Difference between ME and Fibromyalgia

[filfla4]

Can anyone refer me to some reliable information on the medical difference between ME and Fibromyalgia? I know the obvious....can be co-morbid; etc etc however I need something which is quotable and will be used by my local media.

 

[Valentijn]

According to the Canadian Consensus Criteria (published as "Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Protocols"):

Differences Between ME/CFS and FMS
ME and CFS probably are the same illness but their research definitions have emphasized different aspects of the illness. The diagnosis of myalgic encephalomyelitis and chronic fatigue syndrome are generally used interchangeably in Canada. The clinical case definition in this document emphasizes both the lack of stamina and fatigue as well as other symptoms that support a multi-system illness, which is referred to as ME/CFS.Ž

A syndrome may be delineated by means of a criterion that reflects a cutoff point on a continuum of symptoms and dysfunctions. Thus ME/CFS and fibromyalgia syndrome (FMS) can be differentiated on the basis of symptom balance in what many believe are variants of the same or similar disease pathogeneses. By criterial definition, pain is the major feature of FMS whereas post exertional malaise and fatigue are the major symptoms of ME/CFS. However the latter often involves significant cognitive dysfunction and pain, and overlap situations are common where both pain and fatigue are of similar prominence. Some FMS patients have complex symptomatology that is often indistinguishable from ME/CFS. Indeed many patients are diagnosed with both ME/CFS and FMS. Approximately 75% of ME/CFS patients also meet the criteria for FMS (49). Some patients have a syndrome pattern that changes from one to the other. For example, FMS can evolve into ME/CFS and visa versa.

Although it may sometimes be difficult to distinguish between ME/CFS and FMS on the basis of symptomology, ME/CFS cases are commonly triggered by a viral infection, whereas physical trauma as well as other initiating events, trigger many FMS cases. Another important difference is in the response to exercise. Patients with mild FMS may be better able to tolerate aerobic exercise whereas it often aggravates the symptoms in ME/CFS patients, who may need alternate forms of exercise and a gentler progression. The possibility of overlap with ME/CFS may give rise to confusion as different situations may require different approaches to exercise.

 

[WillowJ]

Kathy and Alan Light found gene expression differences between FM patients who do not meet criteria for ME/CFS, and ME patients:

FM-only patients showed no postexercise alterations in gene expression, but their pre-exercise baseline mRNA for two sensory ion channels and one cytokine were significantly higher than controls.

and patients with ME/CFS (patients meeting both Canadian and Fukuda criteria):

At least two subgroups of patients with CFS can be identified by gene expression changes following exercise.

The larger subgroup showed increases in mRNA for sensory and adrenergic receptors and a cytokine.

The smaller subgroup contained most of the patients with CFS with orthostatic intolerance, showed no postexercise increases in any gene and was defined by decreases in mRNA for α-2A

In control subjects, exercise did not increase ratings of mental fatigue or pain at any time point; and physical fatigue was increased only at mid-exercise and not at any post-exercise time. In sharp contrast, exercise caused significant increases in all fatigue and pain measures at all time points during and after exercise in CFS only and in CFS+FM patients.

The present study confirms our prior findings [9] that moderate exercise in CFS patients leads to increased expression of certain sensory ion channel, adrenergic, and immune genes (P2X4, P2X5, TRPV1, α-2A, β-2, COMT, and IL10) that do not occur in healthy individuals. The functions of these genes and how they contribute to the symptoms of CFS and FM was discussed in our previous report [9].

They go on to explain that this is a bigger sample, includes people who are less ill, and allows more medications. All of those things could contribute to fewer findings in this study compared to the earlier study.

In the α-2A decrease CFS patients, the very large and consistent decreases in α-2A expression following exercise combined with orthostatic intolerance suggests that different mechanisms cause the debilitating fatigue in this subgroup. The large decreases in α-2A mRNA may reflect a particular type of dysregulation of the sympathetic nervous system. ... These effects would cause inadequate blood flow to working muscles and the brain.

The larger subgroup of patients (α-2A increase CFS patients) demonstrated large gene expression increases following exercise in many different genes....Interestingly, all of the genes measured here are interconnected by [a few molecules shown in other studies to be connected to ME/CFS]... Whether these associations predict, or cause future CFS, should be investigated.

Interestingly, the genes found to be dysregulated in the present study represent most of the pathways hypothesized by others to be altered in CFS. These include the immune system (IL10, and leukocytes in general) [29–31], cellular energy (P2X4 and 5 that encode ATP levels, and TRPV1 encoding temperature) [32], and the cardiovascular system (adrenergic receptors α-2A, β-1, β-2, and the catecholamine processing gene COMT) [33, 34].

Even though they did not show exercise induced increases in gene expression, FM patients were clearly different from healthy controls and from the CFS patients at baseline. Unlike CFS only or CFS+FM, they showed higher baseline mRNA than controls for 2 sensory ion channel genes, P2X4 and TRPV1, and one cytokine, IL10. Given the results for the CFS+FM patients and the similarity of their post-exertional symptoms, this finding was surprising.


What is not surprising is that the affected genes were P2X4, TRPV1 and IL10. In our mouse experiments, genes that seemed most likely to encode noxious levels of muscle produced metabolites were a combination of ASIC3 (and or ASIC1) P2X4, and TRPV1 [6].

The increases in these receptors on leukocytes could make them more sensitive to muscle produced metabolites, and more likely to produce sensitizing cytokines when muscles are activated (see a recent review of how P2X4 on leukocytes could be involved in inflammatory pain [46]). This could lead to more muscle pain at all times.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3175315/

A.R. Light, L. Bateman, D. Jo, R. W. Hughen, T.A. VanHaitsma, A.T. White, and K.C. Light. Gene expression alterations at baseline and following moderate exercise in patients with Chronic Fatigue Syndrome, and Fibromyalgia Syndrome. J Intern Med. 2012 January; 271(1): 64–81. doi: 10.1111/j.1365-2796.2011.02405.x

 

[*GG*]

I recently read these pieces, not sure if you are looking for something not "scientific" talk?:

http://chronicfatigue.about.com/od/faq1/f/How-Can-I-Explain-Fibromyalgia.htm

and

http://chronicfatigue.about.com/od/faqs/f/how-to-explain-chronic-fatigue-syndrome.htm

GG

PS I believe About.com is related to New York Times. FYI

 

[ukxmrv]

This document is a bit old but some of the quotes and references towards the end may be still useful

http://www.meactionuk.org.uk/Additional_considerations_re_MECFS_and_FM.htm