Physical applications
Electrophysical agents (EPA’s)
Final goal of treatment: send the patient home cured or in a much better shape.
The different techniques will allow us to achieve this goal easier, faster, cheaper, with more comfort for the patient
than without.
Overall conclusion
1. Pain decreasing currents & muscle stimulating need to be used:
a. At the right place → anatomical location = pay specific attention to the electrode position
b. At the right time → in the treatment plan = don’t let the momentum slip through your fingers
c. For the right reason → the pathology = check out the indications
d. In the right way → parameter settings = the more you deviate from it, the less you should expect
2. Used unwisely they will do no good at all or possibly make matters worse
HS1: PAIN DECREASING CURRENTS (PDCS)
1. ELECTRIC CURRENT TYPES AND INTRODUCTORY CONCEPTS
1 ELECTRIC CURRENTS RK!
This chapter is about how to deal with electric pain decreasing currents (PDCs).
2 ANALGESIA AND PAIN PATHWAYS
As this chapter is about causing pain relief, it is necessary to study the physiological mechanisms that can reduce
pain and, albeit briefly, explain the neurophysiology of pain. These are particular text items and therefore will only
be explained in the PDF-textbook, they do not appear in the PowerPoint slides.
2.1 PAIN DECREASING MECHANISMS (PDMS) RK!
Electric currents give an incentive to the body with a physiological response as a result, so:
Which physiological reaction results in pain relief?
How strong are these reactions in order to significantly decrease pain?
What are the qualities and where are the limitations?
Literature discusses various complex mechanisms that underlie a reduction in pain perception. More specifically,
electric currents can cause complicated physiological mechanisms to take place in the body. They have effects on:
the periaqueductal gray, the rostral ventromedial medulla, the spinal cord (including the dorsal horn), endorphins
and enkephalins, ascending and descending pathways, GABA, serotonin, substance-P and ATP. The major question is,
how can addressing these complex mechanisms be translated into easy to use applications of TENS and MET
currents?
1
,In order to explain this step by step, three anatomical zones, where the physiological effects can take place, were
defined:
Local effects at the site of stimulation (peripheral effects);
Effects in the dorsal column (spinal effects);
Effects in the brain (central effects).
As explained before, the full content of the physiological effects at these three zones is a very complex matter, it
therefore lies outside of the scope of the EPAs course. As such, in order to translate these complex mechanisms into
easy to use applications, the physiological effects have been described (in a simplified way) as pain decreasing
mechanisms (PDMs).
2.1.1 LOCAL EFFECTS AT THE SITE OF STIMULATION RS + watch Local Effects video!
The local effects can be divided into four groups: slowing down nerve conduction velocity, local hyperaemia,
reduction of substance-P and tissue repair.
Slowing down nerve conduction velocity (NCV)
Mc Dowell & Walsh (1999) proved TENS currents to cause a decrease in the conduction speed of the afferent nerve.
The authors explain that fewer nociceptive stimuli reach the spinal cord causing a pain relief. The effect is significant
but rather short-lived (± 5 minutes); as such it is symptomatic.
Local hyperaemia (LH)
Local hyperaemia is an increased amount of blood appearing as red skin under the contact surface of the electrodes.
It is a well-known effect from many EPAs. In the group of PDCs it can only be caused by monophasic mA (strong
effect) & µA (weak effect) currents, being: DIA, UR, APS and MET. The increased blood flow reaches skin (≤ 500%)
and muscles (≤ 300%), it causes more nutrients to reach the target site and more wastes to be washed away. As such
it increases the metabolism at electrode site. It is believed that this can have a tissue-healing effect, which would
also cause a pain-reducing effect.
The physiological effect is based on the fact that the constant ion transport of a direct current represents a threat to
the cell. This leads to the release of inflammatory mediators (including histamine and bradykinin) that have a
vasodilation effect. Literature remains unclear as to how long treatment is necessary to obtain the tissue-healing
effects, some few specific literature data state a treatment duration of a few weeks to months is necessary.
Reduction of substance-P (SP)
Substance-P is a neuropeptide, acting as a neurotransmitter. Preclinical data support the notion that substance-P is
an important element in pain perception. TENS currents (and probably all mA currents) are known to reduce
substance-P. It remains unclear whether µA currents have the same effect.
