electrical stimulation. The
indifferent electrode should if possible be located on the muscle to be stimulated, close to the stimulus
electrode.
12
2. Treatment examples
Example 1: Atrophy of the quadriceps
Indication: Muscle atrophy after immobilization of the knee (resulting from trauma,
surgery, arthritis, etc) or after recovery from muscular lesion of the
quadriceps.
Number of channels: Three, arranged sequentially or in parallel.
Electrode size: Stimulus electrodes: 5 x 5 cm.
Indifferent electrodes: 9 x 5 cm.
Electrode position: Channel 1: m. vastus medialis.
Channel 2: m. vastus lateralis.
Channel 3: m. rectus femoris.
Position of patient at start: Sitting, knees bent at 30°, supported with a cushion.
Treatment parameters: Pulse form: symmetrical biphasic TENS.
Pulse length: 300 µs.
Frequency: 50 Hz.
Contraction-rest cycle: ramp-up time: 1 sec.
hold time: 5 sec.
ramp-down time: 1 sec.
interval: 5 sec.
Treatment time: 20 min.
Channels: synchronized.
Notes: -
3
1
2
3
1
2
Illustration 1: Electrode positioning atrophy Quadriceps
13
Example 2: Atrophy of the hamstrings
Indication: As case 1, but with the focus on the mm. biceps femoris, semitendinosus
and semimebranosus.
Number of channels: Four.
Electrode position: Channel 1: m. semitendinosus.
Channel 2: m. biceps femoris (caput longum).
Channel 3: m. semimembranosus.
Channel 4: m. biceps femoris (caput breve).
Position of patient at start: Half sitting, hips bent at 90° and knees bent at 30°.
Frequency: 80 Hz.
hold time: 5 sec.
interval: 6 sec.
Notes: -
3 1 4 2 3 4 2 1
Illustration 2: Electrode positioning atrophy Hamstrings
Example 3: Lesion of the anterior cruciate knee ligament
Indication: Agonistic or antagonistic muscular imbalance, preventable by restoration

of the quadriceps and hamstrings, which may be stimulated alternately or
simultaneously, depending on whether the patient also has an anterior
sign at knee-joint height.
Electrode position: Channel 1: m. vastus medialis.
Channel 2: m. vastus lateralis.
Channel 3: m. semitendinosus.
Channel 4: m. biceps femoris (caput longum).
Position of patient at start: Sitting, hips bent at 90° and knees at 45°.
14
Knee without anterior sign (illustration 3a)

Frequency: channels 1 and 2: 50 Hz.
Channels 3 and 4: 80 Hz.
hold time: 5 sec.
interval: 10 sec.
Notes: Alternate stimulation: channels 1 and 2 (quadriceps), rest interval (2
seconds), channels 3 and 4 (hamstrings), rest interval (2 seconds), etc.
Ch. 1
Ch. 2
Illustration 3a: stimulation cyclus
channel 1 t/m 4
Ch. 3
Ch. 4
Knee with anterior sign (illustration 3b)

Frequency: channels 1 and 2: 50 Hz.
channels 3 and 4: 80 Hz.
Contraction-rest cycle channels 1 and 2:
ramp-up time: 3 sec.
hold time: 5 sec.
interval: 8 sec.
hold time: 7 sec.
interval: 8 sec.
Notes: Synchronized stimulation: all channels start simultaneously with the
contraction, but the ramp-up time on channels 1 and 2 is longer than that
on channels 3 and 4. All channels end the contraction simultaneously. In
this way, a contraction of the quadriceps can be induced at the same
time as a contraction of the hamstrings already initiated to prevent
anterior sign of the knee.
Ch. 1
Ch. 2
Illustration 3b: stimulation cyclus
channel 1 t/m 4
Ch. 3
Ch. 4
15
Example 4: NMES for the treatment of abdominal musculature deficiency
Indication: Abdominal muscular deficiency in general, particularly cases of sports

people suffering from lumbar hyper lordosis causing pain in the facet
joints.
Electrode position: Channel 1: m. rectus abdominis (caudal to the umbilicus).
Channel 2: m. rectus abdominis (caudal to the umbilicus).
Channel 3: m. rectus abdominis (cranial to the umbilicus).
Channel 4: m. rectus abdominis (cranial to the umbilicus).
Position of patient at start: Lying on back, legs bent, feet on the treatment table with a cushion
under the knees.
Frequency: 30 Hz.
hold time: 6 sec.
interval: 6 sec.
hold time: 5 sec.
interval: 7 sec.
Notes: Asynchronous stimulation: channels 3 and 4 (abdominal muscles, cranial
group) begin contraction one second after channels 1 and 2 (abdominal
muscles, caudal group), in order to tip the pelvis backwards, but
stimulation via all four channels ends simultaneously.
3 4
1 2
Illustration 4: Electrode positioning abdominal musculature
16
Example 5: NMES for correction of shoulder instability resulting from tendinitis of the rotator cuff or
capsulitis of the glenohumeral joint or AC joint
Indication: Tendinitis of the rotator cuff muscles resulting from lesion of the
acromioclavicular joint.
Electrode position: Channel 1: m. pectoralis major.
Channel 2: m. pectoralis major.
Channel 3: m. latissimus dorsi.
Channel 4: m. latissimus dorsi.
Position of patient at start: Sitting, shoulder joint in 45° abduction, with forearm and elbow supported
on the treatment table.
Pulse length: 200 ms.
Frequency: 35 Hz.
hold time: 7 sec.
interval: 7 sec.
Notes: While the shoulder is abducted at 45° and the elbow is supported,
simultaneous stimulation of the m. latissimus dorsi and m. pectoralis
major causes caudal movement of the head of the humerus in the joint
socket.
2
1
4
3
Illustration 5: Electrode positioning at shoulder instability
17
2. Neuro-Muscular Electrical Stimulation (NMES) following a CVA
Introduction
This chapter considers the use of electrical stimulation (ES) to aid recovery in patients who have suffered
CVAs. ES has been used in post-CVA therapy for some years. It is particularly useful in cases involving tonus
regulation disorders and disabilities such as abnormalities of gait and grip problems. In this context, the
technique is often referred to as Functional Electrical Stimulation (FES), particularly where the object is to
reduce the degree of residual limitation.
When treating patients who have suffered CVA, electrical stimulation (ES) may be used for the following
purposes:
1. Tonus normalization;
2. Contracture prevention;
3. Trophic normalization and pain relief.
1. Tonus normalization
1.1. Introduction
Muscle hypertonia (spasticity) is a clinical phenomenon associated with damage to the central nervous
system. Traumatic brain injuries, CVAs, spinal cord lesions and various other conditions can result in
spasticity of the extremities or the trunk. Generally speaking, spasticity is the result of a disturbance to the
normal balance of neural input to the central nervous system (CNS) and thus to the alpha motor neurons.
Certain CNS conditions can involve an increase in central and peripheral excitatory input to the alpha motor
neurons, and/or a reduction in the inhibitory input to the alpha motor neurons. In most cases, there is both an
increase in excitation and a reduction in inhibition. The result is increased output from the alpha motor
neurons, heightened muscle tonus and impaired motor control.
The increased muscle tonus may involve anything from slight motor dysfunction, to constant muscle
hypertonia or even permanent immobilization of an extremity. The latter will typically lead to contracture of the
musculature and joints.
Physiotherapy seeks to restore the correct balance between excitation and inhibition in various ways. For the
most part, exercise is the preferred route, but electrical stimulation can also be used to influence muscle
hypertonia (spasticity).
The ultimate aim of tonus normalization by means of electrical stimulation is to improve various day-to-day
functions. Thus, the object is to restore not nerve tissue, but the functions impaired by hypertonia. Any
functions remaining intact following, say, a CVA should be actively trained as far as possible. This is
particularly important where the patient has neglected the functions in question. However, if the patient is
unable to independently influence recovery, electrical stimulation can be used to promote function restoration.
In this context, therefore, electrical stimulation is a supplement to active exercise. Although various authors
have reported functional improvements following electrical stimulation, it is not clear whether the effects are
merely temporary. The potential value of electrical stimulation therefore needs to be reconsidered in each
case.
1.2. Electrical stimulation

Before attempting to correct a muscle tonus regulation defect by electrical stimulation, it is necessary to
establish whether the patient is susceptible to stimulation. First, checks should be made to ensure there are
no contraindications, such as the following:
• reluctance to submit to and/or inability to comprehend the nature of the treatment;
• bone fractures or significant malignities in the part of the body where the motor nerves are to be
stimulated;
• sensory abnormalities in the areas where the electrodes are to be located.
18
Next, the degree of muscle tonus should be clinically determined on the Ashworth/Penn scale:
Muscle tonus score Degree of muscle tonus

1 Normal
2 Slightly heightened
3 Heightened
(passive movement possible, but not
active movement)
4 Substantially heightened
(difficulty with passive movement)
5 Seriously heightened
(severe rigidity in all directions of
movement)
The appropriate application should be selected on an exploratory basis. It is necessary to establish whether
the CNS responds when stimulation is applied to the hypertonic or hypotonic musculature with a view to
affecting the muscle tonus. The initial responses indicate whether electrical stimulation is worthwhile.
Continuation of the treatment should be reviewed if the imbalance between the hypotonic and hypertonic
musculature increases when stimulation is applied. In some cases, it may be necessary to adjust the
electrode position or the current intensity. In practice, it is rarely appropriate to continue electrical stimulation
if there is no visible improvement in the first six weeks. The most suitable treatment lenghts are hard to
determine, since the long-term effects have yet to be precisely established.
In line with medical theory, clinical distinction is often made between the stimulation of hypotonic muscles and
stimulation of hypertonic muscles. The notion that stimulation of the peripheral motor nerves can promote
motor learning remains a valid hypothesis, particularly in view of the fact that the peripheral nerves are not
themselves denervated. When muscles contract in response to stimulation via the motor nerves, various
recognition mechanisms may be activated. The possible explanations cannot be considered in any depth
here; suffice it to say that, despite the amount of work done in this field (particularly on the use of electrical
stimulation in combination with EMG), the role of electrical stimulation in relation to these mechanisms is not
yet properly understood.
However, it is important to note that, where motor learning is concerned, no evidence has so far been
presented to indicate that recovery can be induced by the stimulation of a single muscle. We know that
functional movements are achieved by various muscle sequences. It would therefore seem logical that, when
seeking to promote the restoration of natural movement, electrical stimulation should be applied to all the
muscle groups involved, simultaneously, consecutively or in an overlapping sequence.
Treatment example 6: Tonus normalization in a hypotonic arm/hand
Indication: Tonus normalization in a hypotonic arm/hand, whereby all flexors and

extensors in the forearm are facilitated.
Number of channels: Three, sequential.
Electrode size: Round, approx. 2 cm. If larger electrodes are used, it is important to
guard against overflow to areas which should not be stimulated.
If the skin is dry, it can be dampened with a little water.
Electrode position: Channel 1: n. radialis (see figure 6, page 25)
Channel 2: n. ulnaris
Channel 3: n. medianis
Position of patient at start: No particular position should be adopted, but the patient should be
relaxed and the forearm supported. Major movements of the arm under
treatment should be avoided as far as possible.
Treatment parameters: Pulse form: symmetrical biphasic TENS
Pulse length: 50-250 µs.
Frequency: 15-20 Hz.
Contraction-rest cycle: ramp-up time: 1-2 sec.
hold time: 8-9 sec. (ramp-up time + hold time =
10 sec.)
Length of treatment session: Training should be increased gradually to
maintain muscle condition. In this context, an effective practical
regime is to stimulate the muscles three times a day, increasing the
19
session length over a period of fourteen days from ten to sixty
minutes in five-minute steps (see treatment programme 1).
Amplitude: sufficient to induce clearly observable contractions without
causing pain.
Notes: • Sequential stimulation involving stimulation of the flexors first,
followed by the extensors.
• When positioning the electrodes, it is helpful to minimize the amount
of wrist deviation occurring during stimulation, so as to save the
patient undue discomfort.
Illustration 6: see page 56-57
As an alternative to stimulating the nerve pathways, consideration may be given to stimulation of the surface
extensors and flexors in the hand. This can be done by placing the electrodes on the forearm in such a way
that the m. extensor communis and the m. flexor communis are stimulated. Theoretically, this requires only
two channels, since the electrodes used to stimulate the m. flexor communis can be positioned so as to
stimulate the m. flexor pollicis longus as well. When positioning the electrodes, it is helpful to minimize the
amount of wrist deviation occurring during stimulation, so as to save the patient undue discomfort.
Scheme 1
Day Program Duration Daily frequency

