Subgroup of younger CFS people have POTS

Posted on 01/12/2014 by wames

Abstract

OBJECTIVE:

Patients with chronic fatigue syndrome (CFS) are frequently diagnosed with comorbid postural orthostatic tachycardia syndrome (POTS), suggesting a shared pathogenesis. The aim of this study was to examine the relationship between demographic characteristics, autonomic functioning and fatigue levels amongst CFS patients with and without comorbid POTS.

DESIGN AND SETTING:

All patients presenting to the CFS Discovery Clinic between 2009 and 2012 completed a 20-min standing task as part of their initial assessment. Heart rate and pulse pressure were recorded at baseline, at 2-min intervals poststanding, at the end of the task and following a recovery period. Average heart rate and pulse pressure variability were calculated from this data. Age, gender, length of illness and self-reported fatigue scores were also recorded.

POTS patients were diagnosed by an orthostatic increase in heart rate >30 beats per min, concomitant symptoms of orthostatic intolerance and no orthostatic hypotension. Differences in autonomic functioning between POTS and CFS patients were compared using independent samples t-tests, whilst logistic and linear regressions were performed to examine the contribution of autonomic functioning to task completion and perceived fatigue, respectively.

RESULTS:

Comorbidity of CFS and POTS (CFS-POTS) was observed in 11% (33/306) of patients. CFS-POTS patients were significantly younger (P < 0.001), had a shorter length of illness (P = 0.034), experienced greater task difficulty (P = 0.002) and were able to stand for significantly shorter periods compared to the CFS-only patients (P < 0.001). CFS-POTS patients experienced significantly lower baseline diastolic blood pressure (P = 0.002), significantly higher heart rate and lower pulse pressures at each standing measurement. Early heart rate changes (P = 0.002) and overall heart rate change (P < 0.001) were significant predictors of completion status, whereas heart rate variability (P < 0.001) and female gender (P < 0.001) were significant predictors of increased perceived task difficulty.

CONCLUSIONS:

Haemodynamic and demographic differences between CFS-POTS and CFS-only patients suggest that the former group reflects a distinct subgroup of the CFS population. The findings highlight the utility of screening younger patients with fatigue for POTS, and identified heart rate variability as an important marker of fatigue for CFS patients in general.

Comorbidity of postural orthostatic tachycardia syndrome and chronic fatigue syndrome in an Australian cohort, by GK Reynolds, DP Lewis, BA Lidbury, in J Intern Med. 2013 Nov 9. doi: 10.1111/joim.12161. [Epub ahead of print]

 

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Exercise testing and CFS

Posted on 01/10/2014 by wames

Abstract

PURPOSE

Cardiopulmonary exercise testing (CPET) is used to determine the etiology of unexplained exercise symptoms in otherwise healthy patients and those with well defined cardiopulmonary disease. Test results vary by baseline physical activity levels which are difficult to assess objectively.

METHODS

We performed submaximal exercise testing on 40 physically active, healthy control patients as part of a prospective trial to evaluate the exercise response in patients with chronic fatigue syndrome. All patients provided a self-assessment of fitness using a series of previously validated visual analogue scales (VAS). We evaluated the relationship between baseline fitness and physiologic response to exercise.

RESULTS

Mean age and BMI for the group were 30.7±8.8 and 27.0±3.6 respectively. There were 25 males (62.5%), 23 caucasians (57.5%) and 13 (32.5%) African Americans.

On a VAS from one to ten with ten being optimal, patients rated their current endurance, fitness and muscular strength at 7.8±1.5, 7.9±1.1 and 7.3±1.9. Self-assessment of endurance was significantly correlated with maximum respiratory rate (r=-0.34, p=0.03), fitness showed a trend toward correlation with heart rate reserve (r=0.27, p=0.09) and muscular strength was significantly correlated with peak heart rate (r=-0.43, p=0.01), heart rate reserve (r=0.33, p=0.04) and O2-pulse at VO2 max (r=0.37, p=0.02).

Female assessment of fitness and muscle strength showed good correlation with work rate achieved (0.40 and 0.53 respectively).

CONCLUSIONS

In a group of young, physically fit patients self assessment is correlated with aerobic fitness measured on symptom targeted, sub-maximal exercise testing. VAS scores for muscular strength seemed to be a better predictor of the cardiac response to exercise than were scores for endurance or fitness.

