FIBROMYALGIA is a chronic miasmatic disease syndrome characterized by non-specific generalized body pain and an elevated painful response to tactile pressure stimuli. Symptoms other than body pain may include extreme tiredness, sleep disturbances, memory disturbances, joint stiffness, dysphagia, numbness, tingling, muscular spasms, twitching, temperomandibular joint dysfunctions, palpitations, symptomatic hypoglycemia, functional bowel/bladder disturbances, cognitive dysfunctions, diminished attention span, depression, anxiety as well as many symptoms of stress-related disorders such as post-traumatic stress disorders. Not all people with fibromyalgia exhibit all the associated symptoms.
Fibromyalgia is estimated to affect 2-8% of world population, with a female to male incidence ratio of 8:1, which means females are predominantly affected by this disease. The term ‘fibromyalgia’ derives from latin term ‘fibro’(fibrous tissues), combined with greek terms ‘myo’(mucles) and ‘algos’(pain).
The exact eitiology of fibromyalgia is still considered unknown, but is believed to involve multiple factors such as psychological, genetic, neurobiological and environmental. Generalized body pain, the central symptom of fibromyalgia, has been proven to be associated with some neurochemical imbalances and the activation of inflammatory pathways in the brain which results in biochemical abnormalities of pain processing. Fibromyalgia is classed as a ‘neurobiological disorder’, a disorder of pain processing due to abnormalities in how pain signals are processed in the central nervous system. Research evidences suggest that the pain in fibromyalgia results primarily from abnormal functioning of pain processing pathways. Hyper-excitability of pain processing pathways as well as under-activity of inhibitory pain pathways in the central nervous system jointly results in the pain sensation experienced by fibromyalgia patients. Some neurochemical abnormalities happening in fibromyalgia affect the biochemical systems that regulate sleep, mood and energy, which explain the concomitant symptoms of fibromyalgia.
Some references have included fibromyalgia in the list of autoimmune diseases, with cautious ‘qualifiers’ such as “a co-morbidity common among people with autoimmune disease, but with no evidence of being itself caused by autoimmunity”, and “disease is only caused by autoimmunity in only a fraction of those who suffer from it”. Immune-related aspects of fibromyalgia remain still under study.
According to MIT perspective, fibromyalgia has to be considered as a chronic ‘miasmatic’ syndrom. In this context, the concept of ‘miasm’ is used as “chronic disease dispositions caused by ‘off-target’ actions of antibodies generated in the body in response to invasions by endogenous or exogenous ‘alien protiens’ such as infectious agents, vaccines etc”. In the absence of a scientific understanding of miasms as ‘antibody-mediated diseases’, such diseases are presently classified in medical literature along with ‘autoimmune diseases’.
MIT considers fibromyalgia as a chronic disease condition arising from ‘residual effects’ of different kinds of ‘viral fevers’ that were characterized by severe generalized body pains, such as influenza, chikunguniya, chicken pox etc. Of course, vaccinations against these viral infections also would have similar ‘miasmatic’ effects, since vaccinations inevitably result in production of antibodies, which will be similar to the antibodies generated during actual infections. These antibodies remain in the body for long periods, and attack the enzymes associated with the expression of genes involved in the synthesis of various neuro receptors and neuromediators. Inhibition of such enzyme systems lead to faulty or diminished synthesis of neuroreceptors such as ‘dopamine receptors’ that are essential for maintaining healthy neurotransmission and ‘pain processing’ pathways. Breakdown in these pathways ultimately lead to a cascading effects upon various biomolecular pathways in central nervous system and neuroendocrine system, which are expressed through the mind and body symptoms of FIBROMYALGIA. Disruption of neuroendocrine pathways results in abnormalities of hormones under the direct or indirect control of growth hormone(GH), including insulin-like growth factor 1 (IGF-), cortisol, leptin and neuropeptide Y as seen in people with fibromyalgia. This explains the observation that people with fibromyalgia have alterations of normal neuroendocrine function, characterized by mild hypocortisolemia, hyperreactivity of pituitary adrenocorticotropin hormone (ACTH) release in response to challenge, and glucocorticoid feedback resistance. It also explains other abnormalities such as reduced responsivity of thyrotropin and thyroid hormones to thyroid-releasing hormone, elevation of prolactin levels with disinhibition of prolactin release in response to challenge and hyposecretion of adrenal androgens.
