Cognitive performance affected by poor muscle function in CFS & FM

Posted on 07/30/2014 by wames

Abstract

BACKGROUND:
Both good physical and cognitive functioning have a positive influence on the execution of activities of daily living. Patients with chronic fatigue syndrome (CFS) as well as patients with fibromyalgia have marked cognitive deficits. Furthermore, a good physical and functional health status may have a positive impact on a variety of cognitive skills-a link that has been observed in young and old individuals who are healthy, although evidence is limited in patients with CFS.

OBJECTIVE:
The purpose of this study was to examine whether recovery of upper limb muscle function could be a significant predictor of cognitive performance in patients with CFS and in patients with CFS and comorbid fibromyalgia. Furthermore, this study determined whether cognitive performance is different between these patient groups.

DESIGN:
A case-control design was used.

METHODS:
Seventy-eight participants were included in the study: 18 patients with CFS only (CFS group), 30 patients with CFS and comorbid fibromyalgia (CFS+FM group), and 30 individuals who were healthy and inactive (control group) were studied. Participants first completed 3 performance-based cognitive tests designed to assess selective and sustained attention, cognitive inhibition, and working memory capacity. Seven days later, they performed a fatiguing upper limb exercise test, with subsequent recovery measures.

RESULTS:
Recovery of upper limb muscle function was found to be a significant predictor of cognitive performance in patients with CFS. Participants in the CFS+FM group but not those in the CFS group showed significantly decreased cognitive performance compared with the control group.

LIMITATIONS:
The cross-sectional nature of this study does not allow for inferences of causation.

CONCLUSIONS:
The results suggest that better physical health status could predict better mental health in patients with CFS. Furthermore, they underline disease heterogeneity, suggesting that reducing this factor in future research is important to better understand and uncover mechanisms regarding the nature of diverse impairments in these patients.

Can recovery of peripheral muscle function predict cognitive task performance in chronic fatigue syndrome with and without fibromyalgia? by K Ickmans et al in Phys Ther. 2014 Apr;94(4):511-22

Comment on the research by Cort Johnson: A Muscle Brain Connection in Chronic Fatigue Syndrome Revealed

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Why ineffective psychotherapies appear to work

Posted on 07/29/2014 by wames

Article abstract:
The past 40 years have generated numerous insights regarding errors in human reasoning.

Arguably, clinical practice is the domain of applied psychology in which acknowledging and mitigating these errors is most crucial. We address one such set of errors here, namely, the tendency of some psychologists and other mental health professionals to assume that they can rely on informal clinical observations to infer whether treatments are effective.

We delineate four broad, underlying cognitive impediments to accurately evaluating improvement in psychotherapy

  • naive realism
  • confirmation bias
  • illusory causation
  • illusion of control.

We then describe 26 causes of spurious therapeutic effectiveness (CSTEs), organized into a taxonomy of three overarching categories:

  • (a) the perception of client change in its actual absence,
  • (b) misinterpretations of actual client change stemming from extratherapeutic factors, and
  • (c) misinterpretations of actual client change stemming from nonspecific treatment factors. These inferential errors can lead clinicians, clients, and researchers to misperceive useless or even harmful psychotherapies as effective.

We (a) examine how methodological safeguards help to control for different CSTEs, (b) delineate fruitful directions for research on CSTEs, and (c) consider the implications of CSTEs for everyday clinical practice. An enhanced appreciation of the inferential problems posed by CSTEs may narrow the science-practice gap and foster a heightened appreciation of the need for the methodological safeguards afforded by evidence-based practice.

Why ineffective psychotherapies appear to work: a taxonomy of causes of spurious therapeutic effectiveness, by Scott O. Lilienfeld, Lorie Ritschel, Steven Jay Lynn, Robert D Latzman in Perspectives on Psychological Science 9(4):355-387, July 2014

 

 

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Methylation may have role in immunological changes in CFS/ME

Posted on 07/28/2014 by wames

Abstract

Objective: Methylation is known to regulate biological processes and alterations in methylation patterns have been associated with a variety of diseases. Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) is an unexplained disorder associated with immunological and molecular changes.

CD4+T cells specifically, regulatory Tcells (Tregs) have been implicated in CFS/ME patients where significant increases in Tregs have been observed in these patients. Therefore the objective of this study was to examine methylation in CD4+T cells from CFS/ME patients.

Methods: The study comprised twenty-five CFS/ME participants and eighteen controls aged between 25-60 years. A volume of 20 ml whole blood was collected from each participant and peripheral blood mononuclear cells were isolated via density gradient centrifugation. A negative isolation kit was used to isolate the CD4+T cells from the peripheral blood samples.