CLINICAL IMPLICATIONS

Visual analogue scales can be used to provide a baseline assessment of fitness, In conjunction with other factors known to predict responses to exercise these scales could theoretically help better define normality for a given patient.

Self-Assessment Using a Validated Visual Analogue Scale Predicts Response to Submaximal Exercise Testing, by T Hauser & A Holley in Chest Journal, 1 October 2013

 

 

 

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Cytokines and neuropathic pain

Posted on 12/18/2013 by wames

Abstract

Cytokines and chemokines are proteins that coordinate the immune response throughout the body. The dysregulation of cytokines and chemokines is a central feature in the development of neuroinflammation, neurodegeneration, and demyelination both in the central and peripheral nervous systems and in conditions of neuropathic pain.

Pathological states within the nervous system can lead to activation of microglia. The latter may mediate neuronal and glial cell injury and death through production of proinflammatory factors such as cytokines and chemokines. These then help to mobilize the adaptive immune response.

Although inflammation may induce beneficial effects such as pathogen clearance and phagocytosis of apoptotic cells, uncontrolled inflammation can result in detrimental outcomes via the production of neurotoxic factors that exacerbate neurodegenerative pathology.

In states of prolonged inflammation, continual activation and recruitment of effector cells can establish a feedback loop that perpetuates inflammation and ultimately results in neuronal injury. A critical balance between repair and proinflammatory factors determines the outcome of a neurodegenerative process.

This review will focus on how cytokines and chemokines affect neuroinflammation and disease pathogenesis in bacterial meningitis and brain abscesses, Lyme neuroborreliosis, human immunodeficiency virus encephalitis, and neuropathic pain.

Cytokines and Chemokines at the Crossroads of Neuroinflammation, Neurodegeneration, and Neuropathic Pain, by Geeta Ramesh, Andrew G. MacLean, and Mario T. Philipp in Mediators of inflammation Vol 2013

 

 

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Childhood stressors in the development of CFS and FM

Posted on 12/18/2013 by wames

Review Abstract

Background

Chronic fatigue syndrome (CFS) and fibromyalgia (FM) are both highly prevalent conditions associated with extreme disability and with the development of co-morbid psychiatric disorders, such as depression and anxiety. Childhood stressors have been shown to induce persistent changes in the function of biological systems potentially relevant to the pathogenesis of both CFS and FM, such as the inflammatory system and the hypothalamic–pituitary–adrenal (HPA) axis. In this review, we examined whether multiple forms of childhood stressors are contributing factors to the development of these disorders, and of the associated psychiatric symptoms.

Method

Using PubMed, we identified 31 papers relevant to this narrative review. We included cohort studies and case-control studies, without any exclusion in terms of age and gender. No study characteristics or publication date restrictions were imposed.

Results

Most studies across the literature consistently show that there is a strong association between experiences of childhood stressors and the presence of CFS and FM, with rates of CFS/FM being two- to three-fold higher in exposed than in unexposed subjects. We also found evidence for an increased risk for the development of additional symptoms, such as depression, anxiety and pain, in individuals with CFS and FM with a previous history of childhood stressors, compared with individuals with CFS/FM and no such history.

Conclusions

Our review confirms that exposure to childhood stressors is associated with the subsequent development of fatigue syndromes such as CFS and FM, and related symptoms. Further studies are needed to identify the mechanisms underlying these associations.

Childhood stressors in the development of fatigue syndromes: a review of the past 20 years of research, by A. Borsini, N. Hepgul, V. Mondelli1, T. Chalder and C. M. Pariante in Psychological Medicine, Vol 44 Issue 9, July 2014

 

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Functional capacity evaluation in CFS

Posted on 12/18/2013 by wames

Abstract

Background: Objective measurements of function often form the basis for legal decisions about whether a patient is fit for return to work, or conversely, entitled to disability compensation. The functional capacity evaluation (FCE) is regarded as the gold standard for measuring work capacity in plaintiffs seeking disability benefits. Yet the FCE often fails to link the unremitting fatigue of chronic fatigue syndrome (CFS) to the ability to work.

Purpose: To review the legal rationale and scientific evidence related to functional capacity measurements used to establish disability in individuals with CFS.

Methods: Narrative review.

