Tag: fibromyalgia

Finding benefit in stressful uncertain circumstances: relations to social support and stigma among women with unexplained illnesses

Abstract:

Living with a chronic illness can be challenging, but the ability to derive benefits and grow from this experience may enhance well-being. However, the possibility of obtaining such benefits may be dependent on the levels of stigmatization and lack of social support experienced by an individual as a result of the illness.

Chronic fatigue syndrome (CFS) and fibromyalgia are chronic conditions that remain largely unexplained and those with these conditions must often contend with stigma and skepticism from others. Individuals with CFS/fibromyalgia often display stress-related biological alterations and the experience of stressful life events has been associated with illness development.

The present study demonstrated that women with CFS/fibromyalgia (n = 40) as well as community participants who were depressed/anxious (n = 37), reported higher stigma levels than healthy women (n = 33). Moreover, women with CFS/fibromyalgia and those with depression/anxiety also reported greater levels of stigma than women with a chronic yet more widely accepted condition (n = 35; rheumatoid arthritis, osteoarthritis and multiple sclerosis).

Secrecy related to stigma among those with CFS/fibromyalgia declined with increased social support, but this was not apparent among those with other chronic conditions. In addition, posttraumatic growth was lower among women with CFS/fibromyalgia compared to those with other chronic conditions.

Qualitative analysis examining both negative impacts and positive changes stemming from illness experience revealed many similarities between women with CFS/fibromyalgia and those with other chronic conditions, including elevated appreciation for life, personal growth and compassion for others. However, women with CFS/fibromyalgia tended to report less positive change regarding interpersonal relationships compared to women with other chronic conditions.

In general, unexplained illnesses were also accompanied by stigmatization which might ultimately contribute to women’s lower ability to derive positive growth from their illness experience.

 

Source: McInnis OA, McQuaid RJ, Bombay A, Matheson K, Anisman H. Finding benefit in stressful uncertain circumstances: relations to social support and stigma among women with unexplained illnesses. Stress. 2015;18(2):169-77. doi: 10.3109/10253890.2014.1001975. Epub 2015 Jan 23. https://www.ncbi.nlm.nih.gov/pubmed/25544022

 

Chronic fatigue syndrome and non-celiac gluten sensitivity. Association or cause?

To the editor:

In their letter to the editor Response to: Fibromyalgia and chronic fatigue caused by non-celiac gluten sensitivity, Qanneta et al. pose a conceptual problem between the association of chronic fatigue syndrome (CFS) with non-celiac gluten sensitivity (SGNC) from the prevalent conception of considering chronic fatigue as a distinct disease. From this perspective, being chronic fatigue the central disease associated with other processes, they consider NCGS as a comorbid condition and not as an underlying cause.

You can read the rest of this letter here: http://www.reumatologiaclinica.org/en/chronic-fatigue-syndrome-non-celiac-gluten/articulo/S2173574314001762/

Comment on

 

Source: Isasi Zaragozá C. Chronic fatigue syndrome and non-celiac gluten sensitivity. Association or cause?Reumatol Clin. 2015 May-Jun;11(3):184. doi: 10.1016/j.reuma.2014.10.010. Epub 2014 Dec 10. http://www.reumatologiaclinica.org/en/chronic-fatigue-syndrome-non-celiac-gluten/articulo/S2173574314001762/ (Full article)

 

Response to: fibromyalgia and chronic fatigue syndrome caused by non-celiac gluten sensitivity

Dear Editor:

We have closely read the article published by Isasi et al.1 in Reumatologia Clínica presenting a case of fibromyalgia (FM) and chronic fatigue syndrome (CFS) caused by non-celiac sensitivity to gluten (NGCD). We would like to comment our experience with this attractive topic regarding patients with FM/CFS, which I hope will contribute to an improved knowledge of this association. The authors have reasonably ruled out celiac disease (CD) and have hypothesized that NGCD is the cause of FM and CFS in their patient; upon complete remission (CR) of symptoms, both digestive and musculoskeletal, with a gluten-free diet (GFD).