Genome wide methylation studies were performed on isolated CD4+T cells using the Illumina Infinium 450 K Human methylation array system. Data analysis was performed using Genome studio and Partek Enrichment software.

Results: 120 CpGs were observed to be differentially methylated in the CFS/ME patients in comparison to the controls. Of these 70 were associated with known genes. The majority of the differential methylated regions in the CFS/ME patients were hypomethylated.

Additionally, most of the genes with differentially methylated regions in the CFS/ME patients were responsible for apoptosis, cell development, cell function and metabolic activity.

Conclusion: The present study demonstrates that epigenetic changes in CD4+T cells may have a potential role in the immunological changes observed in CFS/ME patients

Methylation Profile of CD4+ T Cells in Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis by Ekua W Brenu, Donald R Staines and Sonya M Marshall-Gradisnik in J Clin Cell Immunol 2014 Vol 5, Issue 3

 

 

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Review of SNS dysfunction in Orthostatic Intolerance

Posted on 07/22/2014 by wames

Review abstract

Orthostatic intolerance is the inability to tolerate the upright posture and is relieved by recumbence. It most commonly affects young women and has a major impact on quality of life and psychosocial well being. Several forms of orthostatic intolerance have been described.

The most common one is the recurrent vasovagal syncope (VVS) phenotype which presents as a transient and abrupt loss of consciousness and postural tone that is followed by rapid recovery. Another common type of orthostatic intolerance is the postural orthostatic tachycardia syndrome (POTS) which is characterized by an excessive rise in heart rate upon standing and is associated with symptoms of presyncope such as light-headedness, fatigue, palpitations and nausea.

Maintenance of arterial pressure under condition of reduced central blood volume during the orthostasis is accomplished in large part through sympathetic efferent nerve traffic to the peripheral vasculature. Therefore sympathetic nervous system (SNS) dysfunction is high on the list of possible contributors to the pathophysiology of orthostatic intolerance. Investigations into the role of the SNS in orthostatic intolerance have yielded mixed results.

This review outlines the current knowledge of the function of the SNS in both VVS and POTS.

Sympathetic dysfunction in vasovagal syncope and the postural orthostatic tachycardia syndrome, by Elisabeth Lambert and Gavin W Lambert in Front. Physiol. 2014 5:280.

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Impaired range of motion found in teenagers with CFS

Posted on 07/22/2014 by wames

Abstract

Objective

To determine whether adolescents and young adults with chronic fatigue syndrome (CFS) have a greater prevalence of impaired range of motion (ROM) of the limbs and spine than healthy control patients.

Study design

Case-control study comparing rates of abnormal ROM in 48 consecutive adolescents and young adults with CFS and 48 healthy control patients matched by sex and joint hypermobility. We examined range of ankle dorsiflexion, passive straight-leg raise, seated slump, upper-limb neurodynamic test, prone knee bend, and prone press-up. Abnormal ROM was defined before the study began. The number of abnormal responses ranged from 0 (normal ROM throughout) to 11 (impaired ROM in all areas tested).

Results

The median number of areas with impaired ROM was greater in patients with CFS at the onset of stretch in the involved limb (5 vs 2, P < .001) and at end-range (2 vs 0, P < .001). Patients with CFS were more likely to have greater than 3 areas of impaired ROM (OR 6.0, 95% CI 2.1-17.3; P < .001) and were more likely to develop abnormal symptomatic responses to the individual tests and to the overall assessment (40% vs 4%; P < .001).

Conclusions

Impaired ROM is more common in subjects with CFS than in healthy adolescents and young adults matched by sex and joint hypermobility. Adding a longitudinal strain to the nerves and soft tissues provoked symptoms in some subjects with CFS. The causes, functional impact, and optimal treatment of these abnormalities warrant further study.

Impaired Range of Motion of Limbs and Spine in Chronic Fatigue Syndrome by PC Rowe et al in J Pediatr. 2014 Jun 11.

Cort Johnson explains and comments on Peter Rowe’s research:
Strained – are neuromuscular problems causing Chronic Fatigue Syndrome?

Cort Johnson interviews Peter Rowe:

Unrestrained: Dr. Peter Rowe on Neuromuscular Strain in Chronic Fatigue Syndrome (ME/CFS)

 

 

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Intracellular bacteria interfere with dendritic cell functions

Posted on 07/19/2014 by wames

Abstract

 

Dendritic cells (DCs) orchestrate host defenses against microorganisms. In infectious diseases due to intracellular bacteria, the inefficiency of the immune system to eradicate microorganisms has been attributed to the hijacking of DC functions.