Results: Several legal cases demonstrate problems with the FCE as determinative of the ability to work in people with CFS. In addition, scientific studies are lacking to support the reliability and validity of the FCE in this population. The putative metabolic pathology of CFS suggests that maximal cardiopulmonary exercise testing, which combines direct measurements of functioning and metabolic status, may be more appropriate to establish ability and disability than the FCE in this population.

Conclusion: Utilization of the FCE in legal cases to establish disability in individuals with CFS may yield erroneous findings that can be addressed with the use of alternative validated measurements.

Scientific and legal challenges to the functional capacity evaluation in chronic fatigue syndrome, by E. Ciccolella & Todd E. Davenport in Fatigue: Biomedicine, Health & Behavior, Vol 1, Issue 4, 2013

 

 

 

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Which term best describes the key ME symptom for you?

Posted on 12/09/2013 by Pixelwave

Which term best describes a key symptom for you?

  • Post-Exertional Malaise (PEM) (40%, 4 Votes)
  • Post-Exertional Neuroimmune Exhaustion (PENE) (40%, 4 Votes)
  • ill and weak (10%, 1 Votes)
  • exhaustion (10%, 1 Votes)
  • low / fluctuating energy (0%, 0 Votes)
  • fatigue (0%, 0 Votes)
  • other (0%, 0 Votes)

Total Voters: 10

Loading ... Loading ...

Email us if you chose option 7, or have any comments on this poll.

Definitions:

Post-Exertional Malaise (PEM) – inappropriate loss of physical and mental stamina, rapid muscular and cognitive fatigability, malaise and/or fatigue, and/or pain and a tendency for other symptoms to worsen, with a slow recovery period [Canadian guidelines]

Post- Exertional Neuroimmune Exhaustion (PENE) – pathological low threshold of physical and mental fatigability, exhaustion, pain, and an abnormal exacerbation of symptoms in response to exertion. It is followed by a prolonged recovery period. [International guidelines]

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Accuracy of memory of CFS symptoms

Posted on 11/01/2013 by wames

Abstract

This study serves as an investigation of the reliability of symptom data as reported by individuals with chronic fatigue syndrome (CFS), across three recall time frames (the past week, the past month, and the past 6 months), and at two assessment points (with 1 week in between each assessment).

Multilevel model analyses were used to determine the optimal recall time frame, in terms of test-retest reliability, for each of the Fukuda et al. (1994) case defining symptoms.

Results suggested that the optimal time frame for reliably reporting CFS symptoms was six months for sore throat, lymph node pain, muscle pain, post-exertional malaise, headaches, memory/concentration difficulties, and unrefreshing sleep.

For joint pain, the optimal time frame was one month.

Researchers who are interested in the assessment of CFS symptoms need to take recall time frame into account, especially when the intended goal is to standardize and improve the methods used to reliably and accurately diagnose this complex illness.

Effects of Time Frame on the Recall Reliability of CFS Symptoms, by Evans M, Jason LA, in Evaluation and the Health Professions, 23 September 2013. [Epub ahead of print]

 

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Possible causes of mitochondrial dysfunctions in ME

Posted on 10/27/2013 by wames

Abstract

Myalgic encephalomyelitis / chronic fatigue syndrome (ME/cfs) is classified by the World Health Organization as a disorder of the central nervous system. ME/cfs is an neuro-immune disorder accompanied by chronic low-grade inflammation, increased levels of oxidative and nitrosative stress (O&NS), O&NS-mediated damage to fatty acids, DNA and proteins, autoimmune reactions directed against neoantigens and brain disorders.

Mitochondrial dysfunctions have been found in ME/cfs, e.g. lowered ATP production, impaired oxidative phosphorylation and mitochondrial damage. This paper reviews the pathways that may explain mitochondrial dysfunctions in ME/cfs. Increased levels of pro-inflammatory cytokines, such as interleukin-1 and tumor necrosis factor-a, and elastase, and increased O&NS may inhibit mitochondrial respiration, decrease the activities of the electron transport chain and mitochondrial membrane potential, increase mitochondrial membrane permeability, interfere with ATP production and cause mitochondrial shutdown.

The activated O&NS pathways may additionally lead to damage of mitochondrial DNA and membranes thus decreasing membrane fluidity. Lowered levels of antioxidants, zinc and coenzyme Q10, and Omega 3 polyunsaturated fatty acids in ME/cfs may further aggravate the activated immuno-inflammatory and O&NS pathways.

