Dr Myhill video – Biological basis & treatment of CFS/ME

Posted on 07/01/2016 by wames

Dr Myhill gave a talk to the AGM of OMEGA on Sat 5 March 2016.

Dr Sarah Myhill

This talk covered:

  • The Biological Basis of CFS/ME – the “theory”
  • The Treatment of CFS/ME – the “treatment”

You can access the full PowerPoint slide show at this new webpage:

Watch the video

 

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Cardiac abnormality and low blood volume confirmed in CFS

Posted on 06/30/2016 by wames

Research abstract:

Objectives:

To explore potential mechanisms that underpin the cardiac abnormalities seen in chronic fatigue syndrome (CFS) using non-invasive cardiac impedance, red cell mass and plasma volume measurements.

Methods

Crdiac MR (MR) examinations were performed using 3 T Philips Intera Achieva scanner (Best, NL) in participants with CFS (Fukuda; n=47) and matched case-by-case controls. Total volume (TV), red cell volume (RCV) and plasma volume (PV) measurements were performed (41 CFS and 10 controls) using the indicator dilution technique using simultaneous 51-chromium labelling of red blood cells and 125-iodine labelling of serum albumin.

Results

Te CFS group length of history (mean±SD) was 14±10 years. Patients with CFS had significantly reduced end-systolic and end-diastolic volumes together with reduced end-diastolic wall masses (all p<0.0001). Mean±SD RCV was 1565±443 mL with 26/41 (63%) having values below 95% of expected. PV was 2659±529 mL with 13/41 (32%) <95% expected. There were strong positive correlations between TV, RCV and PV and cardiac end-diastolic wall mass (all p<0.0001; r2=0.5). Increasing fatigue severity correlated negatively with lower PV (p=0.04; r2=0.2). There were no relationships between any MR or volume measurements and length of history, suggesting that deconditioning was unlikely to be the cause of these abnormalities.

Conclusions

This study confirms an association between reduced cardiac volumes and blood volume in CFS. Lack of relationship between length of disease, cardiac and plasma volumes suggests findings are not secondary to deconditioning. The relationship between plasma volume and severity of fatigue symptoms suggests a potential therapeutic target in CFS.

Key questions

What is already known about this subject?

  • Chronic fatigue syndrome (CFS) has been shown to be associated with a range of cardiac abnormalities.
  • Studies, to date, have suggested that these abnormalities probably arise because of deconditioning.

What does this study add?

  • This study has confirmed in a large cohort that there are reductions in cardiac volume in CFS measured using cardiac MRI.
  • The degree of these end-diastolic and end-systolic volume abnormalities associates with blood volume.
  • The abnormalities seen are not arising secondary to deconditioning.
  • Reductions in plasma volume associate with fatigue severity.

How might this impact on clinical practice?

  • This study reinforces, using state-of-the art MRI, previous findings that there is a cardiac abnormality in those with CFS.
  • The finding of hypovolaemia in association with cardiac structural abnormalities and fatigue severity represents a potential therapeutic target.

Reduced cardiac volumes in chronic fatigue syndrome associate with plasma volume but not length of disease: a cohort study, by Julia L Newton, Andreas Finkelmeyer, George Petrides, James Frith, Tim Hodgson, Laura Maclachlan, Guy MacGowan and Andrew M Blamire in Open Heart Vol 3, Issue 1 2016

Funded by the (UK) Medical Research Council & ME Research UK

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ME/CFS: the small heart disease

Posted on 06/30/2016 by wames

Health rising blog post, by Cort Johnson, 27 Jun 27 2016: Chronic Fatigue Syndrome: the small heart disease

Did you know that you probably have a smaller heart than normal? Four studies suggest that if you have chronic fatigue syndrome (ME/CFS) you probably do.  The word on the small hearts for years has been that they’re probably caused by inactivity or deconditioning. This study suggested that they probably are indeed caused by inactivity – but not by deconditioning at all.

Small hearts appear to be common on ME/CFS – but not in the way the medical community has thought.

Newton’s earlier small study had found reduced heart mass and significantly reduced blood pumping by the heart, and Miwa in Japan has produced three studies showing that smaller hearts are present in people with chronic fatigue syndrome (ME/CFS).

Mirroring Dr. Cheney’s unpublished findings, both Newton and Miwa have also found reduced diastolic volume (30%).  The diastolic phase of the heart cycle is the filling phase. During diastole, the ventricles relax and then, in an energy intensive process, expand so that they can fill with oxygen enriched blood. Reduced diastolic volume or preload indicates that  the heart is not being filled as much as normal.

Both Newton’s and Miwa’s study published last year found significantly reduced diastolic volume and mass, stroke volume index and cardiac output.  (Miwa targeted and consistently found reduced left ventricular volume and density. He did not measure right ventricular functioning. He or she also appears to be the first Japanese researcher to drop the term CFS and use myalgic encephalomyelitis exclusively throughout the latest paper. )

The Study

Now Newton is back doing more tests with a much larger and better defined cohort (n=41 ME/CFS patients / 10 healthy controls).

Newton measured how much blood entered the heart during the diastolic phase (end-diastolic volume) and systolic phases (end-systolic volume) then how much it spate out (stroke volume). She also assessed the size or mass of the heart.

