The use of ozone in the hypertonic musculature
Trigger
points are one of the most frequent causes musculoskeletal pains. However, in
the last few years has appropriate attention been given to this trigger points,
except for the earlier work by a few pioneers in this field.
|
Myofascial pain syndromes (MPS) as percentage of all forms of chronic
pain affecting the locomotor system |
|
Skootsky
1989
30% |
|
Fishbain
1989
85% |
|
Fricton
1990
55% |
|
Gervin
1995
93% |
Since the practical significance of trigger points was discovered, there has been a veritable boom both in basic research and in the therapeutic possibilities. As jet, the diagnosis myofascial trigger point can be made only clinically, but not based on laboratory-chemical or radiological findings.
Tissular
pO2 measurements of the chronically hypertonic M. erector spinae in
20 patients, compared with 10 healthy controls were carried out by Brückle.
Interestingly, the pO2 levels in the hypertonic musculature rose
proportionately to the degree of hypertonia musculature. The mean tissular pO2
level was 38.5 mmHg, which was 9 mmHg more than that of the healthy controls,
with a standardised mean reference value of 29.5 mmHg.
The
objection, that the pain is caused by small, scattered islands of hypoxia in the
hypertonic musculature, could be refuted by the measurement technology used.
Various
authors have found significantly low levels of adenophosphate in the
hypertonic musculature, with high pO2 level. It can therefore be
resumed that the raised pO2 levels result from deficient oxygen
utilisation due to an inadequate supply of high-energy phosphates.
Myogeloses are olive- to plum-sized areas of hardening in the muscles.
The
histological pictures show a degeration of the myofibrils, or necroses with a
“moth-eaten” appearance (ragged red fibres), as well as large amounts of
glycogen and mitochondrial material.
The
tissular pO2 measurements showed raised pO2 levels at the margin of the
myogeloses, which towards the centre fell to hypoxic levels of under 5 mmHg*.

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The
explanation for this is the occlusion of the microcirculation at the margin of
the myogeloses. This is possibly triggered by compression due to spasm of muscle
fibres surrounding the blood vessels within the muscle. Compression of the
microcirculation causes local hypoxia, with subsequent acidosis due to the
formation of lactate. The lowering of the pH value leads to loss of flexibility
of the erythrocytes and occlusion of the already stenosed vessels. Also
vasoneuroactive substances histamine, bradykinin, substance P (SP) and
calcitonin gene-related peptides (CGRP) are released. As a result, an oedema is
formed which further compresses the vessels and exacerbates the hypoxia. The
oxygen can then pass from the margin into the interior of the myogelosis only by
diffusion, because of which there is a gradual lowering of the pO2 level towards
the centre.
As already mentioned, mediators of inflammation and vasoactive substances are
formed, which sensitises the nociceptors in the sense of hyperalgesia. On the
other hand, the inflammatory metabolism leads to the creation of oxygen
radicals, the formation of which is promoted by the raised pO2 level
in the hypertonic muscle. The excess of oxygen radicals causes a dekompensation
of the enzymatic scavenger system. The obvious assumption is that the free
radicals can lead to further destruction of muscle tissue and nerve tissue –
with an increase in the hyperalgesia.

The
following factors, among others, are important for the physiological development
of muscular contraction:
Ø
A supply
of oxygen sufficient for an aerobic contraction.
Ø
An amount
of glycogen, which as an energy carrier with an adequate supply of oxygen
provides the necessary energy.
Ø
High-energy phosphates, which facilitate utilisation of the oxygen.
Ø
Adequate
amount and composition of electrolytes that are important for the muscular
contraction.
Ø
Elimination of iron, folic acid and vitamins B1, B6, B12,
c deficiency, hypothyroidism and hypoglycaemia.
Ø
Elimination of any excess of free radicals.
Ozone
acts on the metabolism in the following ways, among others:
Ø
Amounts of ozone stimulate the formation of glutathione peroxidase, which
activates glycolysis.
Ø
Glycolysis leads to the formation of 2,3-DPG and ATP.
Ø
2,3-DPG facilitates the release of oxygen to the tissue.
Ø
Low ozone concentration activate the enzymatic scavenger system, mainly the
glutathione peroxidase, catalase and superoxide dismutase. They break down the
oxygen radicals that are formed by degenerative and inflammatory processes.
Ø
The rheological properties of the blood are increased.
This
mode of action of ozone aims at the above-mentioned pathological processes in
the hypertonic musculature and in the myogeloses, and forms the therapeutic
basis for extensive normalisation of the pathological states in the hypertonic
musculature and the myogeloses.
Method
used
From the point of view of clinical practice, the following main criteria, in decreasing order of specificity, may be used for the diagnosis of trigger points:
Main clinical criteria for the diagnosis of myofascial trigger
points, in decreasing order of specificity |
Local pain on pressure within a hard, hypertonic muscle strand
|
|
A
hard, hypertonic muscle strand, palpable from its origin to its point of
insertion |
Local twitch response with twitching of the muscle fibres within a taut
band as a reaction of mechanical stimulation of the MTrP
|
Radiating of a characteristic referred pain as a reaction of mechanical
simulation
|
Renewed recognition of the pain by the patient
|
The frequency of the treatment is determined by the number and the mass of the affected muscles. It can be between once and five times a week.
Two types
of injections can be used: Precisely targeted injections into the trigger points
respectively myogeloses and multiple or fan-shaped infiltrations into large
muscles.
Whenever
possible, fine calibre cannulas should be used corresponded to the intended
depth of the injection.
At first
is lidocaine or procaine injected. The amount of lidocaine ½ percentage: 1 to 20
cc and lidocaine 1%: 1 to 10 cc. Procaine 1%: 1 to 10 cc. After injection of
local anaesthetic, an ozone/oxygen mixture will be injected through the same
cannula. Depending on the size of the muscle and the mode of application
(injection in the hypertonic mass or at a given point), the amount of ozone
injected should be 1 to 10 or eve 20 cc of a 15 to 20
µg/ml
solution per muscle. The ozone should be insufflated slowly in order to avoid
pain as far as possible.
During
the injection the muscle should be massaged in order to obtain better
distribution of the ozone.
Whenever
possible, passive stretching of the shortened muscles should be carried out at
the end of the tonanalgesic therapy and the patient should be given appropriate
instructions for daily active muscle stretching exercises. Muscle-stabilizing
exercises should also be performed during and after the end of the treatment.
Reactive
muscle pain may happen, as an occasional, insignificant side effect.
It is
interpreted as being a result of insufficient distribution of the ozone/oxygen
mixture in the muscle or due to the injection of a relatively too large amount
of ozone. The results are some times markedly better than after painless
injections.
*
This pO2 value corresponds to the oxygen tension observed in peripheral
occlusive arterial disease POAD), in the painful phase.