scholarly journals Understanding Muscle Dysfunction in Chronic Fatigue Syndrome

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Gina Rutherford ◽  
Philip Manning ◽  
Julia L. Newton

Introduction. Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a debilitating disorder of unknown aetiology, characterised by severe disabling fatigue in the absence of alternative diagnosis. Historically, there has been a tendency to draw psychological explanations for the origin of fatigue; however, this model is at odds with findings that fatigue and accompanying symptoms may be explained by central and peripheral pathophysiological mechanisms, including effects of the immune, oxidative, mitochondrial, and neuronal pathways. For example, patient descriptions of their fatigue regularly cite difficulty in maintaining muscle activity due to perceived lack of energy. This narrative review examined the literature for evidence of biochemical dysfunction in CFS/ME at the skeletal muscle level.Methods.Literature was examined following searches of PUB MED, MEDLINE, and Google Scholar, using key words such as CFS/ME, immune, autoimmune, mitochondria, muscle, and acidosis.Results. Studies show evidence for skeletal muscle biochemical abnormality in CFS/ME patients, particularly in relation to bioenergetic dysfunction.Discussion.Bioenergetic muscle dysfunction is evident in CFS/ME, with a tendency towards an overutilisation of the lactate dehydrogenase pathway following low-level exercise, in addition to slowed acid clearance after exercise. Potentially, these abnormalities may lead to the perception of severe fatigue in CFS/ME.

1995 ◽  
Vol 4 (4) ◽  
pp. 751-754 ◽  
Author(s):  
Chunfang Zhang ◽  
Alessandra Baumer ◽  
Ian R. Mackay ◽  
Anthony W. Linnane ◽  
Phillip Nagley

2011 ◽  
Vol 26 (S2) ◽  
pp. 1574-1574
Author(s):  
N. Sáez Francàs ◽  
J. Alegre ◽  
N. Calvo Piñero ◽  
J.A. Ramos Quiroga ◽  
E. Ruiz ◽  
...  

IntroductionChronic Fatigue Syndrome (CFS) is characterized by severe fatigue associated with pain, sleep disturbance, attentional impairment and headaches. Evidence points towards a prominent role for Central Nervous System in its pathogenesis, and alterations in serotoninergic and dopaminergic neurotransmission have been described.Attention-deficit Hyperactivity Disorder (ADHD) courses with inattention, impulsivity, and hyperactivity. It affects children and persists into adulthood in 50% of patients. Dopamine transporter abnormalities lead to impaired neurotransmission of catecholaminergic frontal-subcortical-cerebellar circuits.ObjectivesTo describe the prevalence of ADHD in a sample of CFS patients, and the clinical implications of the association.AimsTo study the relationship between CFS and ADHD.MethodsThe initial sample consisted of 142 patients, of whom 9 were excluded because of severe psychopathology or incomplete evaluation. All the patients (age 49 ± 87; 94,7 women) received CFS diagnoses according to Fukuda criteria. ADHD was assessed with a diagnostic interview (CAADID), ADHD Rating Scale and the scale WURS, for childhood diagnose. The scales FIS-40, HAD, STAI and Pluthik Risk of Suicide (RS) were administrated.Results38 patients (28,8%) were diagnosed of childhood ADHD (4 combined, 22 hyperactive-impulsive, 12 inattentive) and persisted into adulthood in 28 (21,1%; 5 combined, 4 hyperactive-impulsive, 19 inattentive). There were no differences in Fukuda criteria profile and FIS-40 between groups. ADHD patients scored higher in HAD-Anxiety (9,88 ± 4,82 vs. 12,57 ± 3,49; p = 0,007), HAD-Depression (9,69 ± 4,84 vs. 12,04 ± 4,53; p = 0,023), STAI-E (30,55 ± 14,53 vs. 38,41 ± 11,35; p = 0,012), and RS (6,13 ± 3,48 vs. 8,49 ± 3,07; p = 0,002).ConclusionsADHD is frequent in CFS patients and it is associated with more severe clinical profile.