You can read the rest of this letter here: http://www.reumatologiaclinica.org/en/response-to-fibromyalgia-chronic-fatigue/articulo/S217357431400166X/

 

Source: Qanneta R, Fontova R, Castel A. Response to: fibromyalgia and chronic fatigue syndrome caused by non-celiac gluten sensitivity. Reumatol Clin. 2015 May-Jun;11(3):185. doi: 10.1016/j.reuma.2014.09.008. Epub 2014 Nov 7. http://www.reumatologiaclinica.org/en/response-to-fibromyalgia-chronic-fatigue/articulo/S217357431400166X/ (Full article)

Sympathetic nervous system dysfunction in fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, and interstitial cystitis: a review of case-control studies

Abstract:

BACKGROUND: Fibromyalgia often coexists and overlaps with other syndromes such as chronic fatigue, irritable bowel syndrome, and interstitial cystitis. Chronic stress has been implicated in the pathogenesis of these illnesses. The sympathetic nervous system is a key element of the stress response system. Sympathetic dysfunction has been reported in these syndromes, raising the possibility that such dysautonomia could be their common clustering underlying pathogenesis.

OBJECTIVE: The objective of this study was to carry out a review of all published comparative case-control studies investigating sympathetic nervous system performance in fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, and interstitial cystitis.

METHODS: Online databases PubMed and EMBASE were accessed using the following key words: autonomic (OR) sympathetic (AND) fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, and interstitial cystitis. All entries up to December 10th 2012 were reviewed by 2 independent investigators searching for case-control studies in humans. The Method for Evaluating Research and Guidelines Evidence adapted to the Scottish Intercollegiate Guidelines Network was used to rank the level of evidence contained in the selected articles.

RESULTS: A total of 196 articles are included in this review. The most often used methods to assess sympathetic functionality were heart rate variability analysis, sympathetic skin response, tilt table testing, and genetic studies. The majority of studies (65%) described sympathetic nervous system predominance in these overlapping syndromes. In contrast, 7% of the studies found parasympathetic predominance.

CONCLUSIONS: This review demonstrates that sympathetic nervous system predominance is common in fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, and interstitial cystitis. This concordance raises the possibility that sympathetic dysfunction could be their common underlying pathogenesis that brings on overlapping clinical features. The recognition of sympathetic predominance in these 4 syndromes may have potential clinical implications. It may be worth exploring the use of nonpharmacological measures as well as drug therapies aimed to regain autonomic balance.

 

Source: Martínez-Martínez LA, Mora T, Vargas A, Fuentes-Iniestra M, Martínez-Lavín M. Sympathetic nervous system dysfunction in fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, and interstitial cystitis: a review of case-control studies. J Clin Rheumatol. 2014 Apr;20(3):146-50. doi: 10.1097/RHU.0000000000000089. https://www.ncbi.nlm.nih.gov/pubmed/24662556

 

Conditions, controversies and contradictions between Central Sensitivity Syndrome and Depressive Disorders

Abstract:

We present a description of the Central Sensitivity Syndrome (CSS) and some of its main components such as Multiple Chemical Sensitivity Syndrome, Chronic Fatigue Syndrome and Fibromyalgia. We review the changes in pain perception, describing the physiology and pathophysiology of the painful experience from the medulla horn to the CNS. We explain the theory of central sensitization as the basis to the syndrome. We refer to the differences between fibromyalgia and depressive disorders, is spite of their frequent presentation in comorbidity.

We state the main clinical and neurobiological differences. We point out the main psychoneuroimmunoendocrinologic differences such as adrenal activity (hypoactivity vs. hyperactivity, DST hypersuppressive response vs. DST non suppression, hypersensitivity of central glucocorticoid receptors vs. desensitization of these, among others), thyroid (probable reverse T3 vs. flat stimuli TSH response curve) and growth hormone secretion (probable increase vs. disruption of normal circadian rhythm) that makes CSS resemble PTSD. We describe differential changes in sleep patterns (alpha-delta intrusion vs. altered sleep time, REM latency, and stage 3/4) and immunological disturbances almost opposite in each pathological entity. We finally argue which medical specialty should treat these complex syndromes.

