Oh, pain go away! Fibromyalgia syndrome – a widespread disease?

Irene Kolbe, Naturopathic Practitioner, Hanover, Germany

1. Introduction

Welcome

Dear Colleagues, Dear REGUMED Management and Employees, Thank you for the invitation to speak online at the 2021 autumn congress.

Acute and chronic pain

We deal with this issue in our practices time and again and come across patients who have often already undergone a whole range of procedures from A for acupuncture to Z for Zen therapy. What strikes me here is that, as a regulative treatment, bioresonance can often bring about a change in what is happening, allowing other therapeutic procedures to begin to take effect in parallel. It is not easy to talk about fibromyalgia syndrome without addressing the issue of pain in general.

2. PAIN – How can we define and measure it?

Basically, pain is an involuntary protective effect.

We are familiar with numerical and visual scales that permit us to estimate the intensity of pain, but yet pain cannot be weighed, counted, microscopically examined, we cannot express it in percent and say that this is where pain begins. “What you (meaning the patient) have so far referred to as pain is not pain at all.” So there is no clear statement about the quantity and quality of this event, when it begins, at what threshold we can expect pain and when it might even be incompatible with life.

So it is not surprising that pain is described as elusive in its definition by ISAP (International Association for the Study of Pain).

“An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”

The definition also goes on to state that pain is always perceived as an expression of tissue damage, even if there is no such damage.

The translation of the Greek root smerdnos/smerdoléos as terrible, dreadful, horrible, shows in comparison the possible subjective perception of a pain event.

Objectively, or rather in the context of physiological observation, we can now describe the development and continuation of pain based on anatomical structures.

a) Nociception, noxic stimuli, nociceptors and nociceptive system

The expression of nociception deals with the processes by which the nervous system absorbs and processes corresponding stimuli (noxic stimuli).

Noxic stimuli are mechanical, chemical and thermal stimuli that can cause damage. These are recognised by pain receptors, the nociceptors, and processed by the nociceptive system. These are therefore “damage detectors” (lat. nocere = damage).

There is an exception in special cases, e.g. loss of limbs during traumatic events when, if the damage is existentially dangerous, the body switches to “survival mode” and can bypass this system for a short time by releasing adrenaline. Recent research has also shown that nociception has an analgesic descending system in addition to its ascending pain mediating system. Endorphins and encephalin play an essential role here. This is the only way we can explain to ourselves how, for example, victims of anti-personnel mines can travel even extended distances to escape a danger zone or seek help.

Nociceptors are primary afferent “first” neurons that receive damaging stimuli at their sensory endings in tissue. They supply all organs and synaptically activate the central nervous nociceptive system.

This system consists of neurons of the spinal cord and the trigeminal nucleus, which is responsible in particular for the head area. This also involves the thalamocortical system, which is important for the conscious perception of pain.

Fibres run from the cortex and hypothalamus (“the gateway to consciousness”) to the brain stem, where efferent pathways originate. These inhibit or enhance processing in the spinal cord.

b) Peripheral mechanisms in the development of pain mediators excite nociception:

Pathophysiological processes:

First, injury to tissue results in the release of ATP, protons, oxygen radicals, potassium ions and arachidonic acid.

The enzyme cyclooxygenase is expressed in endothelial cells (COX1) and in migrating leukocytes (COX2). This converts the arachidonic acid released from the cell membranes of the damaged cells into prostaglandin E2.

Kinins, which also originate from the injured endothelium, are converted into bradykinin.

Mast cells release histamine, among other things.

Inflammatory mediators (especially bradykinin and serotonin) cause vasodilation, meaning that leukocytes can migrate more easily.

The cytokines IL-1 and IL-6 as well as TNF also lead to an increase in temperature all the way up to fever. In addition, all pain mediators excite the nociceptors via specific receptors, i.e. the free nerve endings that are responsible for the transmission of pain. This excitation causes a neurogenic reflex (described under the nociceptive system).

The nociceptors secrete nerve growth factor (NGF) and calcitonin gene-related peptides (CGRP), both of which are neuropeptides.

This results in two things:

1. The nociceptors sensitise themselves and excite what are known as sleeping pain receptors in the immediate environment, thus increasing the pain stimulus, and neurogenic inflammation occurs.

2. NGF induces nerve fibres to grow, also penetrating the surrounding tissue. This together with the activation of sleeping receptors leads to the tissue adjacent to the damage also becoming sensitive to pain.

3. FIBROMYALGIA

Approximately 3 % of Germans suffer from this, with a growing prevalence also among young people. The disease is classified under the rheumatic form (“soft tissue rheumatism”) – however, the term “pain disease” better describes this syndrome.

The ratio between affected women and men is 8:1.

Fibromyalgia syndrome has been listed in ICD 10 since 2005, which is important for those affected because the disease now has a name and thus the stigma of hypochondria could (might?) be stopped.

The fibromyalgia criteria of the ACR (American College of Rheumatology) have also supported this since 2010.