This time, suspecting that reduced blood volume played a role in the poor cardiac performances, she analyzed blood volume three ways: total blood volume (TV), red blood cell volume (RCV) and plasma volume (PV).

As before, Newton found reduced blood volume during both the diastolic and systolic phases of the heart cycle and not just minor reductions either; ME/CFS patients had a whopping 25% less blood entering their hearts than the healthy controls. They also had about 25% less stroke volume and index and almost 30% smaller heart mass.  These appear to be very large reductions in both heart mass and heart functioning in ME/CFS patients.

Blood pressure was affected as well; ME/CFS patients had significantly lower systolic (125-109) and diastolic (76-70) blood pressures than the healthy controls.  The reduced blood pressure and stroke volumes could result from the poor heart functioning or they could produce the poor heart functioning by not pushing the heart to work harder.

Dr. Cheney appears to believe that reduced heart energetics are interfering with the hearts ability to contract enough to accommodate the blood entering it.  Another possibility is that reductions in blood pressure have resulted in smaller hearts.

Another possibility is that there’s  something wrong with the vascular system leading to the heart which is reducing blood flows to the heart. Reduced blood flows would result in a smaller heart. That’s the option Dr. Newton appears to be most interested in.

Non Compliant Veins?

Dr. Newton questioned whether a problem with “venous compliance” was present.  Since 2/3rd’s of our blood is locked up in our veins the reduced diastolic volume or preload found in ME/CFS could reflect large amounts of blood that has somehow gotten stuck in our veins.

Venous compliance refers to the ability of veins to “push back” once they get extended with fluid. The more full of fluid they are, the more the veins should – like a rubber band that has been stretched – exert pressure on the fluid to  move. If ME/CFS patients veins are non-compliant; that is, if they’re kind of flaccid in response to filling they may not be moving the blood along as they should.

That could lead to reduced preload (reduced diastolic volume).
Venous compliance can be affected by a number of factors including vasodilators and vasoconstrictors, the muscle tone of the smooth muscle tissue, and the renin–angiotensin system. One wonders if connective tissue problems (eg Ehlers Danlos Syndrome) could come into play as well.

Blood Volume

The blood volume results were assessed according to the norms expected. Blood volume was lower in the ME/CFS patients, but perhaps not to the extent that might have been expected.  About half the ME/CFS patients had normal red blood cell volume and about half fell below the 95th percentile expected. About a third of ME/CFS patients had plasma volumes below the 95th percentile.

On the other hand, statistical analyses suggested that the reduced red blood volumes were strongly associated with reduced ventricular mass in ME/CFS.  That suggests the ventricles may be smaller they’re not getting as much blood as usual.

There’s quite a bit of increased interest in blood volume right now.  Medow’s study on the effects of saline solution on ME/CFS should be published soon. He is currently examining whether the World Health Organization’s oral rehydration formula could be helpful in ME/CFS. His ability to use phenylephrine to increase blood flows to the brain and completely knock out POTS during a tilt test was astonishing.

Dr. Newton proposes to increase the blood volumes of ME/CFS patients and see if the size of their heart’s increase to normal size.

Is Arnold Peckerman Smiling Somewhere?

Arnold Peckerman apparently passed away a couple of years ago but one wonders what he would be thinking of all this.  Peckerman, LeManca and others working at Dr.  Ben Natelson’s NIAID funded ME/CFS research center were hot on the trail of cardiovascular issues when NIAID pulled the plug on its ME/CFS research.

The group had produced some interesting results. The first heart study in 1999 showed increased heart rates and reduced blood flows during a tilt test and presaged the attention on orthostatic intolerance and POTS.  The declines in heart rates and blood pressure during a stressful cognitive test they found may have been the first indication that the autonomic nervous system was prone to poop out under stress.

In 2003 their finding that people with ME/CFS were trying as hard as healthy controls knocked the legs out from under a prominent psychological interpretation. Next, Peckerman showed that people with severe ME/CFS (but not moderate ME/CFS) had a significantly lower stroke volume than healthy controls. Then he showed that the blood pressure responses of ME/CFS patients were off during exercise.

Could reduced heart blood flows after exercise help explain post-exertional malaise?
These results were positive but it was the last study, whose results were never published, which was a potential game-changer.

An MD, Peckerman, had seen post exertional malaise in some of his heart patients after the blood flows through their hearts had been stunted. Peckerman, therefore, decided to measured heart functioning before and after exercise in ME/CFS.

It was a small study – just 16 ME/CFS patients and four healthy controls but the results were astounding, and if they had been published and held up could have produced a simple and effective exercise test. Peckerman didn’t measure VO2 max – he measured blood flows – and it didn’t take him two exhausting exercise tests to get his result; he simply measured heart blood flows at rest, had his subjects exercise, and then measured blood flows at rest again.

In 2003 at the American Physiological Association conference Peckerman reported that 13/16 ME/CFS patients had significantly reduced blood flows at rest after exercise.  WebMD ran a story titled “Tricky Heart May Cause Chronic Fatigue Syndrome” in which Peckerman, obviously no shrinking violet, stated that the reduction of blood flows he had seen was the very definition of heart failure.