1 Three-channel stimulation 10 min. 3x
Note: The initial response to electrical stimulation determines whether treatment should be
continued or modified. If the patient experiences muscle pain, muscle stiffness or skin
irritation, the build-up should be more gradual. Conversely, the build-up may be accelerated if
the patient responds well.
20
1.3. Tonus normalization in hypertonic musculature
Electrical stimulation was first used to normalize hypertonic (spastic) musculature by Duchenne as long ago
as 1871. Duchenne’s approach was based upon stimulating the antagonistic musculature. Since 1950,
numerous further studies have been carried out into the use of ES to influence spasticity. Most of these
studies have focused on the musculature of the forearm and hand in hemiplegic patients, but some have
involved stimulation of the muscles in the lower leg. Precisely how ES of the antagonists influences
hypertonic musculature remains somewhat unclear, and this is not the appropriate context for an examination
of the possible explanations. It is nevertheless important to point out that increasing scientific understanding
of the motor system and motor dysfunctions has led to the proposal of new hypotheses with practical
implications. In practice, for example, one does not often come across a patient with hemiplegic spasticity in
just one muscle group. Hence, there is a practical basis for the stimulation of contraction patterns in
antagonistic musculature in order to reduce the tonus of hypertonic musculature. Stimulation of gripping and
reaching movements in the upper extremities are most common.
It is also possible to reduce muscle tonus by prolonged electrical stimulation of the hypertonic (spastic)
musculature itself. Alfieri is among the researchers who have described this application of ES.
When treating hypertonic musculature, the training procedure is much the same as that for hypotonic
arm/hand musculature. If a patient is suffering from hypertonia, there is by definition an imbalance in his or
her muscle tonus. There is a risk that electrical stimulation will make this imbalance worse. It is therefore
important to proceed cautiously during the initial phase of treatment and during the trials carried out before
implementing a full training programme.
Treatment example 7 describes the procedure for stimulating the extensors of the forearm/hand only.
Because these muscles form a relatively small group, this can be done using just one or two channels.
However, when stimulating the entire motor chain, including the extensors of both the forearm and the upper
arm, the use of three or possibly even four channels may be appropriate.
Treatment example 7: Tonus normalization in a hypertonic arm/hand
Indication: Preparatory training for tonus normalization in a hypertonic arm/hand,

whereby the extensors of the forearm and hand only are to be facilitated.
Number of channels: Two.
hold time: 8-9 sec. (ramp-up time + hold time =
10 sec.)
Treatment time: Training should be increased gradually to develop
sufficient muscle condition. In this context, an effective practical
regime is to stimulate the muscles three times a day, increasing the
session length over a period of fourteen days from ten to twenty
minutes in five-minute steps (see treatment programme 2).
Amplitude: sufficient to induce clearly observable contractions without
causing pain.
21
Notes: • When positioning the electrodes, it is helpful to minimize the amount
of wrist deviation occurring during stimulation, so as to save the
patient undue discomfort.
• If the patient responds well, a treatment programme similar to that
recommended for hypotonic hand muscles can be initiated after three
days.
Scheme 2:
Day Treatment Duration Daily frequency

1 Two-channel stimulation 10 min. 3x
Three-channel stimulation 5 min.
Two-channel stimulation 10 min.
Note: The initial response to electrical stimulation determines whether treatment should be
continued or modified. If the patient experiences muscle pain, muscle stiffness or skin
irritation, the build-up should be more gradual. Conversely, the build-up may be accelerated if
the patient responds well.
22
2. Contracture prevention
A contracture is generally regarded as the result of a muscle imbalance in the vicinity of a joint. Burke
contends that the characteristic hemi position of the arm is not the result of spasticity but of heightened
stimulation of the flexor motor neurons. It therefore follows, his argument runs, that the primary problem is
not the spasm but the inability to actively contract or lack of strength in the agonistic muscles that extend the
hand. This theory is gaining more and more ground in medical circles.
Whatever the cause, certain muscles become shortened. In a patient who has suffered a CVA, it is normally
the flexors that are affected in this way. The shortened muscles initially bring about a myogenic contracture.
However, without proper treatment, this can develop into a capsular contracture. Once a myogenic or
capsular contracture is established, the chances of recovery are slim. The connective tissue undergoes a
morphological change, such that new connective tissue will form only in the event of trauma. Yet
traumatization will activate the nervous system, which is liable to aggravate the spasticity. It is therefore
important that all available means, including ES, are used to prevent a contracture becoming established.
If a contracture is not prevented, the associated tissue changes are not reversible using ES. Nevertheless,
some degree of flexibility can be restored, albeit briefly. In this context, therefore, ES supplements other
forms of therapy, such as passive and active stretching. The frequency of the treatment required is such that
the patient should have personal access to a stimulator.
Treatment example 3 deals with stimulation of the extensor group, with a view to preventing flexion
contracture. To ensure that the effect is as localized as possible, only the extensors of the n. radialis should
be stimulated, using a single channel. However, a second channel may be used for simultaneous stimulation
of the n. ulnaris in order to extend muscular activity. Three-channel stimulation is rarely used for contracture
prevention.
Treatment example 8: The prevention of flexion contracture in the forearm
Indication: The prevention of flexion contracture in the forearm. Mobility is improved

by stimulating extension.
hold time: 4 sec.
Treatment time: Three half-hour sessions per day, with a gradual build-
up of muscle condition.
Amplitude: sufficient to induce very marked contractions and even slight
muscle ache, provided that hypertonia is avoided.
Notes: As an alternative to stimulating the nerve pathways, the m. Extensor
communis may be stimulated via channel 1 and the m. Abductor pollicis
via channel 2.
23
3. Trophic improvement and pain relief
Neurophysiological, humoral, neuropsychological, hormonal and other changes can result in circulatory and
trophic disorders of the soft tissues in parts of the body affected by a CVA. These changes, which may
involve the skin, the subcutaneous connective tissue, the musculature or the joint capsules, can be
aggravated by inactivity or movement-related injury. Tissues affected by diminished circulation and trophic
disorders are typically weak. As a result, they are easily damaged, leading to the development of conditions
such as decubitus or hypermobile joint capsules at pressure-sensitive and stretch-sensitive points, e.g. the
ischium node or the shoulder joint. The consequence is often considerable pain and sometimes sub-luxations
or even luxations. Patients can also complain of subjective symptoms, such as cold or “clumsy” hands and
feet, resulting from temperature regulation dysfunctions.
The hypothesis is that by improving local nourishment and circulation in the muscles and surrounding tissues,
these subjective symptoms can be relieved. The level of atrophy may be reduced by stimulation of the
muscles, which can be effected by ES, provided that there has been no damage to the CNS. However, it
cannot be assumed that this is the case following a CVA, which is liable to affect the hypothalamus, for
example. ES cannot therefore be used in the conventional manner to influence pain or trophic problems.
Instead, trials must be carried out before initiating a programme of therapy.
The procedure for the trials is set out in the sections on pain and the correction of trophic problems. At this
point, it should nevertheless be emphasized that the treatment of trophic disorders and pain in CVA patients
is essential, and that all available resources should therefore be employed.
Treatment example 9: Trophic improvement in the upper extremity
Indication: Trophic improvement in the upper extremity in a patient suffering from a

sub-luxation of the glenohumeral joint (see Pouran).
Number of channels: One.
Electrode size: 9 x 5 cm.
Electrode position: With one electrode placed at thoracic level, an area exhibiting
heightened sensitivity (hyperalgesia) is identified, stimulation of which
produces a diffuse/heavy sensation in the arm. The patient cannot
identify this spot independently.
On the hyperalgesic area of the thorax, at the level of the Th4-9
segments. Two electrodes in line vertically.
Position of patient at start: Lying on the side in a relaxed position.
Frequency: 100 Hz.
hold time: 8-10 sec.
interval: 2 sec.
Treatment time: Training is built up from 1.5 to 6 hours per day and
the ratio between the contraction and rest periods progressively adjusted
from 10/12 seconds to 30/2 seconds over a period of five weeks, with
two-second intervals.
Amplitude: sufficient to be clearly discernible.
Notes: -
In addition to stimulating the afferent nerves in the skin to influence trophic processes and pain, trophism can
be promoted by inducing muscular contractions. Before this can be done, however, it is necessary to check
the sympathetic nervous system. If, following a CVA, the patient does not exhibit any disorders affecting the
hypothalamus, so that control is still possible, the induction of muscle contractions is likely to be beneficial. It
will, however, be necessary to stimulate large muscle groups. ES should therefore be used as a supplement
to active exercise therapy. Hence, multi-channel stimulation to induce generalized muscle contraction and
activate the pump function of the muscles is the best approach. In many cases, activation of both the
proximal and distal musculature by means of parallel and overlapping four-channel stimulation should be
considered. It is important to additionally stimulate the cardiorespiratory system to promote effective
circulation.
24
The possibilities outlined above are illustrated in treatment example 10.
Treatment example 10: Trophic improvement in the upper extremity
Indication: Trophic improvement in the upper extremity in a patient suffering from a

(sub-)luxation of the glenohumeral joint and pain in the shoulder.
Number of channels: Between one and three (in accordance with programme 10).
Electrode size: Relative to extent of musculature to be stimulated.
Electrode position: On musculature around the shoulder (particularly m. deltoideus), around
the upper arm (m. biceps brachii and m. triceps brachii) and around the
forearm (extensors/flexors).
Position of patient at start: Relaxed sitting position with the arm slightly bent.
Frequency: 35 Hz.
hold time: 10 sec.
interval: 12 sec.
Treatment time: variable. It is recommended that training should be built
up from half an hour a day to several hours a day and the ratio between
the contraction and rest periods progressively adjusted from 10/12
seconds to 30/2 seconds over a period of several weeks, given a
positive response.
Amplitude: sufficient to induce contractions.
Notes: Treatment as described is only possible if the patient exhibits clear
hypotonia but no pronounced muscular imbalance.
n. medianis
n. radialis
n. ulnaris
Figure 6:
Electrode positioning n. medianis, n. radialis en n. ulnaris
25
3. Neuro-Muscular Electrical Stimulation (NMES) following a transverse
lesion
Introduction
Over the years, electrical stimulation (ES) has for various reasons been used to treat patients following a
transverse lesion (Andrews,1995). ES should be considered where, despite a complete or partial transverse
upper motor neuron lesion (UMNL), no serious damage has been done to the lower motor neuron (LMN). In
such cases, the musculature below the lesion remains sensitive to electrical stimulation, opening the way for
the induction of muscle contractions for various purposes.
It is important to ensure that the patient understands that the effect of (functional) electrical stimulation,
insofar as it is linked to muscle activity, relates directly to the actual use made of the stimulated musculature.
The treatment cannot bring about recovery from the neuro-muscular lesion. In many cases, as soon as
electrical stimulation ceases, the associated stimulus to move will be lost and the patient will have to start
physical exercises. In this context, therefore, electrical stimulation serves as a supplementary treatment for
patients who have suffered an incomplete transverse lesion. The use of electrical stimulation to replace or aid
a movement necessary for a day-to-day activity is referred to as Functional Electrical Stimulation (FES). FES
is often used in combination with orthoses to retain posture or enable a particular movement. However, a
comprehensive review of FES treatment and its effectiveness is outside the scope of this chapter, which is
intended to briefly outline the background to and application of FES by reference to treatment examples.
When treating a patient who has suffered a transverse lesion, the main aims of (functional) electrical
stimulation are:
• to restore functionality (standing, walking, arm/hand functions);
• to provide cardiovascular training;
• to reduce spasticity;
• to improve trophic processes.
In the following paragraphs, the theoretical background to the use of ES for each of these purposes is
explained and a specimen case illustrating each application is presented.
NB: Within this diagnosis group, sensibility loss is common. It is therefore very important to inspect the
skin thoroughly before and after treatment. If any change in skin condition is observed, a cautious approach
to stimulation and dosages should be adopted. During treatment, which will usually entail movement, frequent
checks need to be made to ensure that the electrodes remain in good contact with the skin.
1. The stimulation of functionality (associated with standing)
1.1. Introduction
A transverse lesion normally leads to muscle atrophy. This is due partly to inactivity (the non-use of the
muscles in question) and partly to the lack of innervation. In practice, it is hard to distinguish between the two
processes. It proves that the (monoarticular) extensors (e.g. the vasti of the m. quadriceps) are prone to
particularly rapid atrophy and consequently lose both power and endurance.
Inactivity-related atrophy is accompanied by hystochemical conversion of type I (slow-twitch aerobic) fibres to

type II (fast-twitch, anaerobic, low-endurance) fibres, and by a fall in mitochondrion density, a reduction in
oxidative enzyme concentration and a drop in the capillary count (Kralj et al, 1989; Ragnarson, et al, 1987).
In addition to inactivity-related atrophy, denervation-related atrophy takes place in the segments close to or at
the level of the lesion. This is the result of damage of the motor neurons in the spinal cord or the motor
nerves in the ventral root. The power that a muscle can generate depends partly on the degree of innervation.
Research has shown that in cases of partial denervation, sprouting can lead to almost complete re-
innervation of the affected muscle fibres, provided that at least 15 per cent of the original nerves remain intact
(Gordon et al, 1994).
In view of the considerations outlined above, it is advisable to train the affected muscles by means of
electrical stimulation before beginning exercises aimed at the restoration of functions associated with day-to-
day activities such as standing.
It has been demonstrated that the principles applied when training patients who have not suffered lesions are
equally valid in relation to FES. Hence, strength can be built up by inducing dynamic contractions with
26
increasing and comparatively high loads, intervals and a relatively low number of repetitions. Unless the load
applied in training is gradually raised, the strength of the muscle will not increase (see chapter on NMES in
the treatment of sports injuries). It also proves that the initial muscle length is an important factor. Increasing
muscle length (stretch) promotes protein synthesis (Gordon et al, 1994). To develop stamina, however, it is
necessary to use relatively low loads and long training sessions (one to two hours). Prolonged training without
any load results in a reduction of muscle fibre volume and strength. Where it is necessary to develop both
strength and stamina, training should alternate between short intense sessions and long, less intense
sessions.
The definite increase in strength and stamina associated with FES is attributable to local (peripheral)
physiological changes such as muscle hypertrophy, the conversion of ‘fast-twitch’ fibres into ‘slow-twitch’
fibres, sprouting, increased metabolic enzyme concentrations and greater capillary density.
1.2. Facilitation of standing by stimulation of mm. quadriceps and mm. gluteus maximus
1.2.1. Selection criteria

