Premorbid Functioning, Welfare Issues and Ethics in Chronic Fatigue Syndrome

2003 ◽  
Vol 11 (3) ◽  
pp. 312-318
Author(s):  
Chris Cantor ◽  
Kerryn Neulinger

Objective: To assess former activity levels in chronic fatigue syndrome (CFS) subjects, identify differentiating variables and discuss ethical issues arising. Method: File review of 91 CFS patients from a private psychiatric practice, presenting multiple case reports, with limited case comparison data. Results: The CFS subjects appeared formerly more athletically inclined than controls. Other helpful differentiating variables included exercise intolerance, excessive need for sleep, hopefulness and subjective memory problems. Conclusions: Former exercise and other achievement levels warrant systematic research study and consideration in the assessment of CFS patients. Omissions of consideration of premorbid functioning in medicolegal evaluations raise ethical concerns.

2021 ◽  
Vol 8 ◽  
pp. 204993612110093
Author(s):  
Sonia Poenaru ◽  
Sara J. Abdallah ◽  
Vicente Corrales-Medina ◽  
Juthaporn Cowan

Coronavirus disease 2019 (COVID-19) is a viral infection which can cause a variety of respiratory, gastrointestinal, and vascular symptoms. The acute illness phase generally lasts no more than 2–3 weeks. However, there is increasing evidence that a proportion of COVID-19 patients experience a prolonged convalescence and continue to have symptoms lasting several months after the initial infection. A variety of chronic symptoms have been reported including fatigue, dyspnea, myalgia, exercise intolerance, sleep disturbances, difficulty concentrating, anxiety, fever, headache, malaise, and vertigo. These symptoms are similar to those seen in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a chronic multi-system illness characterized by profound fatigue, sleep disturbances, neurocognitive changes, orthostatic intolerance, and post-exertional malaise. ME/CFS symptoms are exacerbated by exercise or stress and occur in the absence of any significant clinical or laboratory findings. The pathology of ME/CFS is not known: it is thought to be multifactorial, resulting from the dysregulation of multiple systems in response to a particular trigger. Although not exclusively considered a post-infectious entity, ME/CFS has been associated with several infectious agents including Epstein–Barr Virus, Q fever, influenza, and other coronaviruses. There are important similarities between post-acute COVID-19 symptoms and ME/CFS. However, there is currently insufficient evidence to establish COVID-19 as an infectious trigger for ME/CFS. Further research is required to determine the natural history of this condition, as well as to define risk factors, prevalence, and possible interventional strategies.


1999 ◽  
Vol 97 (5) ◽  
pp. 603-608 ◽  
Author(s):  
Kevin K. MCCULLY ◽  
Benjamin H. NATELSON

The purpose of this study was to determine if chronic fatigue syndrome (CFS) is associated with reduced oxygen delivery to muscles. Patients with CFS according to CDC (Center for Disease Control) criteria (n = 20) were compared with normal sedentary subjects (n = 12). Muscle oxygen delivery was measured as the rate of post-exercise and post-ischaemia oxygen-haem resaturation. Oxygen-haem resaturation was measured in the medial gastrocnemius muscle using continuous-wavelength near-IR spectroscopy. Phosphocreatine resynthesis was measured simultaneously using 31P magnetic resonance spectroscopy. The time constant of oxygen delivery was significantly reduced in CFS patients after exercise (46.5±16 s; mean±S.D.) compared with that in controls (29.4±6.9 s). The time constant of oxygen delivery was also reduced (20.0±12 s) compared with controls (12.0±2.8 s) after cuff ischaemia. Oxidative metabolism was also reduced by 20% in CFS patients, and a significant correlation was found between oxidative metabolism and recovery of oxygen delivery. In conclusion, oxygen delivery was reduced in CFS patients compared with that in sedentary controls. This result is consistent with previous studies showing abnormal autonomic control of blood flow. Reduced oxidative delivery in CFS patients could be specifically related to CFS, or could be a non-specific effect of reduced activity levels in these patients. While these results suggest that reduced oxygen delivery could result in reduced oxidative metabolism and muscle fatigue, further studies will be needed to address this issue.


Diagnostics ◽  
2019 ◽  
Vol 9 (2) ◽  
pp. 41 ◽  
Author(s):  
Nacul ◽  
de Barros ◽  
Kingdon ◽  
Cliff ◽  
Clark ◽  
...  

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disease presenting with extreme fatigue, post-exertional malaise, and other symptoms. In the absence of a diagnostic biomarker, ME/CFS is diagnosed clinically, although laboratory tests are routinely used to exclude alternative diagnoses. In this analytical cross-sectional study, we aimed to explore potential haematological and biochemical markers for ME/CFS, and disease severity. We reviewed laboratory test results from 272 people with ME/CFS and 136 healthy controls participating in the UK ME/CFS Biobank (UKMEB). After corrections for multiple comparisons, most results were within the normal range, but people with severe ME/CFS presented with lower median values (p < 0.001) of serum creatine kinase (CK; median = 54 U/L), compared to healthy controls (HCs; median = 101.5 U/L) and non-severe ME/CFS (median = 84 U/L). The differences in CK concentrations persisted after adjusting for sex, age, body mass index, muscle mass, disease duration, and activity levels (odds ratio (OR) for being a severe case = 0.05 (95% confidence interval (CI) = 0.02–0.15) compared to controls, and OR = 0.16 (95% CI = 0.07–0.40), compared to mild cases). This is the first report that serum CK concentrations are markedly reduced in severe ME/CFS, and these results suggest that serum CK merits further investigation as a biomarker for severe ME/CFS.