Tissue repair (TR)
The fact that EPAs can have a tissue repairing (tissue-healing) effect is a more recent discovery. Within the PDCs this
effect is only caused by MET and albeit probably to a lesser extent, HV. The underlying mechanisms are not yet fully
understood, but they can certainly be categorised as cellular effects. Five physiological effects emerge from the
reliable literature. There may be more but either they are not well described or very hypothetical etc. Fortunately,
this gap is filled with a number of clinical studies. Anyway, if the tissue heals the cause of pain disappears; hence it is
pain decreasing.
2
,Cell activity requires a continuous transport of substances through the cell membrane. The quality of cells to respond
to adequate stimuli with specific changes in membrane permeability is described as "gating". This is the opening and
closing of physiological channels in response to changes in the membrane potential initiated by electrical stimuli. It is
generally assumed that microcurrent has an important effect at this level. It opens the so-called "voltage-sensitive
channels". These ion channels open as a result of a change in the electrical potential. MET would thus be able to
increase the intracellular concentration of calcium and sodium. MET is therefore biologically important as a regulator
of Ca2+ and Na+ influx. Furthermore, the mechanism is probably not fully understood, but the changes in membrane
potential translate into altered intracellular Ca2+ concentrations. Given that voltage-gated Na+ channels are at the
basis of action potentials for nerve impulses, this may explain the pain decreasing effect from MET.
There are more influences at cellular level. One of the known basic mechanisms for transmembrane transport is the
"primary active transport". Here, a transport protein will guide a substance through the membrane against an
existing electrical, chemical or pressure gradient. The energy for this is provided by the metabolism in the form of
ATP. Cheng et al (1982) did an interesting study in this context. They measured ATP values in the skin of rats under
the influence of microcurrent, which were up to 500% higher than in the control group. Peak values were reached at
±500 µA and decreased at 750 µA. The uptake of GABA, necessary for protein synthesis and transmembrane
transport, increased at 10 µA with a drastic reduction at 750 µA; peak values are at 30 to 40%. Van Papendorp,
Joubert et al (2002) have made the same observations in a similar study.
Studies also show that fibroblasts, young connective tissue cells from which connective tissue fibres originate, are
sensitive to electrical stimulation. Several studies show an increased fibroblast activity with an impact on the
production of collagen as a result. Nessler and Mass (1987) investigated the influence on proline and hydroxyproline.
The uptake of proline is a measure of cell activity and its conversion to hydroxyproline provides a measurement
value for collagen synthesis. In their research, the authors describe, at an intensity of 7 µA, an uptake of proline in
tendon tissue that is 91% higher than the control values. For hydroxyproline, the value reaches a level that is 255%
higher than the controls. Given the important role of fibroblasts in tissue repair, it is believed that electrical
stimulation plays a role in the tissue repairing effect of electric currents.
In addition to the methods described in the previous sections to reverse the nocisensory stimulation, an influence on
the cell itself is perhaps the most drastic way to realise pain relief. In particular, an effect that restores the damaged
cell wall (responsible for leaks of pain-causing substances) could be a very causal type of pain decreasing
electrotherapy. Among the pain-causing substances mentioned are bradykinin, histamine and lactic acid. It is
postulated that, due to its restorative influence on the cell wall, microcurrent would possess this quality.
To avoid exaltation, a number of things must be put into perspective. In the first place, there is not enough scientific
background for these theories. Still, Koel (1991), whose work is about TENS and not MET, mentions DC potentials in
a wound demonstrated in studies. This shows an analogy with a part of the explanations about the physiological
background of MET. A therapy that promotes tissue repair has long been considered the mythical "Eldorado". In the
past this was also assumed from other techniques; wrongly as it turned out afterwards. Based on the experience
already gained, it can only be stated that the statements sound reasonably logical and could possibly fit in with the
results achieved. Only in the past 10 years clinical research showed significant tissue healing effects from some EPAs,
MET is with them.
2.1.2 SPINAL EFFECTS ≈ spinal pain modulation (SPM) RS + watch Gate Control video!
The "Gate Control Theory of Pain" proposed by Melzack and Wall in 1965 is
one of many models used in science to explain pain relief. A sensory stimulus
can create action potentials that are conducted through both thick (L in figure
1) and thin (S in figure 1) fibres, each type of fibre has their own function (see
table 1). If the stimulus is nociceptive, the thin fibres conduct at a higher
intensity. Both the thick and thin fibresactivate the transmission cells or T-cells
(T in figure 1) which in turn pass on the information to the brain. The T-cells lie
in the dorsal horn in lamina V (figure 3), they are activated when a certain
stimulus threshold is reached.