An Emory cardiologist in the story agreed. The finding of reduced heart blood flows was, in fact, what he saw in people with serious heart disease:

 “Typically we see this in people with three-vessel heart disease. A drop in [blood pumped by the heart] during exercise is not a typical response. It is actually a marker of significant coronary artery obstruction.”

Dr. Natelson described being quite excited at the results but we now know that “heart failure” is not present in ME/CFS.  Heart failure is a progressive condition that ultimately ends in death for just about everyone who has it, and, the fact that ME/CFS patients were not dropping dead from heart failure puzzled both Peckerman and Miller.  They both recommended that further study be done.

The study was never published, however, and we don’t know why.  After one more study on ME/CFS – which did not find differences in cognition before or after exercise – Peckerman was done. He’d participated in 13 studies on ME/CFS and GWS and never published again.

The cardiovascular connection to ME/CFS has never died, however.  As noted above both Newton and Miwa have found significantly reduced blood flows and filling in their studies. It now appears that those issues probably reflect significant problems with the cardiovascular system not the heart.

The outstanding question remaining from Peckerman’s unpublished study, though, is what happened during exercise to so dramatically affect the blood flows to the hearts of his ME/CFS cohort the next day?   The vascular system in ME/CFS and FM is a subject that continues to fascinate.

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Unexpected findings & promoting monocausal claims, a cautionary tale

Posted on 06/30/2016 by wames

Article abstract:

Stories of serendipitous discoveries in medicine incorrectly imply that the path from an unexpected observation to major discovery is straightforward or guaranteed.

In this paper, I examine a case from the field of research about chronic fatigue syndrome (CFS). In Norway, an unexpected positive result during clinical care has led to the
development of a research programme into the potential for the immunosuppressant drug rituximab to relieve the symptoms of CFS. The media and public have taken up researchers’ speculations that their research results indicate a causal mechanism for CFS – consequently, patients now have great hope that ‘the cause’ of CFS has been found, and
thus, a cure is sure to follow.

I argue that a monocausal claim cannot be correctly asserted, either on the basis of the single case of an unexpected, although positive, result or on the basis of the empirical
research that has followed up on that result. Further, assertion and promotion of this claim will have specific harmful effects: it threatens to inappropriately narrow the scope of research on CFS, might misdirect research altogether, and could directly and indirectly harm patients.

Therefore, the CFS case presents a cautionary tale, illustrating the risks involved in drawing a theoretical hypothesis from an unexpected observation. Further, I draw attention to the tendency in contemporary clinical research with CFS to promote new research directions on the basis of reductive causal models of that syndrome.  Particularly, in the case of CFS research, underdetermination and causal complexity undermine the potential value of a monocausal claim.

In sum, when an unexpected finding occurs in clinical practice or medical research, the value of following up on that finding is to be found not in the projected value of a singular causal relationship inferred from the finding but rather in the process of research that follows.

Unexpected findings and promoting monocausal claims, a cautionary tale, by Samantha Marie Copeland in Journal of Evaluation in Clinical Practice [Published online 10 Jun 2016]

NB The Norwegian researchers have never made a ‘monocausal claim’ for CFS and there is no sign that research has been limited as a result of their speculation.

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Negotiating trust on health-related online forums

Posted on 06/29/2016 by wames

Research abstract:

The internet is increasingly being used as a source of health advice and information by individuals with long term conditions (LTCs). Specifically, online forums allow people to interact with others with similar conditions. However, it is not clear how online health information is assessed by those with LTCs.

This study aims to address this gap by exploring how individuals with contested and uncontested LTCs utilise internet forums. Semi-structured interviews were conducted with 20 participants with ME/CFS and 21 participants with type 1 and 2 diabetes and analysed using thematic analysis.

Participants were recruited via online and offline routes, namely forums, email lists, newsletters, and face-to-face support groups. The findings indicate that the use of online forums was a complex and nuanced process and was influenced by a number of individual and illness-specific factors.

Participants trusted those with similar experiences and perspectives as themselves, while also valuing conventional biomedical information and advice. By accessing support online, forum users were able to draw on a personalised form of support based on the lived experiences of their peers. However, the role of digital literacy in developing and maintaining online relationships must be acknowledged.

‘You get to know the people and whether they’re talking sense or not’: Negotiating trust on health-related forums, by Ellen Brady, Julia Segar, Caroline Sanders in Social Science & Medicine, vol 162, Aug 2016, pp 151–157 [published online 18 June 2016]

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The ‘all in the mind’ myth of ME/CFS

Posted on 06/29/2016 by wames

Nursing in practice article, by Dr Keith Geraghty, 27 June 2016: The ‘all in the mind’ myth of myalgic encephalomyelitis/chronic fatigue syndrome

Health professionals should be made aware that ME/CFS is not a psychological illness and in order to improve patient care, nurses need to better understand this illness and its impact on patients.