ES is not appropriate in all cases where a patient has difficulty standing. Patients should therefore be
selected for treatment on the basis of certain criteria, in consultation with the doctor in charge, so as to avoid
any unnecessary risks.
• The primary criterion is that electrical stimulation of the mm. quadriceps and mm. gluteus maximus
should be possible. To ascertain whether this is the case, a stimulus with a phase duration of 0.3 msec, a
frequency of 30 Hz and an intensity of no more than 140 mA should be applied. The muscle may be
considered susceptible to stimulation if a contraction is clearly discernible. After training, the m.
quadriceps should be capable of lifting 10 to 15 per cent of the patient’s body weight (attached at ankle
height) when FES is applied.
NB: Standing can be facilitated by stimulation of the mm. quadriceps, without stimulation of the mm.
gluteus maximus. However, both rising to and remaining in a standing position will be more difficult
without stimulation of the mm. gluteus maximus.
NB: Another option is to stimulate the mm. hamstrings while the patient is standing, while also stimulating
the quadriceps. This approach can reduce lordosis, thereby improving the patient’s standing posture.
• The patient should exhibit normal mobility of the lower extremity (LE). It is particularly important that hip
and knee extension is not restricted if the patient is to stand properly. Slightly restricted dorsal flexion can,
however, be offset by increased heel height.
• The LE should not be affected by any serious orthopaedic problems, such as osteoporosis, sub-luxations
or the like. Additional X-ray examination is strongly advised.
• Upper extremity (UE) function should be such that the patient is able to support his or her body weight on
his/her arms. Standing up requires support from the UE.
• The patient’s general physical condition (in particular his or her cardiorespiratory condition) should be
sufficient to enable physical effort. The patient should not be liable to giddiness when standing.
Experience has shown that, in cases involving complete lesions, the patient’s body weight should not be
more than about 75 kg.
• Spasticity does not necessarily constitute a contraindication. Indeed, the use of FES has sometimes been
found to lead to reduced spasticity. It is necessary to establish on an exploratory basis whether a
particular patient’s spasm is an obstacle to standing or maintaining a suitable standing posture. A certain
amount of compensation is often possible using orthoses.
• The patient must be suitably motivated and have realistic expectations. FES, which remains an
experimental technique, can be used to restore a limited standing function. The limitations of the
technique need to be recognized by the patient. The possibilities should therefore be clearly explained and
the patient encouraged to form realistic expectations, with a view to avoiding disappointment.
27
1.2.2. Preparatory training for standing
The preparatory training phase begins with stimulation of the mm. quadriceps and the mm. gluteus maximus
by FES. This is necessary to restore atrophied muscles to the point where they have the power and stamina
necessary for standing.
Training mm. Quadriceps and mm Gluteus maximus.
There is disagreement in the published academic literature as to the most appropriate training protocol.
Various treatment programmes with a range of on/off cycles are described. However, the protocol set out
below has been in use at Het Roessingh rehabilitation centre for some years.
n=10 Pre-training moment Post-training moment Increase

(Nm) (Nm)
Average 11.4 37.8 395%
Standard deviation 6.4 19.4
Treatment example 11: Preparatory training for standing
Indication: Preparatory training for standing.

Number of channels: Four, parallel.
Electrode position: Channel 1: mm quadriceps, left.
Channel 2: mm gluteus maximus, left.
Channel 3: mm quadriceps, right.
Channel 4: mm gluteus maximus, right.
NB: If the skin is dry, it can be dampened with a little water.
Position of patient at start: Supported sitting position with legs partially extended and a large
cushion under the knees (knees at an angle of approx. 45°).
NB: To prevent decubitus, consideration should be given to the provision
of a soft surface on the treatment table.
Frequency: 30 Hz.
hold time: 3 sec.
interval: 0 sec.
Treatment time: Training should be stopped once the muscles clearly
begin to tire. Signs of tiredness include inability to continue lifting the heel
clear of the surface of the treatment table and the cessation of
discernible contractions (see note).
Amplitude: mm quadriceps: sufficient to effect full extension of the knee,
subject to a maximum of 140 mA. If contractions diminish during the
course of the training session, the intensity may be increased before
continuing, provided that this results in a corresponding increase in
movement.
mm gluteus maximus: sufficient to induce a strong contraction. If
contractions diminish during the course of the training session, the
intensity may be increased before continuing.
Notes: • The muscles in each leg should be activated simultaneously, which is
why parallel stimulation is recommended. However, if a patient’s
muscles exhibit clear variations in contraction time, sequential or
overlapping stimulation can be used.
• The right leg and left leg should be stimulated alternately. The
channels should be set so that each four-second stimulation period is
followed by an eight-second interval.
• The training described above should be preceded by a five-minute
warm-up. During the warm-up, the muscles should be activated using
lower-intensity stimuli, sufficient to induce clear contractions but not
sufficient to extend the leg fully.
• Adequate padding should be provided to prevent tissue damage to
28
the back of the heel as it drops back to the surface of the treatment
table.
Note:
Once the musculature has sufficient strength to straighten the knee for half an hour, a 1 kg weight can be
attached at ankle height. The weight can be increased in 1-kg steps each time the point is reached where the
patient is able to fully lift the weight repeatedly for half an hour, up to a maximum of 10 to 15 per cent of the
patient’s body weight.
Treatment example 12: Standing
Indication: Standing.
Electrode position: Channel 1: mm quadriceps, left.
Channel 2: mm gluteus maximus, left.
Channel 3: mm quadriceps, right.
Channel 4: mm gluteus maximus, right.
Position of patient at start: Sitting in a chair in front of parallel bars.
Frequency: 30 Hz.
Treatment time: Training should stop once contraction of the mm
Quadriceps diminishes as a result of fatigue.
Amplitude: same as for preparatory training.
Procedure: When stimulation is started (by pressing the start button), the patient
stands, holding on to the bars and using his or her arms to help support
his/her weight. Much depends on getting the timing right. The patient
also needs to learn how to make use of the power generated by his or
her leg muscles when standing. The standing position adopted should be
with the hips stretched and the back slightly hollow. Stimulation of the
quadriceps can be combined with stimulation of the hamstrings, with a
view to avoiding excessive lordosis and enabling the patient to adopt a
better standing posture. This also reduces the need for the patient to use
his or her arms. It is important to check whether the m. Quadriceps are
still taut, so that the patient does not suddenly buckle at the knees. In
order to sit, the patient first bends his or her knees, then, as s/he begins
to lower his/her body, the stimulator is turned off.
Notes: • The muscles in each leg should be activated simultaneously, which is
why parallel stimulation is recommended.
• Once started, stimulation is continuous.
• The intensity of the current and the length of the treatment session
depend on how quickly the patient tires, which will vary from one
individual to another. It is very important not to continue stimulation
too long, since, once the patient tires, there is a serious risk of muscle
injury. The afferent nerves will always be stimulated along with the
motor nerves, which can result in sensations of pain or increased
spasmodic intensity. Decisions regarding the continuation of
treatment should be made on the basis of exploratory stimulation and
discussions with the patient. The occurrence of spasms and/or
unpleasant sensations does not necessarily constitute
contraindications.
29
2. Cardiovascular training
A transverse lesion can result in serious conditions affecting both the neuro-muscular system (lack of
available active muscle mass) and the vegetative nervous system (a lesion above Th 6 will lead to
sympathetic decentralization).
Measurements made during ADL (Janssen et al 1994) indicate that brief load peaks leading to rapid fatigue
are commonplace. These load peaks are associated with a heightened risk of injury to the muscular and
cardiovascular systems (Pentland and Twomey, 1994; Yekutiel et al, 1989). It has also been established that
day-to-day activities are not sufficient to increase or maintain stamina levels (Hoffman, 1986, Janssen et al,
1994). Ultimately, therefore, a vicious circle is established, whereby the individual is obliged to adopt an
increasingly sedentary life style, leading to further loss of physical condition and hence to further diminution of
the ability to undertake ADL, recreational activities, work, etc. A sedentary life style also increases the risk of
respiratory and cardiovascular disease. Such diseases are the ultimate cause of death in 46 per cent of
people who suffer high transverse lesions (Le and Price 1982).
Research has shown that traditional forms of condition training based on arm exercises result in hardly any
increase in the amount of blood circulated by the heart per minute or per beat. Furthermore, the upper
extremities are in any case subject to abnormally high levels of usage following a transverse lesion. It is
therefore possible that the use of arm exercises for condition training could lead to undue strain. It proves
that the patient’s starting position during exercise is important in this context: the stroke volume is higher
when the patient is lying than when he or she is sitting, since the venous return is greater.
As well as benefiting the cardiovascular system, training also influences the metabolic mechanisms (Hooker,
1989, Apple, 1996). It has been shown that training of a reasonably high intensity (60 to 70 per cent) can
bring down overall cholesterol concentrations by as much as 8 per cent. Low-density lipoprotein-cholesterol
(LDL-C) concentrations fall (15 per cent) and high-density lipoprotein-cholesterol (HDL-C) concentrations rise
(20 per cent). Such changes can reduce the risk of cardiovascular disease by 20 per cent.
Functional electrical stimulation (FES) can be used in conjunction with other forms of training. The
combination of FES of the legs with “arm crank exercises” (ACEs) lead to a definite increase in stroke volume
(Hooker, 1992; Laskin, 1993; Faghri, 1992). Conversely, active use of the upper body increases the benefit
from FES (Franken et al, 1997). The research data suggests that the use of FES in combination with upper
extremity exercises is a useful supplement to other forms of cardiovascular training in this diagnosis group.
Treatment example 13: Supplementary cardiovascular training
Indication: Supplementary cardiovascular training.

