Estimated number of people with ME:
Wales 13,000
UK 250,000
World 17-24 million
Every year, for a week surrounding May 12th, people with ME speak out to let the world know we are still here and still suffering. Many of us have been missing from our lives for years, in our own ME self-isolation and Lockdown.
I live with my husband in mid-Wales and we both have ME, having met because of it 23 years ago (through the ME Singles Group) despite living 200 miles away from each other at that time.
Our lives during the Coronavirus lockdown haven’t really changed day to day as we are pretty much housebound for most of the time anyway. We do get out occasionally but only for a very short time, possibly once or twice a week and only if we are both well enough, of course.
“lockdown has brought more things within our reach”
If anything, the lockdown has brought more things within our reach as there is now so much more online – museums to ‘visit’, shows to watch, and virtual tours of places I would never be able to visit and see normally. Our days are ‘full’ as it takes so long to accomplish anything, having to break it down into small manageable chunks with lots of rest in between.
Having Mike with me does ease any feelings of isolation and loneliness but, of course, as many ME sufferers know, feelings of missing out and poignant memories do hit us from time to time, especially as we have always found it so difficult to get others to understand ME and how it affects us. At least Covid-19 sufferers are believed.
The lockdown does remind me of when I first became ill and my whole life radically changed, as it has now for so many at this time of Coronavirus. However, most people still have their health. even though the future is uncertain for them. I think ME sufferers are well used to adapting as we have had no choice. I have heard of some people’s experiences with Coronavirus which remind me of ME, especially in the early days when you don’t know what is happening to your body and brain – crushing fatigue, brain fog and confusion, whole body weakness, headaches, pain, and myriad other symptoms.
One glaringly obvious difference between now and when we became ill with ME is that people’s health problems with this virus are being taken seriously. Becoming ill with ME is devastating not only for what it takes away but also for how others, especially the medical profession, treat you. We have both been to numerous doctors for help over the years but there have been few tests or referrals offered, with symptoms sometimes attributed to psychological reasons which, I find, most insulting.
Doctors also seem to misdiagnose patients with ME when they don’t have it, so more education about what ME is and is not is definitely necessary. We are not believed so we tend to keep quiet and suffer largely alone now. In this pandemic people are listened to and the Coronavirus is taken seriously as the devastating illness it can be; but ME is equally devastating and the isolation associated with disbelief makes it even more so.
It will be interesting to see if there are any long-term consequences to having Coronavirus and if patience and tolerance persist over the coming months for those who find their symptoms linger.
On a practical note, the two supermarkets in mid Wales we usually use to deliver food to us on a regular basis have let us down as we can no longer get delivery slots with them. However, we have found local places who deliver and so still get regular deliveries of food. I aim to continue to use these places in the future after the lockdown to repay their great service.
In addition, we have found two other supermarkets who do deliver to us, as well as to my elderly in-laws in West Wales, even though getting slots has been quite a challenge. I have had emails at 10pm from a friend to tell me to go on a particular shopping website “now!” as there are slots, which has been rather trying but also funny in a way!
Of course, the weather being so lovely over recent weeks has been a bonus as we like to sit on the patio by the back door and listen to the birds, and watch the flowers and trees. We don’t have a lot of contact on a daily basis with others so haven’t found it too onerous to be alone. We have, however, ‘adopted’ two birds – a blackbird and a robin – or rather they have adopted us! They have us well-trained in putting food out for them whenever they want! It’s lovely when the robin sings quite near to us and I find it amazing how loud a song emits from such a little bird!
Let’s hope that, once this pandemic has eased, ME sufferers will get their voices heard by those who hold it in their hands to help us find a cure for this terrible illness.
Karen Rippon, Mid Wales
Patients who have had coronavirus could be at higher risk of developing Myalgic Encephalomyelitis (ME), researchers at the University of Leicester have warned.
From previous studies involving patients with Epstein Barr and SARS, it has been estimated that up to 10% of people recovering from COVID-19 could develop ME. Whilst the exact causes of all cases of ME are not known, viral infection is commonly identified as a trigger.
As part of their rehabilitation, patients who have been critically ill with COVID-19 may require physiotherapy, and so physiotherapists could play an integral role in spotting the initial signs of the disease developing in patients.
Dr Nicola Clague-Baker
, Associate Professor in the School of Allied Health Professions at the University of Leicester said:
“The link between severe viral infection and ME is clear, as evidenced in the previous outbreaks of SARS and Epstein Barr, which saw an 8 – 10% corresponding rise in the number of patients diagnosed with ME.