Nurses often witness close-up the impact of acute and chronic illness on patients. Myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) is one illness that nurses may encounter that causes profound life changes for many sufferers. This controversial illness is sometimes presented as a psychosomatic disorder that requires psychological treatment. However, there is no compelling evidence that ME/CFS is a mental health condition and increasing evidence shows it is a biological disease with a range of complex symptoms. This article discusses how the ‘all in the mind’ myth of ME/CFS has permeated both medical discourse and popular culture, with negative consequences for patients living with this poorly understood condition.

1. Is ME/CFS really a mental illness?

In a recent Nursing in Practice article, Roberts (2016)1 suggests that ME/CFS is a psychosomatic disorder, best treated with psychotherapy and mindfulness. The erroneous idea that mindfulness is an optimum treatment masks a hidden and more important story; that very little is understood about ME/CFS and many health professionals are sceptical about whether ME/CFS is even a real illness. For example, NICE guidelines do not mention mindfulness.2

A GP once exclaimed to me that ‘all these patients need is anti-depressants and a good pair of running shoes’. While discussing my ME/CFS research at a hospital in Leicester a nurse offered me a similar opinion by suggesting that ‘ME/CFS patients would get out of bed if you paid them £5000 per day’. Such negative views among doctors and nurses are not uncommon and are perhaps fueled by misinformation about the illness being psychological.

In a recent book, All in Your Head: True Stories of Imaginary Illness,3 Dr Suzanne O’Sullivan, a London-based consultant neurologist, includes a chapter on ME/CFS. O’Sullivan argues ME/CFS is strongly associated with psychological complaints and illness beliefs. In contrast, a growing body of scientific evidence suggests that ME/CFS is not an imagined illness, nor is it a psychological condition, but a complex biological disease that is often triggered by an infection that causes observable neuro-immune dysfunction. Far from being ‘all in the mind’, sufferers often experience life-changing and disabling physical symptoms and physiological abnormalities (see Table 1).

Table 1: Biological abnormalities observed in ME/CFS

  • Alterations in grey and white brain matter.
  • Muscle cell dysfunction
  • Immune cell abnormalities
  • Raised inflammatory markers
  • Cellular and oxidative stress
  • Autonomic irregularities.
  • Cardiovascular deficiencies.
  • Orthostatic intolerance.

The World Health Organization (WHO) classifies ME as a neurological disorder in the International Classification of Diseases (ICD-10: G 93.3; WHO, 1992).4

The US Institute of Medicine (2015) conducted an extensive review of the evidence and concluded that ME/CFS is ‘a serious, chronic, complex, systemic disease’.5

The US National Institutes for Health confirmed ME/CFS as a disabling physical illness and stated that the medical profession has been responsible for causing distress to patients with ME/CFS by ignoring patients’ calls for medical help and failing to adequately research the disease.6

2. So why is ME/CFS treated with psychotherapy?

Psychiatrists have long been interested in attempting to explain the medically unexplained. Sigmund Freud, the father of modern psychiatry, explored the connection between the mind and health. The famous French neurologist J. Charcot believed traumatic life events may bring about a form of hysteria or paralysis in patients; while George Beard put forward the theory of neurasthenia (exhaustion of energy within the nervous system).7  These theories continue to influence how doctors perceive medically unexplained illnesses, particularly ME/CFS.

A brief time-line of how ME (nuero-immune disease) became CFS (a psychosomatic fatigue syndrome)

1955: Melvin Ramsay describes a viral outbreak illness among staff at the Royal Free Hospital in London as a post-infectious disease affecting brain, nerves and muscle tissue (Myalgic Encephalomyelitis).

1970s: UK psychiatrists McEvedy and Beard state that ME is nothing more than a case of ‘mass hysteria’.

1980s: A London newspaper runs a story about ME being ‘Yuppie Flu’. Since then, ME has been indelibly linked with stressed-out professionals complaining about exhaustion.

1988: The US Centers for Disease Control recommend replacing ME with a new syndrome (Chronic Fatigue Syndrome).

1990s: UK psychiatrist Simon Wessely argues ME (now CFS) is a biopsychosocial syndrome, partly created by social trends and maintained by patients’ illness beliefs and behaviours.

2000s: Colleagues of Wessely, including nurse/researcher Professor Trudie Chalder, conduct clinical trials of psychotherapy to treat CFS, including the £5 million PACE trial testing cognitive behavioural therapy and graded exercise therapy.8

2007: The UK National Institute for Health and Care Excellence (NICE) conducts a review and recommends CBT and GET for the treatment of ME/CFS.2  This decision is criticised by ME/CFS patient groups who deem CBT and GET inappropriate treatments. In particular, GET attracts much criticism.