Kindly remember, functional analysis of the autonomic system in people with fibromyalgia has demonstrated disturbed activity characterized by hyperactivity of the sympathetic nervous system at baseline with reduced sympathoadrenal reactivity in response to a variety of stressors including physical exertion and mental stress. People with fibromyalgia demonstrate lower heart rate variability, an index of sympathetic/parasympathetic balance, indicating sustained sympathetic hyperactivity, especially at night. In addition, plasma levels of neuropeptide Y, which is co-localized with norepinephrine in the sympathetic nervous system, have been reported as low in people with fibromyalgia, while circulating levels of epinephrine and norepinephrine have been variously reported as low, normal and high. Administration of interleukin-6, a cytokine capable of stimulating the release of hypothalamic corticotropin-releasing hormone which in turn stimulates activity within the sympathetic nervous system, results in a dramatic increase in circulating norepinephrine levels and a significantly greater increase in heart rate over baseline in people with fibromyalgia as compared to healthy controls.
One of the most reproduced laboratory finding in people with fibromyalgia is an elevation in cerebrospinal fluid levels of substance P, a putative nociceptive neurotransmitter. Metabolites for the monoamine neurotransmitters serotonin, norepinephrine, and dopamine – all of which play a role in natural analgesia – have been shown to be lower, while concentrations of endogenous opioids such as endorphins and enkephalins appear to be higher. The mean concentration of nerve growth factor, a substance known to participate in structural and functional plasticity of nociceptive pathways within the dorsal root ganglia and spinal cord, is elevated. There is also evidence for increased excitatory amino acid release within cerebrospinal fluid, with a correlation demonstrated between levels for metabolites of glutamate and nitric oxide and clinical indices of pain.
Evidence of abnormal brain involvement in fibromyalgia has been provided via functional neuroimaging. Differential activation in response to painful stimulation has also been demonstrated. People also exhibit neural activation in brain regions associated with pain perception in response to nonpainful stimuli in such areas as the prefrontal, supplemental motor, insular, and cingulate cortices.
Evidence of hippocampal disruption indicated by reduced brain metabolite ratios has been demonstrated by studies. A significant negative correlation was demonstrated between abnormal metabolite ratios and a validated index of the clinical. Correlations between clinical pain severity and concentrations of the excitatory amino acid neurotransmitter glutamate within the insular cortex have also been demonstrated using 1H-MRS.
A significant negative correlation between pain severity and dopamine synthesis was demonstrated within the insular cortex. A subsequent study demonstrated gross disruption of dopaminergic reactivity in response to a tonic pain stimulus within the basal ganglia with a significant positive correlation between the defining feature of the disorder (i.e. tender point index) and dopamine D2 receptor binding potential specifically in the right putamen.
Finally, reduced availability of mu-opioid receptors in the ventral striatum/nucleus accumbens and cingulate cortex has been demonstrated, with a significant negative correlation between affective pain levels and receptor availability in the nucleus accumbens.
All these established factors justify the MIT observation that fibromyalgia is caused by alterations in biomolecular processes in central nervous system and neuroendocrine system, produced by inhibitions of enzyme systems associated with expression of genes involved in synthesis of neuro-transmitters and receptors of neuron synapses.
From MIT perspective, therapeutic management of fibromyalgia essentially involves deactivation of antibodies that are responsible for inhibition of enzymes associated with concerned gene expressions. This could be achieved by administration of ‘molecular imprints’ that can act as ‘artificial binding sites’ for those antibodies, so that they could be deactivated and the biological molecules relieved from inhibitions.
Potentized homeopathic nosodes such as Variolinum 30, Influenzinum 30 etc are found to be very useful for this purpose. Potentized Chikungunia nosode is expected to be a very powerful homeopathic drug for fibromyalgia, as the chronic residual effects of ‘chikungunia’ is found to be symptomatically very similar to fibromyalgia symptoms.
PITUTRIN 30 and ACTH 30 are very important drugs that should be incorporated into any homeopathic treatment plan for fibromyalgia, as they will antidote the hyper-reactivity of pituitary adrenocorticotropin hormone (ACTH) release in response to challenge, and glucocorticoid feedback resistance.
All homeopathic drugs that have ‘generalized body pain’ and pain aggravation by pressure’ could be used to alleviate fibromyalgia pains. From my personal experience, I have found ARNICA 30 a very effective drug for this condition. ‘Multiple drug’ approach consisting of homeopathic similimum, potentized hormones and viral nosodes in frequently repeated doses will be a most ideal strategy from MIT point of view.