“During the national COVID-19 crisis, many physiotherapists will have been redeployed to front-line services, but as time goes on our attention will shift to the rehabilitation of patients that were critically ill with coronavirus.
“Now is the time for physiotherapists to heighten their awareness of this serious complication from viral infection. ME develops from post-viral fatigue syndrome and is usually diagnosed between four and five months from the start of the viral infection.”
ME currently affects approximately 250,000 people in the UK and causes a severity of disability that often exceeds conditions such as heart disease or cancer. Around 25% of patients are completely bedbound, with symptom duration that can last indefinitely.
A defining feature of ME is Post-Exertional Malaise (PEM), which is characterised by a set of symptoms including fever, muscle ache, headache, sensitivities, fatigue and dizziness. PEM is triggered by physical or cognitive exertion, which can be as simple as taking a shower or talking to a relative, and it can last days, weeks, or even months. PEM can manifest up to 24-48 hours after exertion, so it is not always apparent what activity was the trigger.
The challenge for physiotherapists who are working to rehabilitate COVID-19 survivors is to identify those who start to display symptoms of ME so that they can adapt their approach to avoid triggering PEM and worsening the condition.
Dr Clague-Baker recommends looking for indicators that there has been change to the patient’s daily life, for example they may have returned to work but are now having to use their weekends to recover or are finding daily tasks a struggle.
Dr Clague-Baker continues:
“After a period of illness, people will be keen to recover and return to their normal activities, and many may try to ignore symptoms and believe they can ‘push through’ their fatigue.
“Careful questioning and an awareness of the viral infection in their history may help to identify potential new ME patients. It may be several months, or even years, before their symptoms are accurately identified.”
Clinical signs to look for include:
physios4me: Post Covid-19 Rehabilitation
Edwyn’s ME Lockdown view
Purpose:
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating chronic multisystem illness of unknown etiology characterized by profound fatigue and impaired neurocognitive, endocrine and immune functions. Currently, there are no tests or validated biomarkers for the definitive diagnosis of ME/CFS, which is based on exclusion of other medical explanations for symptoms.
While the cause is unknown, there are multiple reports in the literature suggesting a role for viruses, particularly human herpesvirus-6 (HHV-6) and Epstein-Barr virus (EBV) in ME/CFS. In support of this premise, recent studies by our group have demonstrated that 50% of patients with ME/CFS had high levels of antibodies to the deoxyuridine triphosphate nucleotidohydrolase (dUTPase) protein produced by EBV and HHV-6A/B. These results suggest that these viruses can and may contribute to the underlying pathology observed in some ME/CFS patients.
The objective of my project is to determine the mechanism(s) through which EBV-dUTPase may contribute to the neuro-immune dysfunction in ME/CFS using an in vivo model.
Methods:
Gene expression analysis of 30 genes was conducted on brain tissue samples from wild-type and Toll-like receptor 2 (TLR2) knock-out C57Bl/6 mice injected via the intraperitoneal route for 5 days with either EBV-dUTPase protein or vehicle control. The effect of EBV dUTPase on the expression of genes with key functions in brain plasticity, pain, and fatigue as well as the involvement of TLR2 in EBV-dUTPase induced effects on gene expression was examined by qRT-PCR.
Findings:
When compared to wild-type mice treated with EBV-dUTPase, TLR2-KO EBV-dUTPase treated mice showed a trend of up-regulation of the Drd1, Egr1, and Nr4a1 gene expression in the right hemisphere, and down-regulation of the Slc6a3, Slc6a4 and Tph2 gene expression in the left hemisphere, in addition to up-regulation of the Dbh gene in the left hemisphere. EBV-dUTPase also induced an up-regulation of the Gch1 in the left hemisphere and IL-1β genes in both hemispheres in the WT-EBV mice, though it appears to be TLR2 independent.
Implications:
The data suggests that the EBV-dUTPase is capable of modulating the expression of genes (Dbh, Drd1, Egr1, Nr4a1, Slc6a3, Slc6a4, and Tph2) associated with early growth protein, nuclear receptor 77, and dopamine and serotonin pathways in a TLR2-dependent manner and may contribute to the cognitive impairments, neuroinflammation, and pain associated with ME/CFS.
This activity is intended for primary care physicians, nurses, nurse practitioners (NPs), and other healthcare providers (HCPs) involved in the diagnosis and management of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).
