Fibromyalgia: An Environmental Scan
Table of Contents
It is paramount to remember that in trying to understand the presentation and etiology of disease concerning fibromyalgia that to date, no specific pathology has been identified that explains individual patient symptoms. Notably, patients consistently report pain and typically show a variety of other symptoms. Laboratory tests and other diagnostic imaging investigations are regularly unsuccessful in demonstrating specific abnormalities.
Given the cause(s) of fibromyalgia simply elude researchers and clinicians, for clarity in this report, the term triggers is used to denote an event, which when it takes place an individual then develops fibromyalgia. Given there is no empirical, thus conclusive evidence of the cause(s) of fibromyalgia, the discussion focuses on the unfolding of events from a trigger through to the development of fibromyalgia without any assumption to the causal factors of this syndrome. fibromyalgia is a complex culmination of various symptoms and is often precipitated by a trauma, which can be physical, psychological or emotional. Additionally, a trigger can also be an illness such as a viral infection. Research to date has demonstrated that there is no strong correlation between any specific event or illness and the development of fibromyalgia. However, recent developments in research and diagnostic processes have led to some understanding of the role of central nervous system (CNS) and the development of fibromyalgia. Recently, research has focused on examining various neuroendocrine, autonomic nervous system and brain activity processes, which is beginning to show neurochemical abnormalities in patients with fibromyalgia (Wood, Patrick 2008).
External factors are currently viewed as possible triggers albeit there is little understanding of exactly how or why a trigger results in the onset of fibromyalgia. The question is why do some triggers result in the development of fibromyalgia in some people and not in others? It is unclear if characteristics create a predisposition to the condition whereby a trigger results in the manifestation of the syndrome. A major risk factor for developing fibromyalgia is having another relative in the family who has the condition. The clinical observation of familial history of fibromyalgia suggests there may be a certain genetic component responsible for fibromyalgia. Specifically, there is evidence that polymorphisms of genes in the serotoninergic, dopaminergic and catecholaminergic systems may be involved (Buskila, D., and Piercarlo Sarzi-Puttini 206). However, we do not understand what ‘turns on or off’ particular genetic influences.
In the fall of 2009, the Whittemore Peterson Institute, who are focused on neuro-immune diseases reported higher than normal levels of retroviral infection XMRV in blood samples from individuals who had a diagnosis of chronic fatigue syndrome. It is well known how virus infections play a role in inflammatory diseases and specifically the XMRV has nearly exclusively been studied in prostate cancer. This work may prove significant in advancing the understanding of how a virus may either trigger or cause a chronic pain syndrome such as fibromyalgia or CFS (Lombardi et al. 2009). However, the research is in the early stages and importantly such results need to be replicated in much larger study populations and among diverse groups. In addition, there are issues surrounding the accuracy of diagnoses in both fibromyalgia and CFS especially as many patients with CFS also meet the diagnostic criteria for fibromyalgia and vice versa. The potential for misdiagnosis among fibromyalgia can be quite prevalent and in this particular piece of research considering the latent impact of confounding misdiagnosis must be addressed in future studies.
Wallace and Clauw (2005) provide a hypothetical model of the components leading up to the onset of fibromyalgia. An individual often has a predisposition, which in the case of fibromyalgia can be a deficiency in a biogenic amine (e.g., norepinephrine, histamine or serotonin) or a defective protein. An individual then experiences an event (trigger) such as a physical trauma or an illness that produces a neurochemical change in the central nervous system (Wallace and Daniel J Clauw 2005). The central nervous system has a role in causing a sensitization to external stimuli and the resulting central pain processing that takes place. There are a number of neurotransmitter and neuropeptide differences found within the cerebrospinal fluids of individuals with fibromyalgia (Valença et al. 2009) (See Appendix H: Neurochemicals). Furthermore, it is well documented that patients with fibromyalgia can feel pain in the body in a more extreme way, hyperalgesia compared to individuals without fibromyalgia. Hypotheses suggest that there is a different process in the way in which the body of a fibromyalgia patient actually processes pain compared to otherwise healthy individuals. Additionally, pain may be experienced by individuals with fibromyalgia from an external stimulus that would not cause pain under normal circumstances, allodynia (Mease, P. 2005). In clinical terms, changes such as aberrant pain processing, an inhibitory process in pain pathways and the alteration of neurotransmitters all take place within the central nervous systems and are thought to be related to the development of fibromyalgia (Podolecki, T., Podolecki, A., Hrycek, A. 2009)(Aryeh, M., Pillinger, Micheal H., Solitar, Bruce M. and Micha Abeles 2007)(Krypel, Linda L. 2009).
Research into diagnostic imagery and chronic pain has focused on the augmentation of the central pain processing system in the CNS. For example, in Germany a neuroimaging study showed that a structural change in the pain systems is a precondition for the central pain sensitization of fibromyalgia (Burgmer et al. 2009). Other research suggests differences in pain processing in individuals with fibromyalgia compared to healthy controls included the difference in opioid receptors, elevated levels of substance P in the cerebrospinal fluid and a difference in the activation of areas in the brain responsible for pain processing. Such results are important as opioid receptors are responsible for binding with opiates that are painkillers contained in many pharmacological agents used to treat pain. Importantly, having a reduced amount of opiate receptors (as a result from upregulation disturbances) in the central nervous system assists in understanding why individuals with fibromyalgia may have difficulty getting pain relief from standard pharmacological agents for treatment in chronic pain.
Substance P, which is three times beyond normal levels in patients with fibromyalgia, mediates pain threshold, thus determines when a stimuli will become painful. Substance P provides a possible explanation as to why individuals with fibromyalgia have such sensitivity to external stimuli, along with very low pain tolerance or feel pain in situations that would not normally produce a pain response in otherwise healthy individuals. Brain activity research shows increased blood flow to particular areas of the brain among fibromyalgia patients and also demonstrates brain activity is higher in areas that deal specifically with pain. Pain signals are significantly increased, which may result in an abnormal process surrounding an abundance of pain messages in the CNS.
Three other neurochemicals are being investigated for the role in fibromyalgia, serotonin, dopamine and cortisol, which are found in abnormally low levels in fibromyalgia patients or are not used effectively in the brain compared to healthy counterparts. These hormones each play an important part in controlling many of the processes in the body. Serotonin, which is found in lower levels, is vital to a person’s mood, sleep and pain response whereas dopamine, which researchers speculate is not used efficiently in fibromyalgia patients is thought to affect pain processing and cortisol, found in lower than normal levels may result from an alteration in the pituitary-adrenal area of the body (Millea and Holloway 2000). Other research has examined the effect of low dopamine and found that the density of gray matter in the brain was augmented (Glabus et al. 2009).
The culmination of a traumatic event and subsequent stress responses can create the environment for the onset of fibromyalgia. Once fibromyalgia has occurred in the body, the hallmark is then a change or augmentation of the central pain process in the central nervous system (Albin, JN., Neumann, L., and Dan Buskila 2008)(Dadabhoy, D., and Daniel J. Clauw 2006). Additionally, both the development and symptoms of fibromyalgia are overlapping with other diseases for example, Lyme disease and particular triggers such as vaccinations. It is not yet fully understood how infections or other conditions act as triggers for the development of fibromyalgia, but is it becoming clearer that such occurrences are significantly contributing to the onset of fibromyalgia (Albin, JN., Shoenfeld, Y., Bushila, D. 2006). (Albin, JN., Shoenfeld, Y., Bushila, D. 2006)