The following criteria are summarised here:

Triggered pain at the trigger points (myofascial points)

Severity of exhaustion, non-restorative sleep, concentration and memory disorders, listlessness, depressive moods, migraine attacks, morning stiffness and a feeling of swelling throughout the body as well as dizziness and weather sensitivity

4. Causes of FIBROMYALGIA

The causes can be a mixture of physical, psychological and social factors. Egloff et al. were able to demonstrate in 2016 that the posterior horn neurons of the spinal cord increasingly develop pain receptors that make the entire pain-conducting system of patients more sensitive.

In her book “Schmerzen – Notrufe aus dem Körper” (Pain – emergency calls from the body), Hanne Seemann describes how long-term stress eventually leads to the down-regulation of the endocrine stress axis consisting of the hypothalamus, pituitary and adrenal glands. In turn, activation of ACTH distribution can be observed. All this can be seen as an expression of long stress-related hyperactivity in terms of chronic exhaustion. The development leads to stiffening and weakening with accompanying neuronal sensitisation. The increased frequency of the stimuli lowers the stimulus threshold. Neurotransmitter measurements show that serotonin and the body’s own endorphins are lowered. It is therefore important to recognise the patterns that underlie exhaustion and sensitisation in this individual pain disorder.

5. A) Case study: patient B. from S., born 1970

First contact 5 years ago in connection with a cystic struma (known for 10 years). Felt solely responsible for her parents, who lived in the same house. The mother’s Alzheimer’s dementia ultimately made it necessary for her to receive care through recourse to a care service. During this period her thyroid gland nodes grew and her hormone levels deteriorated. Thyroidectomy in 2017. Cold nodes without malignancy with normal calcitonin levels. Adjustment of hormone replacement with L-thyroxine was difficult. Her parents’ domestic situation deteriorated at the start of hormone replacement therapy and fatigue. A nursing home with a dementia residential unit was sought for the mother after her tendency to run away and exhibit aggressive behaviour increased dramatically. The pain syndrome began around this time. In addition to the pain, exhaustion and a number of other typical symptoms now appeared on a massive scale.

Arrangement of a salvia sample with simultaneous micronutrient analysis

Extract: salvia test (Laboratory MVZ Dr Kirkamm, Mainz)

B) Interpretation excerpt

Remarkably low values apparent. With the exception of DHEA, all values are still within the normal range, but with visible depletion at the endocrine level.

The DHEA level in particular should be noted.

DHEA (dehydroepiandrosterone) is a hormone that is mainly produced in the adrenal cortex and is converted into sex hormones (oestrogen, testosterone) in both men and women. Levels of DHEA in the blood accordingly fall by 2% with advancing age from the age of 25 onwards. Another important task is that DHEA is a cortisol antagonist.

Let us return to the interpretation of the extract of the saliva sample:

While cortisol levels are within the normal range, they have decreased compared to the preliminary sample 3 months before due to fibromyalgia. At that time, however, DHEA levels were > 400 pg/ml.

The ratio of DHEA to cortisol should therefore be regarded as a quotient. The antagonist DHEA was “plundered”, thus providing guidance for the choice of programs during treatment besides the subjective pain symptoms.

C) Bioresonance programs for patient B.

First session alongside basic program (exhausted patient):

a) Blockage in tissue 3040.0, 951.1

b) Release blockage (energetic) 918.0, 3084.0

c) Liver / gallbladder regulation 3064.0

Second session: basic program for exhausted patient continued:

a) Blockage in the tissue and removal of the blockage, plus an additional low-frequency program 3017.0

b) Stress 3084.0

c) Continuation of liver / gallbladder regulation 3064.0

d) Depression 3027.0, 428.3, 900.5,

e) (Burnout, Insomnia)

Test and possible change to programs over time.

This was followed by 4 more treatments, then a therapy break of 6 weeks.

Additional medication treatment:

The medicines were tested and repeatedly switched between the corresponding bioresonance testing and programs.

The following medications were used as part of the 6 treatments:

Mucedokehl both in D 5 drop form and alternating as D 4 capsules

Multispectrum 24/7 (Biogena)

Griffonia + capsules 1-2 capsules every morning

DHEA capsules (only available on prescription) In accordance with the saturation phases etc.

Hepatodoron

After the onset of saturation with DHEA, supplement with HSC progesterone in the first cycle phase. (Marktapotheke Rotthalmünster, Pharmacist Greiff) together with Phyto C. (Steierl)

5. B) Case study: patient H. from N., born 1945

First contact at the beginning of 2019, after various changes of doctors ranging from orthopaedists and rheumatologists to pain therapists. Under different medication through to MTX, which was not tolerated. Renewed pain progression before our first contact under cortisone treatment from the GP that had been running for 6 weeks. At the beginning with 50 mg of prednisolone, already reduced to 12.5 mg when we first made contact. The administration of cortisone brought only a marginal improvement and so the patient tried everything on her own to achieve a tolerable improvement with additional painkillers. The program included Novalgin drops, cannabidiol (CBD) etc. The psychotherapy initiated at the same time helped the patient to cope better with the situation emotionally. The most prominent symptoms were fatigue, exhaustion with simultaneous insomnia, the feeling of being “congested” and getting up in the morning with no strength, and “soreness” in her tissues and at the connecting points to tendons.