The goal of this activity is to increase clinicians’ knowledge in the diagnosis and management of patients with ME/CFS.
Upon completion of this activity, participants will:
Have increased knowledge regarding the
The questions within the activity are designed to test your current knowledge. After each question, you will be able to see whether you answered correctly and read evidence-based information that supports the most appropriate answer choice. The questions are designed to challenge you; you will not be penalized for answering the questions incorrectly. At the end of the activity, there will be a short post-test assessment based on the material presented.
The questions after each case study aim to discover the level of knowledge about ME as presented in the IOM Report: Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Redefining an Illness. US Continuing Medical Education accreditation is available.
Introduction:
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a disease with high symptom burden, of unknown etiology, with no established treatment. We observed patients with long-standing ME/CFS who got cancer, and who reported improvement of ME/CFS symptoms after chemotherapy including cyclophosphamide, forming the basis for this prospective trial.
Materials and methods:
This open-label phase II trial included 40 patients with ME/CFS diagnosed by Canadian criteria. Treatment consisted of six intravenous infusions of cyclophosphamide, 600–700 mg/m2, given at four-week intervals with follow-up for 18 months, extended to 4 years. Response was defined by self-reported improvements in symptoms by Fatigue score, supported by Short Form 36 (SF-36) scores, physical activity measures and other instruments. Repeated measures of outcome variables were assessed by General linear models. Responses were correlated with specific Human Leukocyte Antigen (HLA) alleles.
Results:
The overall response rate by Fatigue score was 55.0% (22 of 40 patients). Fatigue score and other outcome variables showed significant improvements compared to baseline. The SF-36 Physical Function score increased from mean 33.0 at baseline to 51.5 at 18 months (all patients), and from mean 35.0 to 69.5 among responders. Mean steps per 24 h increased from mean 3,199 at baseline to 4,347 at 18 months (all patients), and from 3,622 to 5,589 among responders. At extended follow-up to 4 years 68% (15 of 22 responders) were still in remission. Patients positive for HLA-DQB1*03:03 and/or HLA-C*07:04 (n = 12) had significantly higher response rate compared to patients negative for these alleles (n = 28), 83 vs. 43%, respectively. Nausea and constipation were common grade 1–2 adverse events. There were one suspected unexpected serious adverse reaction (aggravated POTS) and 11 serious adverse events in eight patients.
Conclusion:
Intravenous cyclophosphamide treatment was feasible for ME/CFS patients and associated with an acceptable toxicity profile. More than half of the patients responded and with prolonged follow-up, a considerable proportion of patients reported ongoing remission. Without a placebo group, clinical response data must be interpreted with caution. We nevertheless believe a future randomized trial is warranted.
Clinical Trial Registration: www.ClinicalTrials.gov, identifier: NCT02444091.
MEPedia: Cyclo ME study Cyclo ME study part A
Promising results from trial of cancer drug in ME/CFS – but results should be interpreted with caution, according to researchers from Haukeland University Hospital.
From 1st May 2020, when the Countess of Mar retires officially from the House of Lords after almost 45 years’ service, the ME community will be losing a champion of the first rank and a redoubtable campaigner for acceptance of the illness, for research and for the proper treatment from government and the NHS of those affected by ME.
The Countess (her title dates back to c1014 and is the oldest peerage title still extant in the United Kingdom and is held by her in her own right) was, until her retirement, the only hereditary peeress in the House of Lords. She was elected to serve as one of the ninety-two hereditary peers retained in the Lords and sat as a cross-bencher. Her departure is marked by an article in ‘The Daily Telegraph’ of 2nd May (paywall) in which, with typical good humoured directness, she says “I don’t want to be there past my best before date.”
On of the privileges of membership of the House is access to Ministers, politicians, and decision-makers which she utilised to the utmost and to the benefit of those affected by ME.
Her zeal for a revolution in the perception and treatment of ME/CFS stemmed from her own experience of organophosphate poisoning which led to autonomic dysfunction. Concern turned to action and she was a member of several European Community Select Committees – on the environment, agriculture and consumer protection, and secretary of the All-Party Parliamentary Group on Pesticides and Organophosphates and a leading light and vice-chair of the All-Party Parliamentary Group on ME.