 

Source: Maresca T, Covini E, Mato AM. Conditions, controversies and contradictions between Central Sensitivity Syndrome and Depressive Disorders.Vertex. 2013 Sep-Oct;24(111):373-91. [Article in Spanish] https://www.ncbi.nlm.nih.gov/pubmed/24312923

 

Brain dysfunction as one cause of CFS symptoms including difficulty with attention and concentration

Abstract:

We have been able to reduce substantially patient pool heterogeneity by identifying phenotypic markers that allow the researcher to stratify chronic fatigue syndrome (CFS) patients into subgroups. To date, we have shown that stratifying based on the presence or absence of comorbid psychiatric diagnosis leads to a group with evidence of neurological dysfunction across a number of spheres.

We have also found that stratifying based on the presence or absence of comorbid fibromyalgia leads to information that would not have been found on analyzing the entire, unstratified patient group. Objective evidence of orthostatic intolerance (OI) may be another important variable for stratification and may define a group with episodic cerebral hypoxia leading to symptoms.

We hope that this review will encourage other researchers to collect data on discrete phenotypes in CFS to allow this work to continue more broadly. Finding subgroups of CFS suggests different underlying pathophysiological processes responsible for the symptoms seen. Understanding those processes is the first step toward developing discrete treatments for each.

 

Source: Natelson BH. Brain dysfunction as one cause of CFS symptoms including difficulty with attention and concentration. Front Physiol. 2013 May 20;4:109. doi: 10.3389/fphys.2013.00109. ECollection 2013. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3657628/ (Full article)

 

Fear of movement and avoidance behaviour toward physical activity in chronic-fatigue syndrome and fibromyalgia: state of the art and implications for clinical practice

Abstract:

Severe exacerbation of symptoms following physical activity is characteristic for chronic-fatigue syndrome (CFS) and fibromyalgia (FM). These exacerbations make it understandable for people with CFS and FM to develop fear of performing body movement or physical activity and consequently avoidance behaviour toward physical activity. The aims of this article were to review what measures are available for measuring fear of movement and avoidance behaviour, the prevalence fear of movement and avoidance behaviour toward physical activity and the therapeutic options with fear of movement and avoidance behaviour toward physical activity in patients with CFS and FM.

The review revealed that fear of movement and avoidance behaviour toward physical activity is highly prevalent in both the CFS and FM population, and it is related to various clinical characteristics of CFS and FM, including symptom severity and self-reported quality of life and disability. It appears to be crucial for treatment (success) to identify CFS and FM patients displaying fear of movement and avoidance behaviour toward physical activity.

Individually tailored cognitive behavioural therapy plus exercise training, depending on the patient’s classification as avoiding or persisting, appears to be the most promising strategy for treating fear of movement and avoidance behaviour toward physical activity in patients with CFS and FM.

Comment in: Fear of movement and avoidance behaviour toward physical activity in chronic-fatigue syndrome and fibromyalgia: state of the art and implications for clinical practice. [Clin Rheumatol. 2013]

 

Source: Nijs J, Roussel N, Van Oosterwijck J, De Kooning M, Ickmans K, Struyf F, Meeus M, Lundberg M. Fear of movement and avoidance behaviour toward physical activity in chronic-fatigue syndrome and fibromyalgia: state of the art and implications for clinical practice. Clin Rheumatol. 2013 Aug;32(8):1121-9. doi: 10.1007/s10067-013-2277-4. Epub 2013 May 3. https://www.ncbi.nlm.nih.gov/pubmed/23639990

 

Does acetaminophen activate endogenous pain inhibition in chronic fatigue syndrome/fibromyalgia and rheumatoid arthritis? A double-blind randomized controlled cross-over trial

Abstract:

BACKGROUND: Although enhanced temporal summation (TS) and conditioned pain modulation (CPM), as characteristic for central sensitization, has been proved to be impaired in different chronic pain populations, the exact nature is still unknown.

OBJECTIVES: We examined differences in TS and CPM in 2 chronic pain populations, patients with both chronic fatigue syndrome (CFS) and comorbid fibromyalgia (FM) and patients with rheumatoid arthritis (RA), and in sedentary, healthy controls, and evaluated whether activation of serotonergic descending pathways by acetaminophen improves central pain processing.