Therefore, it may be concluded that immuno-inflammatory and O&NS pathways may play a role in the mitochondrial dysfunctions and consequently the bioenergetic abnormalities seen in patients with ME/cfs. Defects in ATP production and the electron transport complex, in turn, are associated with an elevated production of superoxide and hydrogen peroxide in mitochondria creating adaptive and synergistic damage.

It is argued that mitochondrial dysfunctions, e.g. lowered ATP production, may play a role in the onset of ME/cfs symptoms, e.g. fatigue and post exertional malaise, and may explain in part the central metabolic abnormalities observed in ME/cfs, e.g. glucose hypometabolism and cerebral hypoperfusion.

Mitochondrial dysfunctions in Myalgic Encephalomyelitis / chronic fatigue syndrome explained by activated immuno-inflammatory, oxidative and nitrosative stress pathways, by Gerwyn Morris and Michael Maes in Metabolic Brain Disease, September 2013.

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Cytokines and CFS

Posted on 10/18/2013 by wames

Abstract

A major hypothesis for the cause of chronic fatigue syndrome (CFS) is immune dysregulation, thought to reflect upregulated pro-inflammatory cytokines leading to the symptoms characteristic of this illness. Because symptoms worsen with physical exertion or sleep loss, we hypothesized we could use these stressors to magnify underlying potential pathogenic abnormalities in the cytokine systems.

We conducted repeated blood sampling for cytokines from healthy subjects and CFS patients during a post-exercise and total sleep deprivation night, and assayed for protein in serum, message in peripheral blood lymphocytes (PBLs), and function in resting and stimulated PBLs.

We found that these environmental manipulations did not produce clinically significant upregulation of pro-inflammatory cytokines. These data do not support an important role for immune dysregulation in the genesis or stress-induced worsening of this illness.

Cytokines do not change after exercise or sleep deprivation in chronic fatigue syndrome, by T Nakamura et al in Clinical and Vaccine Immunology, 11 September 2013 2013 [Epub ahead of print].

 

 

 

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Fatigue in cancer and CFS

Posted on 10/18/2013 by wames

Abstract

BACKGROUND

Androgen deprivation therapy (ADT) often worsens fatigue in patients with prostate cancer, producing symptoms similar to chronic fatigue syndrome (CFS). Comparing expression (mRNA) of many fatigue-related genes in patients with ADT-treated prostate cancer versus with CFS versus healthy controls, and correlating mRNA with fatigue severity may clarify the differing pathways underlying fatigue in these conditions.

METHODS

Quantitative real-time PCR was performed on leukocytes from 30 fatigued, ADT-treated prostate cancer patients (PCF), 39 patients with CFS and 22 controls aged 40-79, together with ratings of fatigue and pain severity. 46 genes from these pathways were included: (1) adrenergic/monoamine/neuropeptides, (2) immune, (3) metabolite-detecting, (4) mitochondrial/energy, (5) transcription factors.

RESULTS

PCF patients showed higher expression than controls or CFS of 2 immune transcription genes (NR3C1 and TLR4), chemokine CXCR4, and mitochondrial gene SOD2. They showed lower expression of 2 vasodilation-related genes (ADRB2 and VIPR2), 2 cytokines (TNF and LTA), and 2 metabolite-detecting receptors (ASIC3 and P2RX7). CFS patients showed higher P2RX7 and lower HSPA2 versus controls and PCF. Correlations with fatigue severity were similar in PCF and CFS for only DBI, the GABA-A receptor modulator (r=-0.50, p<0.005 and r=-0.34, p<0.05). Purinergic P2RY1 was correlated only with PCF fatigue and pain severity (r=+0.43 and +0.59, p=0.025 and p=0.001).

CONCLUSIONS

PCF patients differed from controls and CFS in mean expression of 10 genes from all 5 pathways. Correlations with fatigue severity implicated DBI for both patient groups and P2RY1 for PCF only. These pathways may provide new targets for interventions to reduce fatigue.

Differing leukocyte gene expression profiles associated with fatigue in patients with prostate cancer versus chronic fatigue syndrome, by KC Light et al in Psychoneuroendocrinology, 6 September 2013. [Epub ahead of print]

 

 

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