Electrode position: Channel 1: mm Quadriceps, left.
Channel 2: mm Hamstrings, right.
Channel 3: mm Quadriceps, right.
Channel 4: mm Hamstrings, left.
Since the training should be intensive, the patient needs to be in a
comfortable position at the outset, so that the maximum effort can be
made without causing irritation or injury.
Frequency: 30 Hz.
hold time: 1 sec.
Treatment time: Sessions should last for between half an hour and an
hour, depending on the degree of local and general fatigue.
Amplitude: mm Quadriceps: sufficient to effect full extension of the knee,
subject to a maximum of 140 mA. If contractions diminish during the
course of the training session, the intensity may be increased before
continuing, provided that this results in a corresponding increase in
movement. It is not necessary to induce particularly great movements,
since the object is simply to generate a pump effect.
mm Hamstrings: sufficient to induce a strong contraction. If contractions
diminish during the course of the training session, the intensity may be
30
increased (up to a maximum of 140 mA) before continuing.
Notes: • Stimulation via channels 1 and 2 is alternated with stimulation via
channels 3 and 4. The channels should be set so that each two-
second stimulation period is followed by a four-second interval.
• The training described above should be preceded by a five-minute
warm-up. During the warm-up, the muscles should be activated using
lower-intensity stimuli, sufficient to induce a clear contraction but not
sufficient to extend the leg fully.
• The training is combined with arm exercises in order to maximize the
effect.
3. Spasticity reduction
A transverse lesion can also lead to spasticity. For clinical purposes, spasticity may be regarded as a motor
dysfunction involving animated tendon reflexes and sometimes clonus, together with speed-dependent
muscle hypertonia during extension of the muscle in question (Lance, 1980). Possible causes of these
phenomena include (Delwaide et al, 1996):
heightened sensitivity of the alpha motor neurons to stimulation;
heightened sensitivity of the gamma motor neurons to stimulation;
reduced presynaptic Ia afferent inhibition;
reduced reciprocal inhibition;
reduced Renshaw (recurrent) inhibition;
reduced non-reciprocal Ib inhibition.
Any of these factors acting on its own or in combination with others may cause spasticity. It is not yet clear
which factors are primarily responsible for spasticity in patients who have suffered a transverse lesion. In
such cases, the manifestation of spasticity generally follows a number of stereotypical patterns (Alfieri et al,
1996). The most common form involves clonic flexion and extension contractions in the lower extremities and
the trunk. Onset of the spasms is often preceded by changes in position. This form of spasticity proves to
respond well to cyclic electrical stimulation of both agonistic and antagonistic musculature (see specimen
case 4). Another form of spasticity entails tonic contraction of the extensors in the trunk and lower
extremities, sometimes accompanied by clonus in the calves. This form can also be influenced by ES,
although focusing primarily on the antagonists or flexion reflex (see specimen case 5). A third form of
spasticity, characterized by very strong flexion activity, responds less well to ES.
In the treatment of spasticity, use is also made of a technique based upon stimulation of areas of the skin
corresponding with the innervation level of the hypertonic musculature. The efficacy of this technique, which
has been clinically demonstrated (Bajd, 1985; Vossius, 1996), may be due to the stimulation of thick afferent
fibres which help to regulate the balance between inhibition and excitation. With this form of ES, the stimuli
used are light and do not induce proper contractions.
It is not yet possible to indicate which electrode positions, parameters, starting positions and so on are most
appropriate for the treatment of patients suffering from spasticity following a transverse lesion. Nevertheless,
ES may be regarded as an effective technique in this context. Clinical studies have shown that ES can bring
about tonus reductions, which usually persist for up to several hours.
31
Treatment example 14: Spasticity reduction
Indication: Reduction of spasticity by cyclic stimulation of agonistic and antagonistic

musculature.
Number of channels: Four (see note).
Electrode position: Channel 1: mm Quadriceps, left.
Channel 2: mm Hamstrings, right.
Channel 3: mm Quadriceps, right.
Channel 4: mm Hamstrings, left.
Any position which causes irritation is liable to aggravate the hypertonia.
It is therefore important to ensure that the patient is comfortable and not
likely to suffer irritation or injury.
Frequency: 30 Hz.
hold time: 2 sec.
Treatment time: Training sessions may last for half an hour or an hour,
provided that the contractions remain visible and that muscle hypertonia
reduction is discernible.
Procedure: Training starts with the parameters as indicated above. The stimulus
intensity is low to start with: sufficient to induce clear contractions, but not
to fully extend the leg. It is important that the muscles respond well to the
start and end of the stimulation cycle. Provided that this is the case (i.e.
that the muscles contract and relax immediately in time with the stimuli
and that no responses are seen elsewhere in the legs or trunk), the
intensity may then be increased. However, it remains important to
continue monitoring the reactions of the various muscle groups. In some
cases, a slight contraction is more effective than a major contraction.
Notes: • The volume of the musculature involved and the extent of the
spasticity determines whether four-channel application is appropriate.
• The degree of spasticity and the sequence in which spasms occur
determines whether stimulation should be parallel or not.
• Stimulation via channels 1 and 2 is alternated with stimulation via
channels 3 and 4. The channels should be set so that each four-
second stimulation period is followed by an eight-second interval.
Treatment example 15: Spasticity reduction
Indication: Reduction of spasticity by stimulation of antagonists or flexion reflex in

lower leg musculature.
Number of channels: Two, parallel.
Electrode size: Round, 4 cm.
Electrode position: Cathode: behind/above the head of the fibula on the n. peroneus
communis.
Anode: on the m. tibialis anterior, about four inches below the knee.
Channel 1 - left, channel 2 - right.
Position of patient at start: • Supported sitting position with legs partially extended and a large
cushion under the knees (knees at an angle of approx. 45°). See also
notes in specimen case 4.
• Sitting in a wheelchair.
Frequency: 30 Hz.
32
hold time: 2 sec.
Treatment time: Training may be sustained for between 15 and 30
minutes, depending on the onset of local muscle fatigue.
intensity is then increased until the leg exhibits a complete flexion
movement/tendency. The response from the musculature needs to be
good and determines the intensity of stimulation. As adaptation occurs,
the flexion reflex can diminish, sometimes making it necessary to
increase the intensity. Care needs to be taken to avoid irritation, which
will increase the reflex considerably.
Notes: • Alternate stimulation of the left leg and right leg. The channels should
be set so that each four-second stimulation period is followed by an
eight-second interval.
• This form of stimulation can be combined with passive movement of
the leg receiving treatment. Passive exercises should be carried out
with the patient lying on his or her back. During stimulation, the leg
should be helped to flex, then extended in the interval.
4. Trophic stimulation
A combination of the inactivity and the neurophysiological, humoral and hormonal dysfunctions associated
with a transverse lesion will lead to local trophic and circulatory impairment. This is particularly unfortunate,
since proper nourishment of the tissues is essential for training of the musculature. The trophic impairment
seen in patients following a transverse lesion affects not only the musculature but also the skin and other soft
tissues. As a result, these structures become weak and vulnerable to both externally induced and
contraction-related injury. In cases where the patient is already showing signs of atrophy, it is therefore
important to improve trophic conditions as soon as possible. The severity of the trophic disorders to be
expected will vary, depending on the height of the lesion, the length of time since its occurrence and the level
of activity maintained by the patient.
Active muscle training is normally the best way of improving local trophic and circulatory conditions in the
muscles and surrounding tissues in order to prevent atrophy. However, active muscle training is not always
possible, and other means of improving the situation must therefore be sought. Hence, electrical stimulation
can be an important aid to rehabilitation. The technique essentially involves inducing muscle contractions in
order to promote local metabolic activity. The effectiveness of the treatment can be judged by reference to
both subjective and objective criteria. If it is working, patients should be less troubled by cold, stiff or “clumsy”
extremities. An increase in the elasticity of the musculature and other soft tissues should also be apparent.
The latter effect may only be expected if the trophic disorders have yet to cause any morphological changes.
33
Treatment example 16: Trophic stimulation
Indication: Trophic improvement brought about by stimulation of forearm

musculature.
Number of channels: Two, parallel (see notes)
Electrode size: Round, 4 cm.
Electrode position: Channel 1: forearm extensors.
Channel 2: one electrode on the base of the thumb, the other on the
forearm flexors.
Position of patient at start: Sitting or lying, with the arms supported.
Frequency: 30 Hz.
hold time: 2 sec.
Treatment time: Stimulation should be continued for as long as good
contractions can be induced, up to a maximum of 30 minutes. The
precise length of the sessions will ultimately depend on the level of
local fatigue.
intensity is then increased until good flexion and contraction are induced
in the fingers.
Notes: • Given that neither the volume of muscle nor the extent of the
contractions involved is very great, two channels are usually
sufficient. However, if the upper arm musculature is to be stimulated
as well in order to promote trophic activity, three or four channels may
be used. The contractions should be as violent as possible, with a
view to activating the local metabolic processes.
• Alternate stimulation via channel 1 and channel 2. The channels
should be set so that each four-second stimulation period is followed
by an eight-second interval.
• Both sides may be stimulated simultaneously if desired. The channels
should then be adjusted so as to produce symmetrical extension and
flexion.
• If the object is to create a functional hand (i.e. to shorten the finger
and thumb flexors) both finger extension and dorsal flexion of the
wrist should be limited. This can be done by giving the patient a
function glove to wear during treatment.
It should be emphasized that trophic stimulation is usually combined with stimulation of the cardiorespiratory
system. Increased circulation will only be effective if the heart and lungs are functioning well enough to effect
an improvement in trophic conditions. As soon as the patient is able to contract his or her muscles actively,
electrical stimulation should cease or gradually be phased out.
34
4. Use of electrical stimulation (ES) for pain modulation
1. Introduction
The perception of pain has been the subject of debate for many years. Injury-related pain is often easy to
understand, but it is a mystery how some conditions can give rise to pain. Schools of thought vary. Does one
sense pain in the brain or in the soul? Or both? Is it a sensory phenomenon, involving specific receptors,
transmission routes through the central nervous system and registration centres, then assessment and
interpretation in the brain, or is pain in fact completely non-specific, arising in response to every stimulus that
exceeds a given threshold? Extensive debate and numerous studies have led to the subject of pain being
thoroughly researched and to the rapid development of thinking in this field. From all this work, a number of
theories with practical implications for the treatment of pain have emerged. These theories include the pattern
theory, the theory of the central summation of stimuli and the sensory interaction theory. It emerges that pain
is in fact modulated, as most clearly explained in the sixties by Melzack and Wall’s Gate Control Theory and
endorsed by various psychological (behavioural) theories.
The International Association for the Study of Pain (IASP) defines pain thus: Pain is an unpleasant sensory
and emotional experience associated with actual or possible tissue damage, or which is described in terms of
such damage.
Various types of pain are recognized, such as acute and chronic pain. Chronic pain in particular contains
physical, psychological and social components and cannot therefore be influenced by physical means alone.
Because chronic pain is a complex phenomenon, the seriousness of the related injury is by no means the
only factor influencing the severity of the pain experienced by an individual. A nociceptive stimulus induces a
response in the brain, which can differ considerably from one person to another and defies classification as a
simple physiological response.
For information regarding anatomy and physiology in relation to the multidimensional phenomenon of pain,
readers are referred to the established textbooks. This book focuses on the use of electricity to modulate the
nervous system in order to alleviate pain.
The general aim of physiotherapy is to enable the patient to function as well as possible within the clinical
context, given the specific possibilities and limitations. To help them achieve this aim, physiotherapists use
various aids, one of which is electricity. Electricity is employed in Transcutaneous Electrical Nerve
Stimulation, or TENS – a non-invasive means of modulating pain. Originally, the technique was developed to
relieve acute pain, on the basis of neuro-physiological research by Melzack and Wall and their ‘Gate Control
Theory of Pain’, published in 1965. The Gate Control Theory was itself derived from earlier theories put
forward by Noordenbos. However, Melzack and Wall believed that their theory did not provide an adequate
foundation for the effective treatment of chronic pain. To this day, these two researchers and many others are
still seeking ways of helping those afflicted by such pain.
Electrotherapy, and in particular the use of transcutaneous techniques such as TENS, has long been a topic
of interest to scientists researching acute and chronic pain. In the late sixties, electrotherapy was
‘rediscovered’ by medical science in response to publication of the Gate Control Theory. The effectiveness of
transcutaneous electrical stimulation for the relief of acute pain has since been investigated in a huge number
of (double-blind, randomized) studies. It remains unclear, however, when and how the technique may be
used in the treatment of chronic pain. Consequently, the application of electrical stimulation in physiotherapy
is based not only upon scientific principles, but also, to a large extent, on personal experience. Clinically
speaking, pain is liable to manifest itself in various ways, so that experience and scientific knowledge are not
in themselves an adequate basis for the use of electrotherapy. In this context, the classification of pain could
be of practical benefit, since not all forms of pain can be influenced by electrotherapy.
The classification of pain syndromes is a difficult task, but of fundamental importance for the formulation of
treatment objectives and application of techniques such as electrical stimulation. Pain problems or
syndromes can be divided into the following broad groups:
1. So-called neuropathic pain (syndromes): Pains in this group are associated with damage to the nervous
system itself. Examples include phantom pain, postherpetic neuralgia, causalgia, radiculopathy etc. Other
causes of neuropathic pain include diabetes mellitus and multiple sclerosis.
2. So-called nociceptive pain syndromes: These syndromes are characterized by continuous stimulation of
the nociceptors. The nociceptive impulses are conducted to the brain via ascending pathways.
35
Ad 1) Neuropathic pain may be subdivided into the following classes:
a. Syndromes associated with nerve trauma (resulting in deafferentation), such as stump pain and phantom
pain, plexus avulsion, radiculopathy, causalgia, etc.);
b. Syndromes associated with medical conditions (such as herpes zoster, diabetes mellitus, multiple
sclerosis, alcoholism, etc.);
c. Type I Complex Regional Pain Syndromes (CRPSs; see page 42-43) involving pain from sympathetic
activity;
d. Central pain, such as in thalamus syndrome or trigeminal neuralgia.
Ad 2) Nociceptive pain includes the following:

1. Musculoskeletal pain, such as lower back pain, associated with structures used to effect movement
(ligaments, capsules, discs, muscles, etc);
2. Myofascial pain syndromes;
3. Fibromyalgia syndrome;
4. Headache;
5. Joint pains associated with forms of arthritis (e.g. rheumatoid arthritis or arthrosis).
To make matters more complex still, neuropathic and nociceptive pain can occur simultaneously. Both types
of pain involve sensitization of polymodal C fibres (IV afferents), increased sensitivity of the neurons in the
posterior horn and other parts of the central nervous system. In the complex interaction of the nervous
system’s modulating, exciting and inhibiting processes, the occurrence of referred pain (RP) plays an
important role. RP is the expression of a fault in these processes, and is felt at a point other than its source.
Such pain can be nociceptive or neuropathic. Pain can be modulated on three levels:
1) the peripheral level, via the sensor and the afferent fibre;
2) the spinal level (posterior horn);
3) the supraspinal or central level (formatio reticularis, thalamus, hypothalamus, hypophysis and cortex,
including the limbic system).
Electrotherapy may be intended to initiate modulation at the spinal level, without involving the central nervous
system, or to activate the central modulating systems. Melzack and Wall’s Gate Control Theory remains the
basis for spinal modulation, but only in cases where modulation of the central systems is not possible.
However, chronic pain can only be alleviated by activating the central modulating systems. In clinical
situations, this is done using various techniques, which may be collectively termed ‘Stimulus Produced
Analgesia’. These techniques are based on principles such as the relief of pain by stimulating the central
release of endorphins (endogenic opiates).
Of course, the classification of pain has consequences for clinical physiotherapy. Should the physiotherapist
seek to influence the patient’s posterior horn neurons only, or the nervous system as a whole? It presently
appears that acute pain is generally caused by activity within the non-myelinized afferent nerve fibres.
Activation of the heavily myelinized afferent nerve fibres inhibits onward transmission to the central part of the
nervous system. If, for example, one bangs one’s elbow, the pain can be relieved by rubbing the arm. By
doing so, one is producing tactile and pressure stimuli, which close the gate on the pain signals from the
elbow. The same effect can be induced by using electricity to directly stimulate the heavily myelinized nerve
fibres. Such stimulation is potentially of particular value in cases where the patient is seeking relief for his or
her central nervous system, precisely because of the high levels of existing activity. Such activity may have
various causes, such as a serious emotional shock. However, such treatment can be equally valuable in, for
example, the case of a person suffering central pain associated with multiple sclerosis.
As indicated earlier, the modulating systems of the central nervous system are complex. Nevertheless, it is
advisable to activate these central systems. In a clinical context, this is referred to as activation of the
descending analgesic systems. Activation of this kind depends on stimulation of the injury-registering
afferents or the IIIb and IV afferents.
In electrotherapy, it is important to work on both these groups of nerve fibres, since the current is capable of
prompting both to discharge.
The academic literature makes distinction between the following:
1. Conventional electrotherapy, which involves the use of non-noxious stimuli to activate the II and III afferent
nerve fibres.
2. Electrotherapy involving the use of noxious stimuli (prompting the II, III and IV afferent nerve fibres to
discharge) in order to activate the central descending modulating systems. This form of electrotherapy
includes procedures such as Stimulus Produces Analgesia (SPA) and acupuncture-like TENS or
hyperstimulation analgesia.
The electrode positions necessary for noxious stimulation vary, but electrodes should always be placed in
sensitive zones. Particular attention is focused on areas known as “trigger points”, “acupuncture points” or
simply “pain points”. These areas (of the skin) are nowadays referred to as allodynic and/or hyperalgesic,
36
indicating that they are extremely sensitive and that discharge of the IV afferent nerve fibres can easily be
induced at these points. Stimulation of such points can cause referred pain as a result of the reduced
modulation of the posterior horn neurons.
When stimulating II and III afferent nerve fibres, by contrast, the electrodes have to be located away from the
sensitized points, so as to avoid simultaneous stimulation of the IV fibres, since this would prevent or limit
closure of the gate.
By choosing the aim of the therapy, impetus is given to the practical consequences. In practice, one of the
first steps is to identify the sensitive points. The nature of the reactions, the size and the strength should all
be monitored in order to assess whether electrotherapy is likely to be capable of alleviating the patient’s pain.
Several other variables need to be taken into account. These include the stimulator settings (e.g. the stimulus
frequency) and the size and number of electrodes. Probably even more critical for the success of the
treatment, however, are patient-related variables. Psychosocial factors and lesion age influence the nervous
system considerably, for instance, and are liable to reduce the likelihood of modulation. Noxious stimulation
may also aggravate nervous system dysfunction if psychosocial influences are particularly active. Clearly,
proper assessment of the multidimensional pain problem is of fundamental importance to the success of the
electrotherapy.
2. Equipment for the modulation of pain

The implementation of an effective pain modulation strategy depends on having equipment that offers a wide
range of channel-independent setting options. The settings used should be selected primarily on the basis of
the clinical symptoms and the (patho-) physiological responses to stimulation. The availability of several
stimulation channels means that gentler peripheral stimuli can be generated at the same time as powerful
afferent stimuli, which can be essential for activation of II and III afferent nerve fibres.
One technique that has recently come to the fore is subtractive frequency modulation (the spectrum). This
technique, which involves subtraction of the modulation frequency from the original stable frequency,
prevents adaptation much more efficiently than previous methods. Its success is due to the fact that the level
of reduction in the afferent action potential frequency (adaptation) induced in the nervous system by cycling
through the lower frequencies is much lower than with traditional methods of additive frequency modulation.
Multi-channel stimulation is an efficient and effective way of using ES across a wide area to modulate pain.
The specimen cases outlined below illustrate how the technique may be used.
37
3. Treatment example
Treatment example 17: Herpes Zoster dex. Th5-Th7
Indication: Pain relief in the acute stage of herpes. Information, advice and
reassurance.
Electrode position: Crosswise Th5-Th7, away from cutaneous eruptions, with the aim of
stimulating II and III afferent nerve fibres.
Position of patient at start: Comfortable sitting position. Where self-stimulation is possible, the
patient will normally be ambulant.
Treatment parameters: Pulse form: asymmetrical biphasic TENS.
Frequency: 100 Hz.
Treatment time: 30-60 min.
Amplitude: subthreshold.
Notes: In the event of adaptation:
Spectrum: 20 per cent (= frequency modulation 80-100 Hz).
Sweep cycle: 1/30/1/30, possibly 12/12.
1
2 3
3
3 4
4
1 1
Illustration 17a: dorsal view Illustration 17b: ventral view
Illustration 17a and 17 b:

Herpes Zoster over segmental levels Th5-Th7, right.
Electrodes positioned above and below the affected areas (crosswise).
38
Treatment example 18: Postherpetic Neuralgia dex. Th5-Th7
Postherpetic neuralgia involves pain in the affected dermatomes, which can persist for thirty days after
eruption of the vesicles. Approximately 10 to 15 per cent of all herpes zoster patients and almost 50 per cent
of those aged over sixty develop postherpetic neuralgia.
Indication: Reduction of pain.

Information, advice and reassurance.
Electrode position: Paravertebral over segments Th4 and Th8.
Position of patient at start: Lying on the unaffected side. Where self-stimulation is possible, the
patient will normally be ambulant.
Treatment parameters: Pulse form: asymmetrical biphasic TENS.
Frequency: 100 Hz.
Amplitude: pain threshold.
Sweep cycle: 12/12, possibly 6/6.
Illustration 18: Electrode position paravertebral

Th4 and Th 8 (zie note).
Note
Herpes Zoster is a neurogenic condition involving inflammation mainly of the heavily myelinized sensible
nerve fibres in the spinal ganglion. When treating patients suffering from chronic neuropathological pain, one
should bear in mind that the condition involves degradation of the endoneurium (the insulating layer of
connective tissue) between heavily and lightly myelinized nerve fibres. In postherpetic neuralgia, the damage
extends up to the spinal ganglion; i.e. proximal to the sensible fibres. If under such circumstances one
selectively stimulates type II and IIIa fibres peripheral to the area of nerve damage, the effect will in all
probability be to aggravate the pain, rather than relieve it. Because there is no adequate insulation between
the II and IIIa fibres and the lightly myelinized IIIb and IV fibres, the stimuli will cross to the latter, leading to
increased nociceptive transmission and pain. In cases of peripheral nerve damage, the electrodes should be
positioned proximal to the lesion. When treating a patient with postherpetic neuralgia, one should consider
paravertebral electrode placement on adjacent segments. This arrangement allows the interneurons at the
affected level to be activated via the dorsolateral tract (Lissauer’s tract). It has the disadvantage, however,
that the patient does not experience the characteristic tingling sensation in the painful region, which normally
confirms electrical stimulation of the appropriate nerves.
N.B. Activation of the central pain modulation system can also be considered in cases where the patient
has already had the condition for some while, with the result that the nervous system is functioning
selectively once more.
39
Treatment example 19: Complex Regional Pain Syndrome (CRPS) type I; status after radius fracture
Indication: Relief of pain caused by dystrophy. Improvement of trophic conditions in

the tissue. Normalization of muscle activity and mobility.
Information, advice and reassurance.
Electrode size: Two paravertebral pairs, 3 x 5 cm, and two peripheral pairs, ∅32 mm.
Electrode position: Channel 1. Paravertebral C4-C7 and fossa supraspinatus.
Channel 2. Subacromial: ventral on trigonum claviculopectoralis, dorsal
fossa infraclavicularis.
Channel 3. Sulcus bicipitalis medialis and regio antebrachii anterior
(n.medianus).
Channel 4. Regio brachialis posterior and dorsolateral side of the hand
(n. radialis).
Position of patient at start: Sitting comfortably with the forearm supported. The same position is
adopted for self-stimulation.
Treatment parameters: Channels 1 and 2:
Pulse form: symmetrical biphasic TENS.
Burst: 4 Hz.
Amplitude: pain tolerance.
Channels 3 and 4:
Pulse form: asymmetrical biphasic TENS.
Frequency: 150 Hz.
Amplitude: Subthreshold.

Sweep cycle: 1/30/1/30.
In practice, it is often difficult to achieve the various general objectives

simultaneously. In such cases, the pain should normally be relieved first,
then trophic stimulation provided. However, if the pain presents a less
immediate problem than the dystrophy, treatment should focus on
modulation of the sympathetic nervous system.
1
1
2 2
4
4
3
Illustration 19: Complex Regional Pain Syndrome (CRPS), type I, caused by fracture of the
radius dex. Electrode positioning for trophic normalization
and pain relief.
40
Treatment example 20: Pseudoradicular syndrome L5-S1, with bilateral irradiation
Indication: Relief of referred pain

Information, advice and reassurance regarding the aetiology (the source
of the nociperception and the cause of reduced modulation of the
posterior horn neurons).
Electrode size: Two paravertebral pairs, 5 x 9 cm, and two peripheral pairs, 3 x 5 cm.
Electrode position: Two paravertebral channels, L5-S1.
Two channels on both dorsal sides of the leg, with one electrode level
with the fossa politea and one in a dorsolateral position level with the
Achilles tendon. Electrodes to be placed at sensitized (hyperalgesic)
points.
Position of patient at start: Lying on the belly.
Treatment parameters: Channels 1 and 2:
Frequency: 50 Hz.
Amplitude: tolerance limit.
Channels 3 and 4: settings depend greatly on level of hyperalgesia; the
following settings are appropriate for a very high level of hyperalgesia:
Frequency: 100 Hz.
Amplitude: just discernible.
Treatment time: approx. 20 minutes, depending on the occurrence and

subsequent relief of referred pain during therapy (indicating occurrence
of modulation).
Notes: In the event of adaptation: channels 1 and 2:
Spectrum: 50 per cent (= frequency modulation 40-80 Hz)
Sweep cycle: 6/6, possibly 1/1.
In the event of adaptation: channels 3 and 4:
Spectrum: 20 per cent (= frequency modulation 120-150 Hz)
Sweep cycle: 1/30/1/30, possibly 12/12.
1 2
1 2
3 4
3
4
Illustration 20:
Pseudoradicular syndrome L5-S1, with bilateral irradiation.
41
5. Electrical stimulation for the promotion of tissue recovery
1. Introduction
Many of the conditions encountered by practising physiotherapists involve impaired tissue recovery and high
levels of tissue vulnerability. Minor traumata cause severe injuries and lead to disproportionately serious
inflammation. Impaired recovery and heightened vulnerability are due partly to ineffective circulation of blood
through the affected tissues. This condition may be regarded as a form of dystrophy. The blood vessels
which carry nutrients to the tissues are subject not only to neuronal influence from the sympathetic nervous
system, but also to metabolic and immunological influences. One should not therefore assume that the
dystrophy one observes is simply a product of the condition of the sympathetic nervous system. Ordinarily,
the immune, humoral and neurological systems will work together to effect recovery by physiological means.
Consequently, when recovery does not occur naturally, it is hard to be sure which systems are not functioning
properly and therefore require stimulation. Stimulation of the nervous system, as in ES, therefore addresses
only one of the factors potentially responsible for impaired recovery and heightened vulnerability.
Using ES, it is possible to stimulate the peripheral (cutaneous) nerves and via these nerves to influence the
central nervous system. This is significant in relation to the treatment of dystrophic conditions, since the
neurons of the sympathetic nervous system, located in the hypothalamus and the lateral horns of the spinal
cord, have considerable influence on trophism in the muscle tissues.
ES can be used to improve peripheral circulation in two ways:

1. reflexively, via the peripheral cutaneous nerves (type III and IV afferents) and the sympathetic nervous
system (the so-called “somatosympathetic reflex”);
2. directly, by inducing muscle contractions, which have a pump-like effect.
In practice, the somatosympathetic reflex is used for physiotherapeutic purposes only in cases where this
nervous system is affected by a disorder. In order to make use of the pump action of the muscles, the
nervous system needs to be functioning properly.
A review of the literature on tissue recovery quickly reveals how difficult it is select a suitable patient
population for an effect study. This is because dystrophy is neither easy to identify nor a really appropriate
inclusion criterion. Conditions such as ulcus cruris, decubitus and Sudeck’s syndrome bear all the hallmarks
of trophic disorders, but can in fact have unrelated causes. The development and rectification of such
disorders are influenced by a wide variety of variables. Some cases involve hyperactivity of the sympathetic
nervous system, but others are more readily attributable to immobility. Immobility can lead to trophic
impairment in individuals unaffected by disorders of the sympathetic nervous system. Trophic disorders
attributable to immobility can be treated by utilizing the muscles’ pump action, since the sympathetic nervous
system may be expected to respond.
Despite the procedural problems, various effect studies have been conducted. As long ago as 1982, for
example, Kaada et al attempted to demonstrate that ES could be used to effect vasodilatation in patients
suffering from sympathetic nervous system disorders, such as Raynaud’s disease and polyneuropathy
brought about by Diabetes Mellitus. In addition to its methodological shortcomings, this study failed to
demonstrate any effect attributable to stimulation below the motor threshold. Higher levels of stimulation are
inherently noxious and activate the IIIb and IV afferent nerve fibres. Other studies confirm that only noxious
stimulation has any effect on peripheral circulation.
2. Complex Regional Pain Syndrome, Type I.
2.1. General
The consequences of trophic impairment include poor healing of surgical wounds, chronic oedema in the
extremities, and classic Type I Complex Regional Pain Syndrome. This syndrome has been given various
names over the years, such as Sudeck’s Dystrophy, Sympathetic Reflex Dystrophy, algodystrophy and post-
traumatic dystrophy, to name but a few. Many of these names reflect the complexity of the condition. It is
doubtful whether the sympathetic nervous system plays any significant role in the development of this
condition. By the time it reaches its inflammatory and trophic phases, however, disorders of the sympathetic
nervous system are likely.
The IASP has opted for the name Complex Regional Pain Syndrome in recognition of the condition’s
complexity and association with regionalized pain. There are two kinds of CRPS. In the first kind, the
dystrophy is pronounced, while in the second the pain (also referred to as causalgia) is particularly severe.
With Type I CRPS, a burning or stabbing pain develops following an injury, accompanied by hyperalgesia in
the affected region. Other symptoms may include vascular dilation, oedema and hyperhidrosis. In time,
general hyperpathia sets in; any stimulus then results in abnormal, persistent pain. Patients are liable to
42
suffer trophic changes in the skin, nails and hair, muscle atrophy, joint stiffness and finally bone atrophy
(osteoporosis). Ultimately, the pain and stiffness have a disabling effect.
The hyperpathia is accompanied by diminished selectivity within the nervous system; in other words, little
differentiation is made between different stimuli. This feature of the condition makes treatment particularly
difficult. The nervous system’s compensation mechanism is severely impaired and any excessive stimulus
can lead to decompensation and aggravation of the overall picture. Even a small skin lesion in the dystrophic
region can severely aggravate the dystrophic process.
Because of the role played by the sympathetic nervous system in relation to this syndrome, sympathicus
blocks were often created in the past, with mixed results. The advisability and effectiveness of blocking the
sympathetic nervous system are still topics of debate. Opinion also varies on the use of ES in the treatment
of this condition. Uncertainty remains regarding the circumstances under which it should be used, how it
should be used and particularly the settings that should be used.
In view of these uncertainties, the following guidelines are proffered:

1. Patients exhibiting symptoms of general nervous system activation, as for example associated with
emotional disorders, are unlikely to benefit from and may even be adversely affected by electrotherapy.
2. Patients exhibiting symptoms of trophic disorders should undergo ES tests before starting a full course of
treatment, in order to establish whether their sympathetic nervous systems can be influenced by
electrotherapy.
3. The electrical stimuli applied should preferably be of noxious intensity (i.e. sufficient to activate the IIIb and
IV afferent nerve fibres) in order to influence the central nervous system.
4. The electrical stimuli should preferably be applied to hyperalgesic regions, provided that these regions are
not affected by any serious trophic disorders.
5. The treatment frequency should be adjusted in line with the response from the sympathetic nervous
system.
6. Electrotherapy should be used in conjunction with other forms of treatment designed to stimulate
trophism. Consideration should, for example, be given to general relaxation therapy and active training of
the cardiorespiratory system in order to promote circulation generally.
Subject to the caveats set out above, CRPS patients may be given ES. The specimen cases outlined below
illustrate how electrotherapy may be used with this diagnosis group.
2.2. Therapy implications

As indicated above, noxious stimulation is preferable, but not always possible. Unfortunately, it is in the most
serious cases of trophic impairment, involving high levels of hyperalgesia and hyperpathia, that noxious
stimulation is least appropriate. The stimuli should be applied outside the affected region. Friction (massage
therapy) and passive or heavy resistance exercises are contraindicated. So too are physiotechnical
treatments that involve high levels of stress, such as Träbert, hot and cold stimuli and UV radiation.
Treatment should be applied over a relatively large area. In this context, readers are referred to literature
listing and examining various treatment methods in relation tot TENS (e.g. Manheimer and Lampe, Abram
and Still and Lundeberg and Otterson). With this diagnosis group, the aim of electrotherapy is to stimulate II
and IIIa afferent nerve fibres in order to reduce transmission by IIIb and IV afferent nerve fibres in the spinal
cord and thus to diminish the level of stimulation in the central nervous system. Deafferentation – the
temporary reduction of influence on the central nervous system – is particularly important in circumstances
where the patient is suffering from a serious trophic disorder combined with psychosocial problems. Once the
psychosocial factors have been addressed and the selective capacity of the nervous system begins to
recover, noxious stimulation is in order.
43
Treatment example 21: Type 1 CRPS, with dystrophic pain and functional disorders, accompanied by
strong indications of psychosocial problems
Indication: Treatment of dystrophy throughout the left leg, status following avulsion
of a fragment of the left malleolus lateralis.
Pain relief and function restoration.
Electrode size: Dependent on the size of the area to be treated and of the regions
affected by hyperpathia and hyperalgesia.
Electrode position: Channel 1 paravertebral thoracolumbal.
Channel 2 paravertebral lumbosacral.
Channel 3 dorsal side of the upper leg.
Channel 4 dorsal side of the lower leg.
All electrodes to be positioned outside hyperalgesic areas.
Position of patient at start: Lying on the belly with the ankles well supported and the knees slightly
bent.
Treatment parameters: High-frequency low-intensity TENS.
The object is to stimulate the II and IIIa afferent nerve fibres.
Treatment frequency: five times a week if possible.
Notes: • Treatment can be combined with manual lymph drainage, light
manipulation of the entire spinal column and breathing exercises.
• At a later stage, the electrodes may be positioned within the
hyperalgesic regions and multi-channel treatment geared to the
number of regions to be stimulated in order to induce sympathetic
nervous system responses. Lower frequencies and higher intensities
should gradually be introduced. The frequency of treatment will be
adjusted in line with the sympathetic responses, but once a week is
likely to be in order.
3. Claudicatio Intermittens
ES can also be used to promote blood circulation by direct mechanical means; electrical stimuli are used to
induce muscle contractions, which have a pump-like action. This approach is particularly useful in the relief of
vascular and ischaemic pain. It should be stressed that this form of therapy is closely associated with the
reflexive form of treatment described above. In practice, the reflexive approach will normally be used first,
with the aim of increasing the selectivity of the nervous system. Once this has been done, local metabolic
processes can be activated.
In order to activate local metabolic processes, it is best to actively stimulate the musculature, with a view to
promoting local blood circulation. However, blood circulation is a complicated mechanism involving
mechanical factors, such as pressure, and chemical processes. The circulatory power source is of course the
heart. Blood is pumped via the arteries and arterioles to the capillaries, where perfusion takes place. In the
capillary network, nutrients and oxygen are exchanged for waste products and carbon dioxide. The blood
then returns to the heart via the venules and veins. The lymph system also transports waste materials, as
well as being important in relation to the body’s immune system.
Stagnation in the venous and/or lymph system leads to increased tissue pressure and oedema, which inhibit
perfusion, leading to biochemical changes in the tissues. Arterial dysfunction can also lead to perfusion-
related problems. Such dysfunction may be brought on by inactivity, or may result from damage to the walls
of the blood vessels. Thickening and fibrosis can inhibit perfusion to such an extent that nutrients and oxygen
are no longer exchanged for waste and carbon dioxide. Hence, the affected tissues suffer dystrophy.
Needless to say, these phenomena are accompanied by certain medical symptoms. Impaired peripheral
blood circulation is known as Claudicatio Intermittens.
The characteristics of this condition are:

• frequent manifestation in the lower extremity;
• pain when walking, sufficient to prevent continuation;
• association with men aged more than fifty, but increasingly with women as well;
• pain in the calves and often in the upper leg;
• muscle cramps, particularly at night;
• inability to walk more than fifty metres;
• persistent tiredness in the legs.
44
In patients with Claudicatio Intermittens, local metabolic processes are best activated by walking exercises
supported by increased inhalation and heart rates. The difficulty with this approach is that the pain brought on
by walking is often sufficient to limit progress considerably and to deter the patient.
The use of electrical stimuli and the promotion of local blood circulation in, for example, patients with
Claudicatio Intermittens are well-established forms of physiotherapy. In the absence of good methodological
studies, however, we cannot describe these practices as “evidence-based therapy”. Various techniques are
used to treat the problems associated with this condition, including hydrotherapy, balneotherapy and pulsed
high-frequency electrotherapy. Furthermore, numerous authors have described the beneficial effects that
TENS can have on peripheral circulation. Some time ago, a number of studies were published, which were
able to demonstrate – on the basis of the Doppler effect – an increase in blood circulation attributable to ES.
However, these studies made use of healthy subjects and involved the induction of strong muscle
contractions; it cannot be assumed that similar results could be obtained when treating patients with vascular
conditions.
The following strategy is recommended. Initially, priority should be given to a reflexive approach. Thereafter,
the muscles’ pump action may be stimulated electrically. Finally, electrical stimulation of the pump action
should be replaced by active stimulation through walking and other exercises.
Treatment example 22 below illustrates the use of TENS to stimulate the local pump action.
Treatment example 22: Claudicatio Intermittens in the lower extremity, involving some pain and a
degree of sympathetic nervous system selectivity
Indication: Stimulation of the muscles’ pump action in order to promote local