2015: A large patient survey finds CBT has little impact on the condition: 74% of patients report that GET makes their symptoms worse, while simple pacing is preferred by patients.9  Such concerns are echoed in scientific studies that suggest exercise therapy may be harmful, given biological abnormalities found in ME/CFS.10

3. So, does cognitive therapy or exercise therapy help anyone with ME/CFS?

The answer to this question is rather complex. ME/CFS is an umbrella term often used for patients with ongoing unexplained fatigue. Hooper (2006) points out that ‘Amorphous definitions and diagnostic symptom criteria have contaminated study cohorts and corrupted research data’.11  Essentially, it may be difficult to differentiate patients with ME/CFS from patients with fatigue or depression, given the generality of the diagnostic criteria for CFS: patients are often lumped together in studies, with depressed patients responding better to CBT compared with ME/CFS patients.12

In addition, CBT may help with the secondary depression or anxiety that occurs in most illness states. Clinical trials of CBT and GET tend to recruit mild to moderately unwell CFS patients, as more severe cases are too unwell to take part. Yet, even if we accept these research biases, the evidence for the success of psychological or exercise therapies in ME/CFS is unconvincing:

  • Cochrane review:A meta-analysis found that while CBT and/or GET may benefit some patients with ME/CFS in the short term, the benefits are short-lived and have little impact on restoring physical function over the long term.13
  • PACE trial:The largest clinical trial of CBT and GET for CFS reported that 22% of patients recovered following CBT/GET added to standard care, while only 7% did after standard care alone.14 However, ‘recovery’ here did not mean a return to normal physical function. A patient could be deemed recovered with a SF-36 (quality of life) score of 60/100 or higher,8 even though a score of 65/100 indicates severe disability with 57/100 being a score of patients with Class II congestive heart failure.15 At follow-up, two years after treatment, there was no clear benefit of adding CBT or GET to standard medical care.8
  • FINE trial: A study of nurse-provided community-based CBT and GET for 296 CFS patients failed to find any evidence for the long-term effectiveness of these therapies.16  FINE stood for ‘Fatigue Intervention by Nurses Evaluation’. CBT-GET was compared against a supportive listening treatment. The FINE investigators found no statistically significant benefits to either pragmatic rehabilitation (CBT-GET) or supportive listening at 70 weeks. The authors concluded that the community setting was inappropriate, rather than the psychotherapy treatment.

4. Why is it important to know the facts?

In a recent Centers for Disease Control ‘Grand Rounds’ event (2016) discussing ME/CFS research, Professor Anthony Komaroff of Harvard University stated that the medical profession were wrong to adopt the name Chronic Fatigue Syndrome in 1988, as this term led to inaccurate perceptions of the illness. Komaroff points out that that there are thousands of published articles on biological dysfunction in ME/CFS, with no compelling evidence to suggest the illness is psychogenic (an illness of the mind).16

Many ME/CFS sufferers and advocacy groups are deeply concerned about the portrayal of the disorder as a psychological illness in medical publications and the wider media. Misinformation may negatively impact patients. Patient surveys consistently reveal that many ME/CFS patients experience medical scepticism, difficult interactions with health professionals and poor care quality (AfME, 2001).17  Sufferers report finding it difficult accessing benefits and social care and often have to fend off accusations of laziness and hypochondria – perhaps a consequence of the perception that the illness is a self-generated psychological illness.

The 25% ME Group, a charity that supports the most severely ill sufferers, state that the medical establishment has largely ignored these ME/CFS patients.18 Many are housebound or bedbound, with family members as full-time care-givers.

We must consider the harrowing case of Miss Sophia Mirza, a young ME sufferer forcibly removed from her home and sectioned under the Mental Health Act to impose psychiatric treatment on her. Miss Mirza died in 2005 and is one of the first patients in the UK to have ME as the official cause of death. The reality that ME/CFS kills some patients and dramatically shortens life expectancy is rarely reported in the media. In addition, ME/CFS sufferers are six times more likely to commit suicide compared to the general population;19 most likely as the result of having to deal with debilitating symptoms, such as chronic pain and sleep deprivation, but perhaps also having to deal with feelings of social isolation and poor medical treatment.

5. What can nurses do to support ME/CFS patients?

Many nurses will encounter ME/CFS patients, particularly in primary care. Nurses often have the capacity to form close therapeutic relationships with patients. Offering empathy and understanding to patients experiencing distressing symptoms is a central part of the nursing role. In the absence of a cure for ME/CFS, nurses are well placed to provide supportive care. By understanding the symptoms generated by the illness, nurses may be able to offer patients better care. ME/CFS severity varies from mild to severe and patients experience the illness in different ways. Some sufferers may be able to continue work on a limited basis, while others may be bed-bound, reliant on family and carers. Retired nurse Greg Crowhurst, a care-giver to a wife with severe ME/CFS, writes eloquently about how nurses may support patients with the illness.19

Practical tips for nursing practice are as follows:

  • Sufferers experience profound fatigue – nurses may be able to ensure patients are not left in waiting areas for long periods of time.
  • Sufferers experience cognitive problems – nurses may assist patients in medical consultations, perhaps asking whether the patient understands the information provided.
  • Sufferers experience sensory overload – nurses may ask patients if they require a quiet area or darkened room, or on home visits, nurses may avoid causing sensory distress by speaking quietly and ensuring mobile phones are turned off.
  • Sufferers symptoms vary and fluctuate – nurses should liaise with family members or care-givers to get a personalised account of the patient’s health status and care needs.
  • Sufferers often feel disbelieved and anxious – nurses may reassure patients, particularly if they convey empathy and knowledge of the illness to the patient.

Nurses also have an another important role as advocates for ME/CFS patients, helping to liaise between the patient and doctor and also helping to promote the patient voice in the public domain. However, to fulfill this important role, nurses need to better understand the illness and to understand that ME/CFS is by no means ‘all-in-the-mind’.