Bioresonance programs for patient H.

Basic program (exhausted patient)

a) Blockage in tissue 3040.0, 951.1

b) more blockage 3084.0, 3017.0

c) Depression, insomnia3027.0 alternating with 428.2 and 900.5

Phytodolor drops via the honeycomb and substances fed in via the 2nd channel.

The sessions were initially at weekly intervals and later every 4 weeks.

Additional medication treatment:

When the Cushing’s threshold is reached at <7.5 mg, I like to use the Pischinger elimination:

Phoenix detoxification (spagyric) over 45 days in three-day alternation of silybum spag., solidago spag., urtica-srsenicum spag. and continuously with all three remedies the great connective tissue remedy thuja-lachesis spag. (However, from experience with pain patients, only half the dose as indicated.)

5. C) Case study: patient K. from H., born 1990

Young man (family history of ankylosing spondylitis), all “normal” tests by the general practitioner without inflammation parameters, rheumatologist without pathological parameters, orthopaedist without results in the laboratory and imaging measures. Out of desperation, I undertook a great deal of research on the Internet, including reports about latent diabetes with fibromyalgia syndrome and improvement through taking metformin. However, since no one wanted to test these, we tested the HbA1 c value here, but with no result.

Thus we proceeded to the intracellular examination (subject of mitochondropathies) via blood laboratory micronutrients/nitrostress, as the patient was increasingly suffering from sleep disturbances, exhaustion syndrome and a “depressive mood”.

This involves a lot of testing for loads and toxic substances in order to find a cause.

Arrangement of a salvia sample with simultaneous micronutrient analysis

Extract: salvia test (Laboratory MVZ Dr Kirkamm, Mainz)

Citrulline increase: inflammatory reactions, inhibition of mitochondrial function, reduction in the formation of serotonin, melatonin, catecholamines etc.

DNA oxidation: mitochondrial damage

Bioresonance programs for patient K.

First session alongside basic program (exhausted patient):

a)Blockage in tissue 3040.0, 951.1

b)move blockage (energetic) 918.0, 3084.0

c)Liver / gallbladder regulation 3077.0

d)Detoxification. 3036.0

e)Inflammation 3037.0

Further session: basic program “exhausted patient” remained, programs from the first session tested out and partly replaced by:

a)Blockagein the tissue and remove blockage plus an additional low-frequency program 3017.0

b)Alternating pain therapy 426 and 425

c)Stress 3084.0

d)Continuation of liver / gallbladder reg. 3064.0

e)Depression (Burnout, insomnia) 3027.0, 428.3, 900.5,

Additional medication treatment:

Biogena substitution: Nitro-Stress Formula II and OPC Polymax 250/30 and vit.

D3/K2 oil drops

Ceres: Daucus comp.

Phytodolor if required

Gelum drops

Other prescriptions in accordance with the “pain pattern” and their causes Bioresonance programs:

a) Improve intestinal flora 3013.0, 3028.0, 562.0

b)Mucosal regulation 3089.0

c) Liver / gallbladder regulation 3064.0, 3063.0, 430.2,

d) Stressed nervous system 3077.0

e) Nerve attenuate 911.1

f) Nerve regulation 3074.0

g) “Rheumatic” pain 3085.0

I would like to conclude with a poem by Christian Morgenstern. I know this is an unusual conclusion to presentation. This poem is an important element in dealing with pain in the context of eurythmy therapy. It shows us a piece of our being, but also of the power inherent in pain. Not resigned acceptance, but the perspective of confronting it, the pain,both as a therapist and as a patient.

What would you be, wind,

if you had no trees

to roar through?

What would you be, spirit,

if you had no bodies

to dwell in?

All life seeks resistance.

All light seeks gloom.

All labour-pain seeks trunk and wall

so that it can work against it.

Thank you for your interest and I wish you all the energy to continue thinking, researching, gaining experience and sharing it with colleagues.

References:

1. Hanne Seemann: Schmerzen – Notrufe aus dem Körper (Pain – Emergency calls from the body) Edition Sept. 2018, Klett-Cotta-Verlag

2. HP Dr vet Anita Kracke: Schmerzen als Erschöpfungsignale erkennen – in Frühwarnsystem für Körper und Seele (Recognising pain as a sign of exhaustion – An early warning system for body and soul), presented at Sanum Converence March 2019

3. Thews-Mutschler-Vaupel, Anatomie, Physiologie, Pathophysiologie des Menschen (Physiology, pathophysiology of humans), Wissenschaftliche Verlagsgesellschaft mbH, Stuttgart, 5th edition

4. Schmidt-Lang-Thews, Physiologie des Menschen mit Pathophysiologie (Human physiology with pathophysiology), Springer Verlag, 29th edition

5. HP Irene Kolbe: Schmerz, eine Herausforderung in der naturheilkundlichen Praxis (Pain, a challenge in the naturopathic practice), presented at Sanum Conference

April 2010 (first published 2011)