metabolism and enable the patient to walk further (in preparation for
exercise therapy).
Number of channels: Three.
Electrode size: Dependent on the size of the extremities.
Electrode position: Upper and lower leg. Two electrodes are placed on the dorsal side of the
lower leg, two more on the ventral side of the upper leg and the last two
on the dorsal side of the upper leg.
Position of patient at start: Sitting with the knees partially extended.
Treatment parameters: Low-frequency high-intensity TENS, above the motor threshold.
Length of treatment session: 30 minutes.
Intensity: sufficient to induce tangible and visible contractions.
Treatment frequency: daily in preparation for exercise therapy, giving
way to daily active exercises.
Notes: If strong muscle contractions are initially not possible, an overlapping
arrangement may be used, to be replaced by a parallel arrangement
once strong contractions can be induced. Under such circumstances, the
duration of treatment should be reduced to about ten minutes. The
contractions should not be so violent as to induce any real pain, but
should be strong enough to bring about a definite sensation of fatigue.
Pain is associated with injury and would cause the sympathetic nervous
system to induce further vasoconstriction.
4. Oedema
Strong parallels exist between the treatment of vascular disorders such as Claudicatio Intermittens and the
procedure adopted in cases of oedema in the lower leg. The contractions induced need to be rhythmic in
order to stimulate blood flow and treatment sessions should be about half an hour long. The aim is to
promote venous and lymphatic drainage by stimulating the muscles’ pump action in circumstances where
active exercise is difficult or impossible. Strong evidence for the effectiveness of electrical stimulation in such
cases is, however, lacking. It would appear that ES is more effective in the treatment of oedema that has only
recently developed than in the treatment of well-established conditions. Other physiotherapeutic means are
also used to control oedema and it is unclear whether ES has an additional benefit. However, ES is the
preferred method of treatment in cases where active exercise is not possible or where the skin is particularly
hyperalgesic. As with many other techniques, the use of ES should be reviewed at the end of the diagnostic
phase to determine whether the initial treatment has been effective and should be continued.
45
Patients affected by poor blood circulation are liable to suffer lesions to the skin, subcutaneous tissue, fasciae
and muscles, which often prove difficult to heal. With Diabetes Mellitus, so-called “leg ulceration” is often
seen following minor skin lesions. Other chronic and potentially immobilizing conditions can involve skin
complications associated with minor injuries. These problems are discussed in the chapter on neurological
conditions such as transverse lesions. TENS is one of several techniques that can be used to promote the
healing of open wounds. Various forms of ES appear to have the same effect when the cells responsible for
tissue repair are stimulated. It is not clear which current forms are the most effective. As long ago as 1988,
Luther Kloth reported that the use of a high-voltage monophasic pulsed current could be effective in
accelerating the healing of wounds. In the years since, numerous publications have appeared, documenting
improved methods. A great deal more research is required, however, before a protocol for this kind of
treatment may be advanced.
46
INDEX
multiple sclerosis .......................................... 35; 36
A
muscle atrophy ................................... 8; 11; 26; 43
acupuncture-like TENS .......................................36 muscle fatigue .......................................... 8; 32; 33
acute pain......................................................35; 36 muscle fibres .................................. 8; 9; 10; 11; 26
allodynic ..............................................................37 Muscle hypertonia ............................ 18; 21; 31; 32
arthritis ..........................................................13; 36 Myofascial pain syndromes ................................ 36
Atrophy of the hamstrings ...................................14
N
Atrophy of the quadriceps ...................................13
neuropathic pain................................................. 35
C
nociceptive pain syndromes ............................... 35
cardiovascular training ..................................26; 30 nociceptive stimulus ........................................... 35
causalgia .................................................35; 36; 42 non-tetanic contractions ..................................... 10
Central pain.........................................................36
O
central summation...............................................35
chronic pain...............................................5; 35; 36 overloading............................................... 8; 10; 11
Claudicatio Intermittens ................................44; 45
P
Complex Regional Pain Syndrome .........36; 40; 42
Contracture prevention .................................18; 23 pain. 5; 7; 16; 18; 19; 20; 21; 22; 24; 35; 42; 44; 45
co-ordination .............................................8; 11; 12 phantom pain................................................ 35; 36
cortex ..................................................................36 plasticity................................................................ 8
crank exercises ...................................................30 postherpetic neuralgia .................................. 35; 39
CVA.....................................................7; 18; 23; 24 Postherpetic Neuralgia dex ................................ 39
Pseudoradicular syndrome................................. 41
D
Q
deficiency of abdominal musculature..................16
diabetes mellitus ...........................................35; 36 Quadriceps ......................................... 9; 13; 27; 28
F R
Fibromyalgia........................................................36 radiculopathy ................................................ 35; 36
formatio reticularis...............................................36 radius fracture .................................................... 40
referred pain ........................................... 36; 37; 41
G
S
Gate Control Theory......................................35; 36
gluteus maximus .....................................27; 28; 29 sensory interaction ............................................. 35
shoulder instability.............................................. 17
H
spasticity......................... 18; 21; 23; 26; 27; 31; 32
Headache............................................................36 sports revalidation ................................ 7; 8; 11; 27
herpes zoster ................................................36; 39 stimulation frequency ..................................... 9; 10
high-density lipoprotein-cholesterol.....................30 Stimulus Produced Analgesia ............................ 36
hyperalgesic ..........................24; 37; 41; 43; 44; 46 strength .............. 7; 8; 9; 10; 11; 12; 23; 27; 29; 37
hyperstimulation analgesia..................................37 stump pain.......................................................... 36
hypophysis ..........................................................36
T
hypothalamus..........................................24; 36; 42
tetanic contractions ...................................... 10; 11
I
thalamus............................................................. 36
Inactivity-related atrophy .....................................26 tissue repair........................................................ 46
International Association for the Study of Pain5; 35 Tonus normalization ............................... 18; 19; 21
transverse lesion .................... 7; 26; 30; 31; 33; 46
L
trigeminal neuralgia ............................................ 36
Lesion of the anterior cruciate knee ligament .....14 Trophic ................................. 18; 24; 25; 33; 34; 42
limbic system ......................................................36 Type I fibres.......................................................... 8
Low-density lipoprotein-cholesterol.....................30 Type II fibres......................................................... 8
M U
m. Quadriceps.....................................................26 upper motor neuron lesion ................................. 26
Metabolic effect...................................................10
mm. Quadriceps .......................................9; 27; 28
47
BIBLIOGRAPHY CHAPTER 1
Adams, G.R., Harris, R.T., Woodard, D., Dudley, G.A.

Mapping of electrical muscle stimulation using MRI
Appl. Physiol. 1993; 74; 532-537
Burke, R.E. & Edgerton, V.R.,

Motor unit properties and selective involvement in movement
Exercise Sport Csi. Rev., 3, 31-69, Avademic Press, New York, 1975
Chae, J., Triolo, R.J., Kilgore, K., Creasey, G.H.

Rehabilitation Medicine, Principles and practice.
Delisa JA, Gans BM. Lippincott - Raven 1998.
Chapter 24 Functional Neuromuscular Stimulation.. 611-635.
Eriksson, E., Häggmarkt, T.

Comparison of isometric muscle training and electrical stimulation supplementing isometric muscle
training in the recovery after major knee ligament surgery.
Am. J. Sports Med. 1979; 7; 169-171
Hannerz, J.
Discharge properties of motor units in relation to recruitment order in voluntary contraction.
Acta Physiol. Scand., 91, 374-384, 1974
Hultman, E., Spriet, L.L.

Skeletal muscle metabolism, contraction force and glycogen utilization during prolonged electrical
stimulation in humans.
J. Physiol. 1986; 374; 493-501
Kottke/ Lehmann.
e
Physical Medicine and Rehabilitation Krusen’s Handbook of. 4 edition 1990 WB Saunders Copany.
Chapter 15 Electrical Therapy. Basford JR. Pp. 375-401
Lambert, H., De Bisschop, F., De Mey, G., De Cuyper, H., Demurie, S., Vanderstraeten, G., Blonde W.
Calculation of electric current distribution in tissue.
Eur. J. Phys. Med. Rehabil., 1, 5, 126-32, 1991
Matheson, G.O., McKenzie, D.C., Georghiu, D., Ellinger, D.C., Quinney, H.A., Allen, P.S.
31P NMR of electricaly stimulated rectus femoris muscle: An in vivo graded exercise model. Magn.
Reson. Med. 1992; 26: 60-70
Morrissey, M.C., Brewster, G.E., Shields, C.L., Brown, M.

The effects of electrical stimulation on the quadriceps during postoperative knee immobilization.
Am. J. Sport Med. 1985; 13: 40-45
Mysiw, W.J., Jackson, R.D.

Physical Medicine & Rehabilitation.
Braddom RL 1996 WB Saunders Company.
Chapter 23 Electrical stimulation.. 464-491.
Snyder-Mackler, L., delitto, A., Stralka, S.W., Bailey, S.,

Use of electrical stimulation to enhance recovery of Quadriceps femoris muscle force production in
patiënts following anterior cruciate ligament reconstruction.
Physical Therapy, vol. 7f4, nr 10, October 1994.
Vanderthommen, M., Cohnen, A., Crielaard, J.M.
Intérét de l’ électromyostimulation de base fréquence dans le cadre d’un alitement prolongé.
Electrostimulation des Nerfs et des Muscles, Pelissier J., & Roques C.F., Ed. Masson, 62-66, 1992
48
Vanderthommen, M., Constant, T., Crielaard, J.M.
Intérét de l’ électromyostimulation de base fréquence dans la reeducation du quadriceps, apres
arthroscopie du genou
Kinésithérapie Scientifique, 308, 21-22, 1992
Vanderthommen, M., Depresseux, J., Bauvir, P., Degueldre, C., Delfiore, G., Peters, J., Sluse,F., Crielaard,
J.
A positron emission tomography study of voluntarily and electrically contracted human quadriceps.
Muscle & Nerve, April 1997, 20:505-507
49
Afieri, V.
Electrical treatment of spasticity: reflex tonic activity in hemiplegic patients and selected specific
electrostimulation.
Scand. J. Rehabil. Med. 1982; 14:177-82
Burke D.
Spasticity as an adaptation to pyramidal trac injury.
Adv. Neurol. 1988; 47: 401-22
George, H. Kraft, MD, Sally, S., Fitts, PhD, Margaret, C., Hammond, MD.
Techniques to improve function of the arm and hand in chronic hemiplegia.
Arch. Phys. Med. Rehabil. Vol.73, march 1992.
Lagasse, P., Kroll, W., Kilmer, W.

Functional electrical stimulation and the treatment of flaccid hemiparesis: a report on three
case studies.
Proceedings of the second biannual Conference of the Canadian Society for biomechanisc.
Ontario: Human Locomation 2 1982; 42-3
Pandyan, A.D., Granat, M.H, Stott, D.J.

Effects of electrical stimulation on flexion contractures in the hemiplegic wrist.
Pouran, P., Taghri, M.D., Mary, M., Rodgers, PhD., Roger, M., Glaser, PhD., John, G., Bors, MD., Charles,
Ho, MD PhD, Pani Akuthota, MD.
The effects of FES on shoulder subluxation, armfunction recovery and shoulderpain in hemiplegic
stroke patients.
Arch. Phys. Med. Rehabil. Vol 75 jan 94, 73-79
Rymer, W.Z., Katz, R.T.

Mechanics of spastic hypertonia.
Phys. Med. Rehabil. 1994; 8: 441-54
Rymer, W.Z., Katz, R.T.

Mechanical quantification of hyper tonia.
Phys. Med. Rehabil. 1994; 8: 454-64
50
Andrews, e.a.
Functional and therapeutic benifits of electrical stimulation after spinal cord injury Current
Opinion in Neurology
1995, 8:461-466
Alfieri ,e.a.
Clinical considerations on spasticity and FES
Neuroprosthetics; from basic research to clinical applications
Springer, ISBN: 3-540-61084-7
1996, pp 447-460
Apple,
Physical fitness: a guide for individuals with spinal injury
Rehabilitation research and development service
1996 (uitgave Department of Veterans Affairs i.v.m. Paralympics)
Bajd, e.a.
Electrical stimulation in treating spasticity resulting from spinal cord injury
Archives of physical medicine and rehabilitation.
1985; 66, 515-517
Delwaide, e.a.
Wich spinal cord neurophysiologic mechanisms are responsible for spasticity.
1996, pp 393-399
Faghri, P., e.a.

Functional electrical stimulation leg cycle ergometer exercise:
Training effects on cardiorespiratory responses of spinal cord injured subjects at rest during
submaximal exercise.
Arch Phys Med Rehab
1992 (vol 73, 1085-1093)
Franken, e.a.
The influence of voluntary upper body exercise on the performance of stimulated paralysed
human quadriceps
J. Electromyogr. Kinesiol.
1997 (vol 7, no 1, 67-77)
Gordon, e.a.
Muscle atrophy and procedures for training after spinal cord injury
Physical therapy
1994; vol 74, jan
Hoffman
Cardiorespiratory fitness and training in quadriplegics and paraplegics.
Sports Medicine
1986 (3, 312-330)
Hooker, e.a.
Metabolic and hemodynamic responses to concurrent voluntary arm cranck and electrical
stimulation leg cycle exercise in quadriplegics
J. Rehab. Research
1992 (vol 29 no 3, 1-11)
51
Hooker, e.a.
Effects of low- and moderate-intensity training in spinal cord-injured persons.
Medicine and science in sports and exercise,
1989 (vol 21, no 1, 18-22)
Janssen, e.a.
Relationship between physical strain during standardized ADL tasks and physical capacity in
men with spinal cord injuries.
Paraplegia
1994 (32, 844-859)
Kralj, e.a
Functional elctrical stimulation: standing and walking after spinal cord injury
CRC Press, inc , ISBN 0-8493-4529-4
1989
Lance
Pathophysiology of spasticity and clinical experience with baclofen
Spasticity: Disordered Motor Control. Year book medical publisher, Chicago and London
1980 pp 185-203
Laskin, J., e.a.