Conclusion: The key message for nurses

Most people feel fatigued following illness, stressful events, or after working long hours. This is quite different from the severe fatigue and the range of symptoms that patients with ME/CFS endure, including: unrelenting painful joints and muscles; cognitive dysfunction, including memory problems; gastrointestinal complaints; transient paralysis; hypersensitivity to light, noise and touch; unrefreshing sleep; post-exertional malaise after minimal effort; and the inability to maintain an upright posture for any significant period.

Overwhelming evidence shows that these symptoms are not psychosomatic. Nurses have a valuable role to play in assisting and supporting patients with ME/CFS. Nurses should not underestimate the power and importance of the nursing position to relieve suffering, prevent harm and promote better care for ME/CFS patients.

References

1. Roberts D. Diagnosing and managing chronic fatigue syndrome. Nursing in Practice 2016, 89.

2. NICE. Chronic fatigue syndrome/myalgic encephalomyelitis (or encephalopathy) – Diagnosis and management of CFS/ME in adults and children. NICE 2007, 53. https://www.nice.org.uk/guidance/cg53/chapter/1-guidance

3. O’Sullivan S. All in Your Head: True Stories of Imaginary Illness, 2016.

4. WHO. International Classification of Diseases, Tenth Revision (ICD-10). WHO 1992; G93.3.

5. IOM (Institute of Medicine). Beyond myalgic encephalomyelitis/chronic fatigue syndrome: redefining an illness. Washington, DC; 2015. ISBN: 978-0-309-31689-7.

6. Green CR, Cowan P, Elk R, O’Neil KM, Rasmussen AL. National Institutes of Health pathways to prevention workshop: Advancing the research on Myalgic Encephalomyelitis/chronic fatigue syndrome. Annals of Internal Medicine 2015;16;162(12):860-865.

7. Beard G. Neurasthenia, or nervous exhaustion. The Boston Medical and Surgical Journal 1869;217-221.

8. White PD, Goldsmith KA, Johnson AL et al. Recovery from chronic fatigue syndrome after treatments given in the PACE trial. Psychological Medicine 2013;43(10):2227-2235.

9. ME Association. ‘ME/CFS Illness Management Survey Results: No decisions about me without me’. Patient Survey, May 2015. http://www.meassociation.org.uk/wp-content/uploads/2015-ME-Association-Illness-Management-Report-No-decisions-about-me-without-me-30.05.15.pdf

10. Twisk F, Geraghty K. Deviant Cellular and Physiological Responses to Exercise in Myalgic Encephalomyelitis and Chronic Fatigue Syndrome. Jacobs Journal of Physiology 2015;1(2):007, 2015.

11. Hooper M. Gibson Inquiry – Day 1 April 18th 2006 – Group Testimonies, Comments by Professor Malcolm Hooper 21st April, 2006. http://www.meactionuk.org.uk/Hooper_on_Gibson_Inquiry_Day_One.htm

12. Jason LA, Torres-Harding S, Brown M et al. Predictors of change following participation in non-pharmacologic interventions for CFS. Tropical Medicine and Health 2008;36(1):23-32. DOI: 10.2149/tmh.36.23.

13. Price JR, Mitchel E, Tidy E, Hunot V. Cognitive behaviour therapy for chronic fatigue syndrome in adults. Cochrane Database of Systematic Reviews 2008, Issue 3.

14. Sharpe M, Goldsmith KA, Johnson AL, Chalder T, Walker J, White PD. Rehabilitative treatments for chronic fatigue syndrome: long-term follow-up from the PACE trial. The Lancet Psychiatry 2015a;2(12):1067-1074.

15. Juenger J, Schellberg D, Kraemer S, Haunstetter A, Zugck C, Herzog W, Haass M. Health related quality of life in patients with congestive heart failure: comparison with other chronic diseases and relation to functional variables. Heart 2002;87(3):235-241. http://dx.doi.org/10.1136/heart.87.3.235

16. Wearden A, Dowrick C, Chew-Graham C et al. Nurse led, home based self help treatment for patients in primary care with chronic fatigue syndrome: randomised controlled trial. British Medical Journal 2010;340:c1777.

16. Komaroff AL. Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Real Illness. Annals of Internal Medicine 2015;162:871-872.

17. Action for ME. ‘Severely neglected’. Patient Survey, 2001.

18. 25% ME Group. Stakeholder Response to NICE CG53 Three Yearly Review, Nov, 2010. http://www.angliameaction.org.uk/docs/25megroup-nice-cg53-response-nov2010.pdf (accessed January 2016).

19. Roberts E, Wessely S, Chalder T et al. Mortality of people with chronic fatigue syndrome: a retrospective cohort study in England and Wales from the South London and Maudsley NHS Foundation Trust Biomedical Research Centre (SLaM BRC) Clinical Record Interactive Search (CRIS) Register, Lancet, (published online Feb 9.), 2016.