Author(s):  
Vsevolod G. V.G.Potapenko ◽  
Marina F. Ballyuzek

Purpose. Presentation of clinical signs and laboratory profiles of the patients with chronic fatigue syndrome, and comparison of their symptoms with those of the patients with iron deficiency anemia. Materials and methods. Retrospective analysis of the patients symptoms referred to the hematologist outpatient clinic during the period between January 2016 and December 2018. Results. There were 560 patients(162 males and 398 females) referred for a primary consultation by a hematologist. Median age was 52.5 (1894) years. The unexplained fatigue was reported by 27 (4.8%) patients (1 male and 26 females), median age 41 (2466) years. Diagnosis chronic fatigue syndrome (CFS) was confirmed based on the criteria in 17 (63%) patients. 10 patients (47%) with symptoms partially meeting the criteria were diagnosed idiopathic fatigue syndrome (SIF). Half of the patients connected the onset of the diseases with emotional trauma (family issues etc.). The prevailing complaints (30%) were represented by: prolonged fatigue, mild memory impairment and distraction, arthralgia and insomnia. The most frequent reason to see a hematologist was fatigue and borderline changes in the blood tests. Five patients with CFS and 2 patients with SIF were known to have previously diagnosed iron deficient anemia (IDA). Median level of hemoglobin in the patients with severe fatigue and IDA was 10.7 (8.411.7) g/dl. Median follow up duration was 28 (640) months. In the observed group (n = 23) 17% of the patients (n = 4) showed spontaneous improvement. The rest of the patients had reported no changes. The comparison group (n = 64) included the patients with IDA. Most of them (n = 38) did not report fatigue as their initial symptoms (median level of hemoglobin was 9.35 (5.511.9) g/dl). Twenty six patients reported fatigue; median level of hemoglobin was 8.15 (5.911.7) g/dl. The difference between the hemoglobin levels in two groups was significant (р 0.05). However, there was no correlation between the level of hemoglobin and fatigue in the patients with CFS and SIF. The correlation was found in the patients with CFS and SIF between fatigue and patients perception. Conclusion. The main symptoms accompanying CFS are fatigue and other non-specific symptoms which are often related to patients emotional status. Considering CFS as a differential diagnosis when dealing with fatigue is essential.


CHEST Journal ◽  
1992 ◽  
Vol 102 (6) ◽  
pp. 1716-1722 ◽  
Author(s):  
Roger Wong ◽  
Gary Lopaschuk ◽  
Gang Zhu ◽  
Dorothy Walker ◽  
Dianne Catellier ◽  
...  

2011 ◽  
Vol 31 (1) ◽  
Author(s):  
Leonard Jason ◽  
Jason Meredyth Evans ◽  
Molly Brown ◽  
Nicole Porter ◽  
Abigail Brown ◽  
...  

<p>Few studies have explored issues of sensitivity and specificity for using the fatigue construct to identify patients meeting chronic fatigue syndrome (CFS) criteria. In this article, we examine the sensitivity and specificity of several fatigue scales that have attempted to define severe fatigue within CFS. Using Receiver Operating Characteristic (ROC) curve analysis, we found most scales and sub-scales had either significant specificity and/or sensitivity problems. However, the post-exertional subscale of the ME/CFS Fatigue Types Questionnaire (Jason, Jessen, et al., 2009) was the most promising in terms of specificity and sensitivity. Among the more traditional fatigue scales, Krupp, LaRocca, Muir-Nash, and Steinberg’s (1989) Fatigue Severity Scale had the best ability to differentiate CFS from healthy controls. Selecting questions, scales and cut off points to measure fatigue must be done with extreme care in order to successfully identify CFS cases.</p>


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.


1993 ◽  
Vol 56 (6) ◽  
pp. 679-683 ◽  
Author(s):  
P R Barnes ◽  
D J Taylor ◽  
G J Kemp ◽  
G K Radda

Sign in / Sign up

Export Citation Format

Share Document