What are fibromyalgia and Chronic Fatigue Syndrome (ME/CFS): Similarities and Differences?

The primary presenting complaint in fibromyalgia is muscle pain, and the primary reason chronic fatigue syndrome (CFS/ME) patients seek treatment, is life altering fatigue and an overwhelming feeling of illness. Though in neither case, is this where symptoms stop.

The diagnostic criteria for fibromyalgia (FM), here,  and  chronic fatigue syndrome (CFS/ME), here,  are very specific to each disorder and are dissimilar in several respects. 

Fibromyalgia and CFS/ME (as we refer to in our book,  chronic fatigue immunodysfunction, CFID) do share some common comorbid conditions, and both are thought to have central nervous system disruption, however, disruptions are different between the two, and newer research is showing a stronger connection to viral, infectious, and immune overload in CFS/ME than seen in FM, though immune problems have been established in fibromyalgia too. (Behm, 2012). These problems are complex and researchers are still weeding through research results which allow them to make new hypothesis and,, hopefully, move the research in a more distinct direction.  Learn more about fibromyalgia comorbid conditions here 

 and CFS.ME here. 

Fibromyalgia and CFS/ME also share autonomic effects such as loss of heart rate variability and POTS, however, in a study done by Light, et al (2011) it was reported “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 [an immune modulator]. The smaller subgroup contained most of the patients with CFS with orthostatic intolerance, showed no post-exercise increases in any gene and was defined by decreases in mRNA for α-2A. FM-only patients can be identified by baseline increases in three genes. Post-exercise increases for four genes meet published criteria as an objective biomarker for CFS and could be useful in guiding treatment selection for different subgroups.”

This leads us the discussion on exercise. Study after study indicates that exercise worsens the symptoms of CFS/ME, yet low impact exercise is one of the treatment protocols for helping improve body-wide pain in FM. I propose this could be due to a higher incidence of orthostatic intolerance in CFS/ME secondary to an underlying viral, infectious, or immune causation. There are studies indicating that FM patients symptoms are also worsened by exercise, but I propose this is due to the presence of untreated myofascial pain syndrome, where the muscles become weak from the presence of myofascial trigger points, learn more here, and primary deregulation of the HPA axis.

   

Repeated studies of FM suggest a disruption of the hypothalamus-pituitary-adrenal axis and oxidative stress, which could result in secondary immunologic deregulation. In contrast, It is quite possible immunologic deregulation in CFS/ME is primary and results from a viral or infectious insult. This is where the differences are exposed.  

Myofascial pain syndrome is thought to overlap in both FM and CFS/ME, which massacres research reliability. Researchers are currently studying muscle tissue irregularities in both FM and CFS/ME. It is my greatest hope that they are considering the presence of myofascial pain syndrome, for without this consideration and examination for the presence of myofascial trigger points; study results once again become skewed.  We discuss this and other considerations at length in our book (Cooper and Miller, 2010).

There are specific biological differences between FM and CFS/ME. Also interesting is a study done by Castro-Marrero et al., who suggest their data leads to “the hypothesis that mitochondrial dysfunction-dependent events could be a marker of differentiation between CFS and FM indicating the mitochondria as a new potential therapeutic target for these conditions” Both are considered neuroendocrineimmune disorders, as is Lyme’s disease, Gulf War Syndrome, Lupus, and others. Though they fall under the same umbrella, they are different.

We explain the differences and the similarities, why they are confused and the importance in having the right diagnosis in Chapter One, “All about Fibromyalgia, Chronic Fatigue Immunodysfunction—The Muster to Master, and Chronic Myofascial Pain—Nerve to Muscle, and Double Cross". here 

All blogs, posts and answers are not meant to replace medical advice.

Resources:

Bardal E, Olsen T, Ettema G et al. 2013. Metabolic rate, cardiac response, and aerobic capacity in fibromyalgia: a case-control study. Scand J Rheumatol. [Mar 26 Epub ahead of print].

Behm FG, Gavin IM, Karpenko O, Lindgren V, Gaitonde S, Gashkoff PA, Gillis BS. Unique immunologic patterns in fibromyalgia. BMC Clin Pathol. 2012 Dec 17;12(1):25. doi: 10.1186/1472-6890-12-25.

Brewer JH, Thrasher JD, Straus DC, Madison RA, Hooper D.. Detection of Mycotoxins in Patients with Chronic Fatigue Syndrome. Toxins (Basel). 2013 Apr 11;5(4):605-17.

Castro-Marrero J, Cordero MD, Saez-Francas N, Jimenez-Gutiérrez C, Aguilar-Montilla FJ, Aliste L, Alegre-Martin J. Could mitochondrial dysfunction be a differentiating marker between Chronic Fatigue Syndrome and Fibromyalgia? Antioxid Redox Signal. 2013 Apr 22. [Epub ahead of print]

Cooper, C and Miller, J. (2010). Integrative Therapies for Fibromyalgia, Chronic Fatigue Syndrome, and Myofascial Pain: The Mind-Body Connection. Vermont: Healing Arts Press.

Ge HY, Nie H, Graven-Nielsen T, Danneskiold-Samsøe B, Arendt-Nielsen L. Descending pain modulation and its interaction with peripheral sensitization following sustained isometric muscle contraction in fibromyalgia. Eur J Pain. 2012 Feb;16(2):196-203.

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