 

In this study, we selected intracellular bacterial pathogens with distinct lifestyles and explored the responses of monocyte-derived DCs (moDCs). Using lipopolysaccharide as a control, we found that Orientia tsutsugamushi, the causative agent of scrub typhus that survives in the cytosol of target cells, induced moDC maturation, as assessed by decreased endocytosis activity, the ability to induce lymphocyte proliferation and the membrane expression of phenotypic markers.

 

In contrast, Coxiella burnetii, the agent of Q fever, and Brucella abortus, the agent of brucellosis, both of which reside in vacuolar compartments, only partly induced the maturation of moDCs, as demonstrated by a phenotypic analysis. To analyze the mechanisms used by C. burnetii and B. abortus to alter moDC activation, we performed microarray and found that C. burnetii and B. abortus induced a specific signature consisting of TLR4, TLR3, STAT1 and interferon response genes. These genes were down-modulated in response to C. burnetii and B. abortus but up-modulated in moDCs activated by lipopolysaccharide and O.  tsutsugamushi. This transcriptional alteration was associated with the defective interferon-β production.

This study demonstrates that intracellular bacteria specifically affect moDC responses and emphasizes how C. burnetii and B. abortus interfere with moDC activation and the antimicrobial immune response. We believe that comparing infection by several bacterial species may be useful for defining new pathways and biomarkers and for developing new treatment strategies. 

 

Intracellular bacteria interfere with dendritic cell functions: role of the type 1 interferon pathway by L Gorvel et al in PLoS One. 2014 Jun 10;9(6)

 

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What do you think of ‘Pacing’?

Posted on 07/18/2014 by wames

What do you think of 'Pacing'? [Pacing’ is a way of balancing activity and rest to help manage symptoms and allow your body to recover]

  • I have tried it and found it helpful. (100%, 4 Votes)
  • I have tried it but didn't find it helpful. (0%, 0 Votes)
  • I haven't tried it but intend to. (0%, 0 Votes)
  • I haven't tried it and don't think it is worth trying. (0%, 0 Votes)
  • I haven't tried it because it would be too difficult. (0%, 0 Votes)
  • I don't know enough about it to have an opinion. (0%, 0 Votes)

Total Voters: 4

Loading ... Loading ...

Email us if you have any comments or questions about this poll. Find out more about pacing from our info sheet by Dr Goudsmit.

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SFPN (small-fiber polyneuropathy) found in children with pain syndromes

Posted on 07/18/2014 by wames

Abstract

 

OBJECTIVE: We tested the hypothesis that acquired small-fiber polyneuropathy (SFPN), previously uncharacterized in children, contributes to unexplained pediatric widespread pain syndromes.

 

METHODS: Forty-one consecutive patients evaluated for unexplained widespread pain beginning before age 21 had medical records comprehensively analyzed regarding objective diagnostic testing for SFPN (neurodiagnostic skin biopsy, nerve biopsy, and autonomic function testing), plus histories, symptoms, signs, other tests, and treatments. Healthy, demographically matched volunteers provided normal controls for SFPN tests.

 

RESULTS: Age at illness onset averaged 12.3 ± 5.7 years; 73% among this poly-ethnic sample were female (P = .001). Sixty-eight percent were chronically disabled, and 68% had hospitalizations. Objective testing diagnosed definite SFPN in 59%, probable SFPN in 17%, and possible SFPN in 22%. Only 1 of 41 had entirely normal SFPN test results.

Ninety-eight percent of patients had other somatic complaints consistent with SFPN dysautonomia (90% cardiovascular, 82% gastrointestinal, and 34% urologic), 83% reported chronic fatigue, and 63% had chronic headache.

Neurologic examinations identified reduced sensation in 68% and vasomotor abnormalities in 55%, including 23% with erythromelalgia. Exhaustive investigations for SFPN causality identified only history of autoimmune illnesses in 33% and serologic markers of disordered immunity in 89%.

Treatment with corticosteroids and/or intravenous immune globulin objectively and subjectively benefited 80% of patients (12/15).

 

CONCLUSIONS: More than half among a large series of patients with childhood-onset, unexplained chronic widespread pain met rigorous, multitest, diagnostic criteria for SFPN, which extends the age range of acquired SFPN into early childhood. Some cases appeared immune-mediated and improved with immunomodulatory therapies.

Evidence of small-fiber polyneuropathy in unexplained, juvenile-onset, widespread pain syndromes, by AL Oaklander, MM Klein in Pediatrics 2013 Apr;131(4), Epub 2013 Mar 11.