3
, Fibres of both diameters reach the substantia gelatinosa (SG in Figure 1), located in laminae II and III of the dorsal
horn (figure 3). This creates a functional unit with ascending and descending pathways on both the homolateral and
heterolateral sides. Activity in the thick fibres stimulates the substantia gelatinosa where activity in the thin fibres
inhibits it. The substantia gelatinosa will inhibit the activity in the T cells. As a result, a balance is created in which
thick and thin fibres, respectively, activate or inhibit the substantia gelatinosa which in turn will inhibit or leave the
T-cells untouched. If the T-cells are inhibited, the information cannot be passed on to the brain. Habituation to mild
stimuli, which were initially guided by thick fibres, is regulated by this mechanism.
For example, the nervous system will adjust when wearing skinny jeans and the original sensation of relatively tight-
fitted clothing will not continue. However, those who have a key ring with keys in the back pocket and sit on their
keys will continue to feel them continuously. In the latter situation there is not only conduction through the thick
fibres, but also, activated by intense stimulation, a conduction through the thinnest fibres.
That activity stimulates substantia gelatinosa and T-cells which in turn pass on the information to the brain to
provide them with the nociceptive information coming from the keys in the back pocket. The continuous inhibitory
information of the thin fibres on the substantia gelatinosa switches off its activity so that the T-cells no longer
receive inhibitory information. The T-cells are now in a situation where they can continuously provide the brain with
nociceptive information. This is finally the often outlined way in which the gate is kept open for painful stimuli. As is
also explained in the stimulus pathways (see next §), the information, in the brain, is given an emotional/affective, a
motivational and a sensory/discriminative component. Wall & Melzack (1965) added a so-called "central control
mechanism" to their model.
According to this mechanism, emotions such as anxiety or arousal can operate the gate from any part of the body.
This makes random motor activity possible despite the supply (via the thinnest afferents) of powerful painful stimuli.
In the use of TENS currents, there is good scientific and clinical evidence for the gate control mechanism. However,
in the use of microcurrent it remains unclear whether this mechanism works. Based on empirical data, the effect
seems to be minimal.
2.1.3 CENTRAL EFFECTS ≈ central pain modulation (CPM) RS + watch Central Effects video!
The central effects can be divided into two groups: ascending/descending pathways and endorphins/ enkephalins.
Ascending and descending pathways (AD)
At frequencies and intensities used clinically, TENS activates large diameter afferent fibres. This afferent input is sent
to the central nervous system to activate descending inhibitory systems to reduce hyperalgesia. The whole
mechanism is a lot more complicated, but in this context it is sufficient to know that descending inhibitory systems
are activated by the electrical stimulus of a TENS current.
Endorphin and enkephalin opiates release (E)
In the 1970s it was discovered that the body is able to produce substances, in particular peptides, which have a
strong analgesic effect. According to the word “encephalon” (brain), where these substances were discovered, they
were named enkephalins. The chemical structure of enkephalins shows similarity with morphine. Following these
initial discoveries, scientists found larger peptides with a more powerful pain-relieving effect. Although there are
chemical differences, they are generally named endorphins. The β-endorphin appears to have the strongest
analgesic properties, followed by enkephalin and dynorphine. Some authors therefore consider β-endorphin as the
only active opiatelike factor in the body.
A great deal of research has been done into origin and properties and as a result it is now fairly certain that the
enkephalins are synthesized in the brain itself. They would then be transported via the axon to the nerve endings
where storage is also provided. Although this would also be the case to a lesser extent for the enkephalins,
endorphins are present in high concentrations in the pituitary gland. The natural stimuli could be rhythmic painful
stimuli. Cappendijck (1996) suggests this after it was determined that only a low level of endorphins was found in the
cerebrospinal fluid of patients with chronic pain.
Also, after a nice long bout of aerobic exercise, some people experience what is known as a “runner’s high”: a feeling
of euphoria engaged in a strenuous running, coupled with reduced anxiety and a lessened ability to feel pain.
Scientists have associated this phenomenon with an increased level in the blood of β-endorphins, opioid peptides
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