20. Crowhurst G. Supporting people with severe myalgic encephalomyelitis. Nursing Standard 2005;19(21):38-43.

About the Author
Dr Keith Geraghty
Honorary Research Fellow, Centre for Primary Care, University of Manchester

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The difficulties of studying whether negative illness beliefs contribute to maintenance of CFS symptoms

Posted on 06/28/2016 by wames

Review abstract:

PURPOSE:

Chronic fatigue syndrome (CFS) is characterized by severe and debilitating fatigue. Studies based on self-report measures suggest negative illness representations, related symptom interpretations, and heightened symptom focusing are maintaining factors of fatigue. This study reviews studies which have investigated these cognitive biases using experimental methods, to (1) review the evidence for information processing biases in CFS; (2) determine the nature of these biases, that is the stages cognitive biases occur and for what type of stimuli; and (3) provide directions for future methodologies in this area.

METHODS:

Studies were included that measured attention and interpretation bias towards negative and illness-related information in people with CFS and in a comparison group of healthy controls. PubMed, Ovid, CINAHL, PsycINFO, Web of Science, and EThOS were searched until December 2014.

RESULTS:

The evidence for cognitive biases was dependent on the methodology employed as well as the type and duration of the stimuli presented.

Modified Stroop studies found weak evidence of an attentional bias in CFS populations, whereas visual-probe studies consistently found an attentional bias in CFS groups for health-threatening information presented for 500 ms or longer. Interpretative bias studies which required elaborative processing, as opposed to a spontaneous response, found an illness-related interpretive bias in the CFS group compared to controls.

CONCLUSIONS:

Some people with CFS have biases in the way they attend to and interpret somatic information. Such cognitive processing biases may maintain illness beliefs and symptoms in people with CFS.

This review highlights methodological issues in experimental design and makes recommendations to aid future research to forge a consistent approach in cognitive processing research.

Statement of contribution

What is already known on this subject? Studies based on self-report measures suggest negative illness representations, related symptom interpretations, and heightened symptom focusing contribute to the maintenance of chronic fatigue. Experimental studies in other clinical populations, such as patients with anxiety, depression, and chronic pain, have identified illness-specific biases in how information is implicitly attended to and interpreted, which has a causal role in these conditions.

What does this study add?

This is the first review of implicit cognitive processes in chronic fatigue syndrome (CFS).
Sustained attention and negative interpretations of somatic information may reinforce negative illness beliefs. Cognitive processes have a role to play in the cognitive behavioural model of CFS.

Attentional and interpretive bias towards illness-related information in chronic fatigue syndrome: A systematic review, by A Hughes, C Hirsch, T Chalder, R Moss-Morris in Br J Health Psychol. 22 June 2016 [Epub ahead of print]

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Activity pacing is associated with better & worse symptoms in long term conditions

Posted on 06/28/2016 by wames

Research abstract:

Background:
Activity pacing has been associated with both improved and worsened symptoms, and its role in reducing disability among patients with long-term conditions has been questioned. However, existing studies have measured pacing according to uni-dimensional subscales, and therefore the empirical evidence for pacing as a multifaceted construct remains unclear. We have developed a 26-item Activity Pacing Questionnaire (APQ-26) for chronic pain/fatigue containing five themes of pacing: activity adjustment, activity consistency, activity progression, activity planning and activity acceptance.

Objective:
To assess the associations between the five APQ-26 pacing themes and symptoms of pain, physical fatigue, depression, avoidance and physical function.

Methods:
Cross-sectional questionnaire design study. Data analysed using multiple regression.

Participants:
257 adult patients with diagnoses of chronic low back pain, chronic widespread pain, fibromyalgia and chronic fatigue syndrome/myalgic encephalomyelitis.

Results:
Hierarchical multiple regression showed that activity adjustment was significantly associated with increased physical fatigue, depression and avoidance, but decreased physical function (all P<=0.030). Activity consistency was associated with decreased pain, physical fatigue, depression and avoidance but increased physical function (all P<=0.003).
Activity planning was associated with reduced physical fatigue (P=0.025) and activity acceptance was associated with increased avoidance (P=0.036).

Conclusion:
Some APQ-26 pacing themes were associated with worse symptoms and others with symptom improvement. Specifically, pacing themes involving adjusting/reducing activities were associated with worse symptoms, whereas pacing themes involving undertaking consistent activities were associated with improved symptoms. Future study will explore the causality of these associations to add clarification regarding the effects of pacing on patients’ symptoms.

Activity pacing is associated with better and worse symptoms for patients with long-term conditions, by Deborah Antcliff, Malcolm Campbell, Steve Woby, Philip Keeley in The Clinical Journal of Pain, 17 June 2016 [Preprint]

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Gastric enterovirus infection: a possible cause of gastroparesis

Posted on 06/27/2016 by wames

Research abstract:

BACKGROUND: Gastroparesis (GP) is a disabling chronic gastroenterologic disorder with high morbidity that severely impacts patients’ quality of life. GP can present acutely after a viral-like gastrointestinal illness resulting in speculation that in some patients, neurologic damage caused by the infection might underlie the pathogenesis of idiopathic gastroparesis (IGP).

AIMS: The aim of this study is to document case reports of Enterovirus (EV) infection as a possible cause of IGP.