STUDY DESIGN: Double-blind randomized controlled trial with cross-over design.

METHODS: Fifty-three women (19 CFS/FM patients, 16 RA patients, and 18 healthy women) were randomly allocated to the experimental group (1 g acetaminophen) or the placebo group (1 g dextrose). Participants underwent an assessment of endogenous pain inhibition, consisting of an evaluation of temporal summation with and without conditioned pain modulation (CPM). Seven days later groups were crossed-over. Patients and assessors were blinded for the allocation.

RESULTS: After intake of acetaminophen, pain thresholds increased slightly in CFS/FM patients, and decreased in the RA and the control group. Temporal summation was reduced in the 3 groups and CPM at the shoulder was better overall, however only statistically significant for the RA group. Healthy controls showed improved CPM for both finger and shoulder after acetaminophen, although not significant.

LIMITATIONS: The influence of acetaminophen on pain processing is inconsistent, especially in the patient groups examined.

CONCLUSION: This is the first study comparing the influence of acetaminophen on central pain processing in healthy controls and patients with CFS/FM and RA. It seems that CFS/FM patients present more central pain processing abnormalities than RA patients, and that acetaminophen may have a limited positive effect on central pain inhibition, but other contributors have to be identified and evaluated.

 

Source: Meeus M, Ickmans K, Struyf F, Hermans L, Van Noesel K, Oderkerk J, Declerck LS, Moorkens G, Hans G, Grosemans S, Nijs J. Does acetaminophen activate endogenous pain inhibition in chronic fatigue syndrome/fibromyalgia and rheumatoid arthritis? A double-blind randomized controlled cross-over trial. Pain Physician. 2013 Mar-Apr;16(2):E61-70. http://www.painphysicianjournal.com/linkout?issn=1533-3159&vol=16&page=E61 (Full article available as PDF file)

 

Chronic fatigue syndrome: 3 cases and a discussion of the natural history of attention-deficit/hyperactivity disorder

Abstract:

Fatigue is commonly reported in the primary care setting; however, its cause is often unclear. This article presents 3 cases involving patients with chronic fatigue syndrome who responded poorly to treatment. After clinical evaluation, all patients were found to meet criteria for attention-deficit/hyperactivity disorder (ADHD) and underwent a standard regimen of a psychostimulant medication.

After treatment with psychostimulants, the 3 patients reported improved symptoms of fatigue and pain, and cognitive and core ADHD symptoms. These cases suggest that ADHD and chronic fatigue syndrome (and possibly fibromyalgia) share a common underlying mechanism. This article presents a model suggesting that over time, ADHD (predominantly inattentive type) develops into a syndrome of chronic fatigue and pain. These cases indicate that fatigue may be an important presenting symptom of adult ADHD. These cases also suggest the need for additional research to determine the prevalence of ADHD in patients who present with fatigue, and, in those meeting criteria for ADHD, the responsiveness of fatigue to psychostimulant treatment.

 

Source: Young JL. Chronic fatigue syndrome: 3 cases and a discussion of the natural history of attention-deficit/hyperactivity disorder. Postgrad Med. 2013 Jan;125(1):162-8. doi: 10.3810/pgm.2013.01.2631. https://www.ncbi.nlm.nih.gov/pubmed/23391682

 

A Brief Historic Overview of Clinical Disorders Associated with Tryptophan: The Relevance to Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM)

Abstract:

Last century there was a short burst of interest in the tryptophan related disorders of pellagra and related abnormalities that are usually presented in infancy.1,2 Nutritional physiologists recognized that a severe human dietary deficiency of either tryptophan or the B group vitamins could result in central nervous system (CNS) sequelae such as ataxia, cognitive dysfunction and dysphoria, accompanied by skin hyperpigmentation.3,4 The current paper will focus on the emerging role of tryptophan in chronic fatigue syndrome (CFS) and fibromyalgia (FM).

 

Source: Blankfield A. A Brief Historic Overview of Clinical Disorders Associated with Tryptophan: The Relevance to Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM). Int J Tryptophan Res. 2012;5:27-32. doi: 10.4137/IJTR.S10085. Epub 2012 Sep 17. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3460668/ (Full article)