Onset Patterns of Chronic Fatigue Syndrome and Myalgic Encephalomyelitis: A Mixed Method Approach

Abstract:

The onset of Chronic fatigue syndrome (CFS) and Myalgic Encephalomyelitis (ME) is considered a key area of inquiry. Case criteria for ME and CFS and much of the academic literature suggest that patients typically experience one of two possible onset patterns: sudden or gradual. The current study provided an in-depth investigation of ME and CFS onset in order to provide insight into early symptoms, onset duration, and the progression of functional disability. We collected qualitative descriptive data to gain a rich description of illness onset from the patients’ point of view.

Overall, qualitative findings revealed detailed descriptions of ME and CFS onset experiences. Major themes that emerged from the data included: onset/illness progression patterns, illness causes, methods of adapting and coping, hardworking and active lives prior to onset, healthy lives prior to onset, prior health problems, comorbid health conditions, emotional responses to onset, exertional effects, the illness as life limiting, stress, traumatic experiences, lack of support, support, and treatment limitations. A closer examination of the onset/illness progression patterns that emerged from the data provided evidence that individuals with ME and CFS experience complex onset patterns.

Furthermore, the study findings suggest that the method of categorizing individuals into sudden versus gradual onset groups fails to capture the more nuanced and varied onset experiences. Prospective research studies that capture the onset period as it is developing could lead to improvements in the way we define and assess ME and CFS onset, and may also lead to methods for early detection, prevention, and individualized treatment approaches.

Source: Meredyth Anne Evans & Leonard A. Jason. Onset Patterns of Chronic Fatigue Syndrome and Myalgic Encephalomyelitis: A Mixed Method Approach. Res Chron Dis (2018) 2(1), 001–0030 (Full article)

A twin study of cognitive function in chronic fatigue syndrome: the effects of sudden illness onset

Abstract:

Variable reports of neuropsychological deficits in individuals with chronic fatigue syndrome (CFS) may, in part, be attributable to methodological limitations. In this study, these limitations were addressed by controlling for genetic and environmental influences and by assessing the effects of comorbid depression and mode of illness onset. Specifically, the researchers conducted a co-twin control study of 22 pairs of monozygotic twins, in which 1 twin met strict criteria for CFS and the co-twin was healthy.

Twins underwent a structured psychiatric interview and comprehensive neuropsychological assessment evaluating 6 cognitive domains. Results indicated that twin groups had similar intellectual and visual memory functioning, but fatigued twins exhibited decreases in motor functions (p = .05), speed of information processing (p = .02), verbal memory (p = .02), and executive functioning (p = .01). Major depression did not affect neuropsychological functioning among fatigued twins, although twins with sudden illness onset demonstrated slowed information processing compared with those with gradual onset (p = .01).

Sudden onset CFS was associated with reduced speed of information processing. If confirmed, these findings suggest the need to distinguish illness onset in future CFS studies and may have implications for treatment, cognitive rehabilitation, and disability determination.

 

Source: Claypoole KH, Noonan C, Mahurin RK, Goldberg J, Erickson T, Buchwald D. A twin study of cognitive function in chronic fatigue syndrome: the effects of sudden illness onset. Neuropsychology. 2007 Jul;21(4):507-13. https://www.ncbi.nlm.nih.gov/pubmed/17605583

 

Gene expression profiling in the chronic fatigue syndrome

Fatigue is a symptom found in many conditions of disease and illness. Although, unfrequently recognized by the medical profession, it is often of major importance for the patients. Chronic fatigue was reported by 5.9% of the Swedish population in a large telephone-based interview with 31 406 individuals in the Swedish twin registry (STR) [1]. The fatigue had lasted for more than 6 months and caused impairment, e.g. >25% reduction of working capacity. When at least four of eight criteria included in the current definition of chronic fatigue syndrome (CFS) [2] was added 2.4% reported that they suffered from a CFS-like illness.

This costly condition is still an intriguing issue for researchers and clinicians, and ambiguities in the definition have recently been focused upon [3, 4]. An empirical test of the definition was performed with data from the STR where five subgroups were identified: ‘CFS-like’, ‘residual’, ‘rheumatic’, ‘depressive’ and ‘acute physical syndrome’ [5].

We wanted to identify genes in peripheral blood mononuclear cells (PBMCs), which may play an important role in the pathogenesis and diagnostics of CFS, using microarray technology. PBMCs can serve as indicators of illness processes occurring in different parts of the human body. Patients with CFS from a clinic of infectious diseases at a university hospital were stratified according to the STR study findings [5] to sex, illness classification (ICD-10), illness onset type, illness duration and number of symptoms (Table 1).

You can read the rest of this article here: http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2005.01548.x/full

 

Source: Gräns H, Nilsson P, Evengard B. Gene expression profiling in the chronic fatigue syndrome. J Intern Med. 2005 Oct;258(4):388-90. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2005.01548.x/full (Full article)

 

Spinal fluid abnormalities in patients with chronic fatigue syndrome

Abstract:

Arguments exist as to the cause of chronic fatigue syndrome (CFS). Some think that it is an example of symptom amplification indicative of functional or psychogenic illness, while our group thinks that some CFS patients may have brain dysfunction. To further pursue our encephalopathy hypothesis, we did spinal taps on 31 women and 13 men fulfilling the 1994 case definition for CFS and on 8 women and 5 men serving as healthy controls.

Our outcome measures were white blood cell count, protein concentration in spinal fluid, and cytokines detectable in spinal fluid. We found that significantly more CFS patients had elevations in either protein levels or number of cells than healthy controls (30 versus 0%), and 13 CFS patients had protein levels and cell numbers that were higher than laboratory norms; patients with abnormal fluid had a lower rate of having comorbid depression than those with normal fluid.

In addition, of the 11 cytokines detectable in spinal fluid, (i) levels of granulocyte-macrophage colony-stimulating factor were lower in patients than controls, (ii) levels of interleukin-8 (IL-8) were higher in patients with sudden, influenza-like onset than in patients with gradual onset or in controls, and (iii) IL-10 levels were higher in the patients with abnormal spinal fluids than in those with normal fluid or controls.

The results support two hypotheses: that some CFS patients have a neurological abnormality that may contribute to the clinical picture of the illness and that immune dysregulation within the central nervous system may be involved in this process.

 

Source: Natelson BH, Weaver SA, Tseng CL, Ottenweller JE. Spinal fluid abnormalities in patients with chronic fatigue syndrome. Clin Diagn Lab Immunol. 2005 Jan;12(1):52-5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC540195/ (Full article)