Electrical stimulation-assisted rowing exercise in spinal cord injured people. A pilot study.
Paraplegia,1993 (31, 534-541)
Le Chap, T., e.a.

Survival from spinal cord injury
J. Chron. Dis.
1982 (vol 35, 487-492
Pentland, e.a.
Quadriplegia and cardiovascular fitness.
The Lancet
1993 (8842, 413-414)
Ragnarson
Physiologic effects of functional electrical stimulation-induced exercises in spinal cord injured
individuals
Clinical orthopaedics and related research
1997 223; aug.
Vossius, e.a.
Parameters controlling antispastic electrical stimulation. Clinical application and theoretical
considerations
1996, pp 437-446
Yekutiel, e.a.
The prevalence of hypertension, ischaemic heart diseases and diabetes in traumatic spinal
cord injured patients and amputees
Paraplegia
1989 (27, 58-62)
52
Bonica, Fordyce and Loeser.

Managementstaf pain: vol. I and II. Lea and Febinger, 1990
Dingemans, W.A., Groenman, N.H., van Kleef et al.

Pijn en Pijnbehandeling: een basaal onderwijs curriculum
Universitaire Pers Maastricht 1993
Giffard, L.
Typical issuses in pain.
Physiotherapy Pain Association Yearbook 1998-1999.
NOI Press Falmouth, Adelaide 1998
Johnson, M.
The Physiology of the sensory dimensions of clinical pain.
Physiotherapy, October 1997, vol. 83, no.10.
Koel G.
Pijnbestrijding en TENS. Hoofdstuk 7, pp. 160-185.
Jaarboek Fysiotherapie Kinesitherapie 1997 Bohn Stafleu Van Loghum Red. Vaes P et al.
Passhier, J., Trijsburg, R.W., de Wit, R., Eerdemans- Dubbelt, S.L.C.

Psychologie van ongebrepen pijn. Hoofdstuk 2: Pijnmeting en Pijnbevordering
van Gorcum en Comp. BV, Assen 1998
Robinson, A.J., Snyder-Machler, L.

Clinical Electrophysiology, second edition
Williams & Wilkins, Baltimore 1994.
Shacklock, M.O.
Moving in on Pain
Butler wordth- Heinemann, Australië 1995
Turk, D.C. and Melzack, R.

Handbook of Pain Assessment.
The Guilford Press, New York 1992
Wall, PW, Melzack R.

e
Textbook of pain. 3 edition Churchill Livingstone 1994
Wall, P.,
The mechanisms by which tissue damage and pain are related: IASP Refresher Course Syllabus, an update
review.
IASP Press 1996
53
Aronson, MD et al
Vidarabine therapy for severe herpes virus infections: An unusual sundrome of chronic varicella and
trasient immunologie deficience.
J. amer. Med ass. 235:1339, 179.
Cash’, J.E.
Textbook of chest, Heart and vascular disorders for physiotherapists.
Faber & Faber, 1977 London and Boston P:261-283.
Jänig, W., Stanton-Hicks, M.

Reflex Sympathetic Dystrophy: a Reappraisal. Progress in pain research and management vol. 6
IASP press 1996. Chapter 5 Boas RA. Complex Regional Pain Syndromes: Symptoms, Signs and
Differential Diagnosis. Pp 79-92.
Kerchofs, E., Lievens, P., Veen, van der Ph., Desloover, N.

Jaarboek Fysiotherapie Kinesitherapie. Hoofdstuk Fysische therapie in engere zin. Een
experimentele benadering van de effecten op de spiercontracties bij de mens en op het
lymfesysteem bij mens en dier; 1999, pag. 127-144.
Bohn Stafleu Van Loghum Houten; onder redactie van Dekker, den JB, Aufdemkampe, G., Ham, van
I., Smits-Engelsman, B.C.M., Vaes, P..
Kloth, L.C., Feedarb, J.A.

Acceleration of wound healing with high voltage monophasic pulsed current.
Phys. Therapy 1988; 68:503-508.
Koel G.
Transcutane Elektrische Neurostimulatie (TENS).
Lochem, De Tijdstroom, 1991.
Ragozinne A.H., Melton L.J., Kurland L.T., et al

Population based study of Herpes Zoster and its sequelae.
Medicine 1982; 61:310.
Robinson, A.J., Snyder-Machler, L.

Clinical Electrophysiology, second edition
Williams & Wilkins, Baltimore 1994.
Salter, R.B.
Textbook of disorders and injuries of the musculoskeletal system.
P. 389-390; the Williams & Wiltins company, Baltimore, 1970.
Sanders, H.W.A.
Herpes Zoster in de huisartsen praktijk.
Academisch proefschrift, Nijmegen 1968.
Sanders, H.W.A.
Beloop en prognose van Herpes Zoster bij niet-geselecteerde patiënten.
Nederlands tijdschrift v. Geneeskunde 1980; 124;61:1023.
Stanton-Hicks, M., Janig, W. et al

Reflex sympatic dystrofia: changing concepts and taxonomy.
Pain 1995; 63:127-33.
Williamson, A.P.
The Varicella Zoster virus in the etiology of serve congenital defects. A report of eleven reported
instances.
Clin. Pediat. 14:553, 1975.
Zutphen, van H.C.F., et al

Nederlands leerboek der fysische therapie in engere zin.
Uitgeverij Bunge, Utrecht, 1991.
54
PROTOCOL REFERENCELIST ENDOMED 481, 482 AND 484
Sorted on protocol number
Protocol Indication Chapter Treatment page

example
2.10 Postherpetic Neuralgia dex. Th5-Th7 4 Number 18 39
2.14 Herpes Zoster dex. Th5-Th7 4 Number 17 38
2.15 CRPS typ 1 4 Number 19 40
2.16 Pseudoradicular syndrome L5-S1 4 Number 20 41
10.1 Trophic improvement upper extremity 2 Number 9 & 10 24, 25
10.2 Prevention flexion contracture 2 Number 8 23
10.3 Tonus normaliz. Hypertonic arm /hand 2 Number 7 21
10.4 Trophic stimulation 3 Number 16 34
10.5 Spasticity reduction (2) 3 Number 15 32
10.6 Tonus normalization hypotonic arm/hand 2 Number 6 19
10.7 Preparatory training for standing 3 Number 11 28
10.8 Standing 3 Number 12 29
10.9 Supplementary cardiovacular training 3 Number 13 30
10.10 Spasticity reduction (1) 3 Number 14 32
11.3 Atrofie van de Quadriceps 1 Number 1 13
11.4 Atrofie van de Hamstrings 1 Number 2 14
12.1 Atrophy of the Quadriceps 1 Number 1 13
12.2 Atrophy of the Hamstrings 1 Number 2 14
12.3 Lesion anterior crutiate ligament (1) 1 Number 3, 6.1 14
12.4 Lesion anterior crutiate ligament (2) 1 Number 3, 6.2 14
12.5 Deficiency abdominal musculature 1 Number 4 16
12.6 Tendinitis rotator cuff 1 Number 5 17
Sorted on number treatment example
Treatment Protocol Indication Chapter page

example
Number 1 11.3 Atrophyof the Quadriceps 1 13
Number 1 12.1 Atrophy of the Hamstrings 1 13
Number 3, 6.1 12.3 Lesion anterior crutiate ligament (1) 1 14
Number 3, 6.2 12.4 Lesion anterior crutiate ligament (2) 1 14
Number 4 12.5 Deficiency abdominal musculature 1 16
Number 5 12.6 Tendinitis rotator cuff 1 17
Number 6 10.6 Tonus normalization hypotonic arm/hand 2 19
Number 7 10.3 Tonus normaliz. Hypertonic arm /hand 2 21
Number 8 10.2 Prevention flexion contracture 2 23
Number 9 & 10 10.1 Trophic improvement upper extremity 2 24, 25
Number 11 10.7 Preparatory training for standing 3 28
Number 12 10.8 Standing 3 29
Number 13 10.9 Supplementary cardiovacular training 3 30
Number 14 10.10 Spasticity reduction (1) 3 32
Number 15 10.5 Spasticity reduction (2) 3 32
Number 16 10.4 Trophic stimulation 3 34
Number 17 2.14 Herpes Zoster dex. Th5-Th7 4 38
Number 18 2.10 Postherpetic Neuralgia dex. Th5-Th7 4 39
Number 19 2.15 CRPS typ 1 4 40
Number 20 2.16 Pseudoradicular syndrome L5-S1 4 41
55
ILLUSTRATIONS
Illustration 6 Illustration 7 and 8
Illustration 9 and 10
Example electrode position
Illustration 11b, 12a

Electrode position Gluteus maximus
Illustration 11a, 12a, 13a, 14a

Electrode position Quadriceps
56
Illustration 13b, 14b
Electrode position Hamstrings
Illustration 15
Illustration 16a Illustration 16b

Electrode position extensors Electrode position on the base of the thumb
of the forearm and flexors of the forearm
57

TENS (Manual Book Endomed 484) Van Der Esch

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TENS (Manual Book Endomed 484) Van Der Esch

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TENS treatment using the Endomed 484:

Published by Enraf-Nonius B.V.,

Chapter 1. Neuro-Muscular Electrical Stimulation (NMES) in the treatment of sports 8

Chapter 2. Neuro-Muscular Electrical Stimulation (NMES) following a CVA 18

Chapter 3. Neuro-Muscular Electrical Stimulation (NMES) following a transverse lesion 26

Chapter 4. Use of electrical stimulation (ES) for pain modulation 35

Protocol Reference List for Endomed 481, 482 and 484 55

M. van der Esch

Various TENS forms and stimulus characteristics

frequency 40-200 Hz freq. 80-120 Hz freq. 60-120 Hz freq. 1-5 Hz

treatment time: variable ± 15-60 min ± 15-20 min ±15-20 min

In this context, the aims of electrical stimulation are:

1.2. What types of muscle fibre are there?

1.4. Influence of NMES intensity

Spatial summation induced by electrical stimulation

1.5. Metabolic effect of NMES-induced contractions

NMES can therefore be used in two basic ways:

Ad 1) Electrical stimulation for the treatment of muscle tissue atrophy

Ad 2) Electrical stimulation for the development of muscular strength

Example 1: Atrophy of the quadriceps

Illustration 1: Electrode positioning atrophy Quadriceps

Illustration 2: Electrode positioning atrophy Hamstrings

Example 3: Lesion of the anterior cruciate knee ligament

Indication: Agonistic or antagonistic muscular imbalance, preventable by restoration

Treatment parameters: Pulse form: symmetrical biphasic TENS.

Knee with anterior sign (illustration 3b)

Treatment parameters: Pulse form: symmetrical biphasic TENS.

Indication: Abdominal muscular deficiency in general, particularly cases of sports

Illustration 4: Electrode positioning abdominal musculature

Illustration 5: Electrode positioning at shoulder instability

1.2. Electrical stimulation

Muscle tonus score Degree of muscle tonus

Treatment example 6: Tonus normalization in a hypotonic arm/hand

Indication: Tonus normalization in a hypotonic arm/hand, whereby all flexors and

Illustration 6: see page 56-57

Day Program Duration Daily frequency

Treatment example 7: Tonus normalization in a hypertonic arm/hand

Indication: Preparatory training for tonus normalization in a hypertonic arm/hand,

Illustration 7: see page 56-57

Day Treatment Duration Daily frequency

Treatment example 8: The prevention of flexion contracture in the forearm

Indication: The prevention of flexion contracture in the forearm. Mobility is improved

Illustration 8: see page 56-57

Treatment example 9: Trophic improvement in the upper extremity

Indication: Trophic improvement in the upper extremity in a patient suffering from a

Illustration 9: see page 56-57

Treatment example 10: Trophic improvement in the upper extremity

Indication: Trophic improvement in the upper extremity in a patient suffering from a

Illustration 10: see page 56-57

1. The stimulation of functionality (associated with standing)

Inactivity-related atrophy is accompanied by hystochemical conversion of type I (slow-twitch aerobic) fibres to

1.2.1. Selection criteria

Training mm. Quadriceps and mm Gluteus maximus.

n=10 Pre-training moment Post-training moment Increase

Treatment example 11: Preparatory training for standing

Indication: Preparatory training for standing.

Illustration 11: see page 56-57

Treatment example 12: Standing

Illustration 12: see page 56-57

Treatment example 13: Supplementary cardiovascular training

Indication: Supplementary cardiovascular training.

Illustration 13: see page 56-57

Indication: Reduction of spasticity by cyclic stimulation of agonistic and antagonistic

Illustration 14: see page 56-57