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Characterisation of impaired NK cells in CFS/ME

Posted on 07/17/2014 by wames

Abstract

OBJECTIVE

Natural Killer (NK) cells are classified into different phenotypes according to the expression of the surface markers CD56 and CD16. Each NK cell phenotype has a role in the immune response through cytotoxic activity or cytokine production. Reduced NK cell cytotoxic activity is a consistent finding in patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) and investigations into the potential causes of reduced NK cell cytotoxic activity have predominantly focused on total NK cells. The purpose of this study was to investigate and characterize four NK cell phenotypes in CFS/ME.

METHODS

Twenty nine CFS/ME patients (mean age ± SEM=48.28 ± 2.63) meeting the 1994 Fukuda definition and 27 healthy controls (mean age ± SEM=49.15 ± 2.51) were included in this study. Flow cytometric protocols identified CD56brightCD16-/dim, CD56dimCD16-, CD56dimCD16+ or CD56-CD16+ NK cells for the measurement of surface markers including adhesion molecules CD2, CD18, CD11a, CD11b and CD11c, natural cytotoxicity receptors, Killer Immunoglobulin Like Receptors, signalling lymphocytic activation molecules and cell maturation (CD57).

Following stimulation, NK cell phenotype expression of CD107a and CD107b was measured as a marker for degranulation. Intracellular staining measured lytic proteins including perforin, Granzyme A and Granzyme B in the four NK cell phenotypes.

RESULTS

In the CFS/ME group, CD56brightCD16-/dim NK cell co-expression of adhesion molecules CD2 and CD18 was significantly reduced. Granzyme B was significantly decreased in CD56dimCD16+ and CD56-CD16+ NK cells from CFS/ME patients. CD57 expression on CD56dimCD16+ NK cells from CFS/ME patients was significantly increased.

CONCLUSION

This is the first study to characterize four NK cell phenotypes in CFS/ME by investigating surface and intracellular molecules necessary for NK cell effector function. The data suggests that a combination of impairments in CD56dimCD16+ NK cells from CFS/ME patients may contribute to reduced cytotoxic activity of this
phenotype.

Characterization of Natural Killer Cell Phenotypes in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis, by Teilah K Huth et al in J Clin Cell Immunol 2014, 5:3

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Is CFS an autoimmune disorder with vasoactive neuropeptide dysfunction?

Posted on 07/15/2014 by wames

Abstract

Chronic fatigue syndrome is a disorder characterised by prolonged fatigue and debility and is mostly associated with post-infection sequelae although ongoing infection is unproven.

Immunological aberration is likely and this may prove to be associated with an expanding group of vasoactive neuropeptides in the context of molecular mimicry and inappropriate immunological memory.

Vasoactive neuropeptides including vasoactive intestinal peptide (VIP) and pituitary adenylate activating polypeptide (PACAP) belong to the secretin/glucagon superfamily and act as hormones, neurotransmitters, immune modulators and neurotrophes. They are readily catalysed to smaller peptide fragments by antibody hydrolysis. They and their binding sites are immunogenic and are known to be associated with a range of autoimmune conditions.

Vasoactive neuropeptides are widely distributed in the body particularly in the central, autonomic and peripheral nervous systems and have been identified in the gut, adrenal gland, reproductive organs, vasculature, blood cells and other tissues. They have a vital role in maintaining vascular flow in organs, and in thermoregulation, memory and concentration. They are co-transmitters for acetylcholine, nitric oxide, endogenous opioids and insulin, are potent immune regulators with primarily anti-inflammatory activity, and have a significant role in protection of the nervous system to toxic assault, promotion of neural development and the maintenance of homeostasis.

This paper describes a biologically plausible mechanism for the development of CFS based on loss of immunological tolerance to the vasoactive neuropeptides following infection, significant physical exercise or de novo. It is proposed that release of these substances is accompanied by a loss of tolerance either to them or their receptor binding sites in CFS. Such an occurrence would have predictably serious consequences resulting from compromised function of the key roles these substances perform.

All documented symptoms of CFS are explained by vasoactive neuropeptide compromise, namely fatigue and nervous system dysfunction through impaired acetylcholine activity, myalgia through nitric oxide and endogenous opioid dysfunction, chemical sensitivity through peroxynitrite and adenosine dysfunction, and immunological disturbance through changes in immune modulation.

Perverse immunological memory established against these substances or their receptors may be the reason for the protracted nature of this condition. The novel status of these substances together with their extremely small concentrations in blood and tissues means that clinical research into them is still in its infancy.

A biologically plausible theory of CFS causation associated with vasoactive neuropeptide dysfunction would promote a coherent and systematic approach to research into this and other possibly associated disabling conditions.

Is chronic fatigue syndrome an autoimmune disorder of endogenous neuropeptides, exogenous infection and molecular mimicry? by DR Staines in Med Hypotheses; 62(5): 646-52, 2004.

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