METHODS: Eleven patients referred with a diagnosis of GP underwent workup to exclude known causes of GP. Those with a history of flu-like symptoms or gastroenteritis prior to onset of GP symptoms had gastric biopsies taken during upper endoscopy to assess for the presence of gastric mucosal EV infection. Data on presenting symptoms, extra-intestinal symptoms and conditions, prior nutritional support requirements, upper endoscopy findings, and response to therapy were cataloged.

RESULTS: Eleven patients were diagnosed as IGP. Nine had active EV infection on gastric biopsies and were included (7/9 female, mean age 43 years). Eight out of nine received EV treatment with antivirals and/or immune therapies, with a wide degree of variability in treatment regimens. Four out of eight who received EV treatment had symptomatic improvement. One patient had stable symptoms. Three patients are currently undergoing therapy.

CONCLUSIONS: Gastric EV infection was frequently detected (82 %) in patients undergoing investigation for IGP. Antiviral and/or immune therapies against EV seem to be favorable, as most of our patients had resolution of their GP symptoms after treatment. This is the first study to identify EV as a possible infectious etiology of IGP.

Gastric Enterovirus Infection: A Possible Causative Etiology of Gastroparesis. by Barkin JA, Czul F, Barkin JS, Klimas NG, Rey IR, Moshiree B. in Dig Dis Sci. 2016 Jun 25. [Epub ahead of print]

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Indicator of CFS found in gut bacteria

Posted on 06/27/2016 by wames

Cornell Chronicle blog post by Krishna Ramanujan, 24 June 2016: Indicator of chronic fatigue syndrome found in gut bacteria

Physicians have been mystified by chronic fatigue syndrome, a condition where normal exertion leads to debilitating fatigue that isn’t alleviated by rest. There are no known triggers, and diagnosis requires lengthy tests administered by an expert.

Due to this lack of information, some people have even suggested the disease may be psychosomatic.

Now, for the first time, Cornell researchers report they have identified biological markers of the disease in gut bacteria and inflammatory microbial agents in the blood.

In a study published June 23 in the journal Microbiome, the team describes how they correctly diagnosed myalgic encephalomyeletis/chronic fatigue syndrome (ME/CFS) in 83 percent of patients through stool samples and blood work, offering a noninvasive diagnosis and a step toward understanding the cause of the disease.

“Our work demonstrates that the gut bacterial microbiome in ME/CFS patients isn’t normal, perhaps leading to gastrointestinal and inflammatory symptoms in victims of the disease,” said Maureen Hanson, the Liberty Hyde Bailey Professor in the Department of Molecular Biology and Genetics and the paper’s senior author. “Furthermore, our detection of a biological abnormality provides further evidence against the ridiculous concept that the disease is psychological in origin.”

Ruth Ley, associate professor in the Departments of Molecular Biology and Genetics and Microbiology, is a co-author.

“In the future, we could see this technique as a complement to other noninvasive diagnoses, but if we have a better idea of what is going on with these gut microbes and patients, maybe clinicians could consider changing diets, using prebiotics such as dietary fibers or probiotics to help treat the disease,” said Ludovic Giloteaux, a postdoctoral researcher in both Hanson’s and Ley’s labs and first author of the study.

Researchers have evidence that an overactive immune system plays a role in chronic fatigue. Symptoms include fatigue even after sleep, muscle and joint pain, migraines and gastrointestinal distress. One hallmark of the condition is post-exertional malaise, meaning patients may take weeks to recover from minor exertion. To test for ME/CFS, clinicians may give patients a cardio-pulmonary exercise test where they ride a bike until they become fatigued. If the test is repeated the following day,  ME/CFS patients usually cannot reproduce their performance from the first day.

“That’s very typical and specific of people with ME/CFS, because healthy people, or even people who have heart disease, can reproduce the exercise on the second day, but these people cannot,” Giloteaux said.

In the study, Ithaca campus researchers collaborated with Dr. Susan Levine, an ME/CFS specialist in New York City, who recruited 48 people diagnosed with ME/CFS and 39 healthy controls to provide stool and blood samples.

The researchers sequenced regions of microbial DNA from the stool samples to identify different types of bacteria. Overall, the diversity of types of bacteria was greatly reduced and there were fewer bacterial species known to be anti-inflammatory in ME/CFS patients compared with healthy people, an observation also seen in people with Crohn’s disease and ulcerative colitis.

At the same time, the researchers discovered specific markers of inflammation in the blood, likely due to a leaky gut from intestinal problems that allow bacteria to enter the blood, Giloteaux said.

Bacteria in the blood will trigger an immune response, which could worsen symptoms.

The researchers have no evidence to distinguish whether the altered gut microbiome is a cause or a whether it is a consequence of disease, Giloteaux added.

In the future, the research team will look for evidence of viruses and fungi in the gut, to see whether one of these or an association of these along with bacteria may be causing or contributing to the illness.

Co-authors include Julia Goodrich, a doctoral student, and William Walters, a postdoctoral researcher, both in Ley’s lab.

The study was funded by the National Institutes of Health.

Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome by Ludovic Giloteaux, Julia K. Goodrich, William A. Walters, Susan M. Levine, Ruth E. Ley and Maureen R. Hanson in Microbiome 2016 4:30 [published 23 June 2016]

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