2021 ◽  
Vol 6 (3) ◽  
pp. 472-478
Author(s):  
Adwitiya Ray ◽  
Neharika Saini ◽  
Ravi Parkash

Coronavirus disease 2019 (COVID-19) is a viral infection that causes various respiratory, gastrointestinal, and vascular symptoms. The acute illness phase lasts for about 2-3 weeks. However, there is increasing evidence that a percentage of COVID-19 patients continue to experience long-lasting symptoms characterized by fatigue, dyspnea, myalgia, exercise intolerance, and sleep disturbances, difficulty concentrating, anxiety, fever, headache, malaise, and vertigo. Similar symptoms are reported by patients who having myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS). ME/CFS pathology is not known: it is thought to be multifactorial, resulting from the dysregulation of multiple systems in response to a particular trigger. There is a resemblance between post-acute COVID-19 symptoms and ME/CFS. However, at present, there is inadequate evidence to establish COVID-19 as an infectious trigger for ME/CFS. Further research is required to determine the natural history of this condition, as well as to define risk factors, prevalence, and possible interventional strategies. Keywords: chronic fatigue syndrome, COVID-19, human coronavirus, myalgic encephalomyelitis, post-infectious fatigue, review.


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Klaus J. Wirth ◽  
Carmen Scheibenbogen

AbstractChronic Fatigue Syndrome or Myalgic Encephaloymelitis (ME/CFS) is a frequent debilitating disease with an enigmatic etiology. The finding of autoantibodies against ß2-adrenergic receptors (ß2AdR) prompted us to hypothesize that ß2AdR dysfunction is of critical importance in the pathophysiology of ME/CFS. Our hypothesis published previously considers ME/CFS as a disease caused by a dysfunctional autonomic nervous system (ANS) system: sympathetic overactivity in the presence of vascular dysregulation by ß2AdR dysfunction causes predominance of vasoconstrictor influences in brain and skeletal muscles, which in the latter is opposed by the metabolically stimulated release of endogenous vasodilators (functional sympatholysis). An enigmatic bioenergetic disturbance in skeletal muscle strongly contributes to this release. Excessive generation of these vasodilators with algesic properties and spillover into the systemic circulation could explain hypovolemia, suppression of renin (paradoxon) and the enigmatic symptoms. In this hypothesis paper the mechanisms underlying the energetic disturbance in muscles will be explained and merged with the first hypothesis. The key information is that ß2AdR also stimulates the Na+/K+-ATPase in skeletal muscles. Appropriate muscular perfusion as well as function of the Na+/K+-ATPase determine muscle fatigability. We presume that dysfunction of the ß2AdR also leads to an insufficient stimulation of the Na+/K+-ATPase causing sodium overload which reverses the transport direction of the sodium-calcium exchanger (NCX) to import calcium instead of exporting it as is also known from the ischemia–reperfusion paradigm. The ensuing calcium overload affects the mitochondria, cytoplasmatic metabolism and the endothelium which further worsens the energetic situation (vicious circle) to explain postexertional malaise, exercise intolerance and chronification. Reduced Na+/K+-ATPase activity is not the only cause for cellular sodium loading. In poor energetic situations increased proton production raises intracellular sodium via sodium-proton-exchanger subtype-1 (NHE1), the most important proton-extruder in skeletal muscle. Finally, sodium overload is due to diminished sodium outward transport and enhanced cellular sodium loading. As soon as this disturbance would have occurred in a severe manner the threshold for re-induction would be strongly lowered, mainly due to an upregulated NHE1, so that it could repeat at low levels of exercise, even by activities of everyday life, re-inducing mitochondrial, metabolic and vascular dysfunction to perpetuate the disease.


Healthcare ◽  
2020 ◽  
Vol 8 (3) ◽  
pp. 211 ◽  
Author(s):  
Nigel Speight

A current problem regarding Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is the large proportion of doctors that are either not trained or refuse to recognize ME/CFS as a genuine clinical entity, and as a result do not diagnose it. An additional problem is that most of the clinical and research studies currently available on ME are focused on patients who are ambulant and able to attend clinics and there is very limited data on patients who are very severe (housebound or bedbound), despite the fact that they constitute an estimated 25% of all ME/CFS cases. This author has personal experience of managing and advising on numerous cases of severe paediatric ME, and offers a series of case reports of individual cases as a means of illustrating various points regarding clinical presentation, together with general principles of appropriate management.


2011 ◽  
Vol 500 ◽  
pp. e14
Author(s):  
Jo Nijs ◽  
Mira Meeus ◽  
Jessica Van Oosterwijck ◽  
Kelly Ickmans ◽  
Inge van Eupen ◽  
...  

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