In 2008 and under her chairmanship, she created the Forward-ME Group, which consists of a broad spectrum of charities and voluntary organisations. The Group’s aim is to promote effective joint working by organisations to maximise impact on behalf of all people with ME and CFS in the UK. From the first meeting, ME Research UK has been a member with our (now) Vice Chair Sue Waddle, a regular attendee.
There have been 50 Minuted Meetings of the Group since the inaugural one on 8 October 2008. The ethos follows that set out in the Opening Statement:
I do hope that all of us here today will develop a strategy for bringing together all those who suffer from ME or are supporters and that we can then move on to transform the ME scene.
It is undoubtedly true that the Group would not have benefited from the opportunity to quiz politicians and the likes of NICE Directors, Officers of various medical Royal Colleges, the CMO of Capita or the Chairman of Optimum Health Care without the leverage that an invitation from a peeress possesses. The speakers, it is fair to say, left meetings under no doubt what challenges were faced by those with ME/CFS due to the decisions/processes that the speakers’ organisations had made.
In the House, Hansard records 36 instances of the Countess speaking to the Chamber specifically about ME/CFS (since such records were indexed from 2006). This does not include contributions to debates regarding neurological conditions or concerning those affected my long-term chronic illnesses in general. The contributions run the full gamut of issues which affect the ME community – social security, personal independence payments, work capability assessments, children and young persons, as well research. Her comments on the PACE trial (6 February 2013), CBT (18 March 2013), and neurological conditions (11 October 2010) are especially noteworthy and informed, and reward a re-visit.
The opportunities offered at Forward-ME for collaboration is illustrated by the commissioning of a survey into the experiences of those with ME/CFS who were offered CBT and GET. The study (funded jointly by ME Research UK and the ME Association) was delivered to NICE as part of a submission to provide hard evidence of the results of both ‘treatments’ and its findings received much publicity and are oft quoted.
In their Lordships’ debate on ME on 2 June 2008 – over a decade before the historic Jan 2019 House of Commons one – the Countess elicited confirmation from the Government (the Parliamentary Under-Secretary of State, Department of Health, Lord Darzil of Denham) “My Lords, the Government accept the World Health Organisation’s classification of CFS/ME as a neurological condition of an unknown cause.” An acceptance which has been used to remind the Department of Work and Pension of the nature of the illness ever since.
Her activities have not been confined to the red benches either. The Countess has been a vociferous letter-writer in defence of those affected by the illness and in challenging misconceptions about the illness e.g. Dr S O’ Sullivan’s book ‘It’s All in Your Head: True Stories of Imaginary Illness’.
Her role has also led to invitations to speak at various events – the launch of the CMRC for example and, in March 2015, to the Royal Society of Medicine to contribute to a lecture on ‘ME/CFS: Frontiers‘. The aim was to give delegates, all members of the Royal Society of Medicine, “a rare opportunity to learn about ME/CFS from a clinical, scientific and political perspective.” Her speech included a quote from Frantz Fanon and was addressed to the medics present
Ladies and gentlemen, I know how very difficult it is to say ‘Sorry, I got it wrong’, especially when your whole career has been based on a particular belief. I have been told that, in medicine, nothing will change until the old guard moves on. The history of medicine is littered with instances of this phenomenon. It is my very sincere wish that the situation will change radically long before the changing of the guard.
Through her work, Margaret has spoken truth unto power and pointed out the injustices that surround ME/CFS and the treatment of those with the condition. Although she will be retiring from the House of Lords, we know that she will not be withdrawing from the fight and we are truly grateful for all that she has done (thus far!) Excepts from Her letter to the members of the Forward-ME Group is reproduced below.
Trustee, Prof Faisel Khan, with ME Research UK Vice-Chair Sue Waddle, Patron The Countess of Mar, and Trustee Jan McKendrick at the launch of the CMRC. Part of email from the Countess of Mar to Forward-ME Group members –
After a great deal of thought and with some initial regrets, I have finally bitten the bullet and have decided to retire as a member of the House of Lords with effect from 1 May. As you know, I haven’t been well for some time and, although I am much better than I was, I have realised that I cannot be relied upon to do my Parliamentary duties to the standard that I would wish. I also find the prospect of travelling and getting about the House daunting.
After reaching my 80th year and having been a member of the House for nearly 45 of those years I feel that, while enjoying the huge privilege that membership has afforded me, I have done my duty.…….. Looking back, I believe that between us we have managed to change the perception of ME by most of both the medical profession and the public. There is still some way to go before we know cause/s and cure, but we are well on the way to finding them. I am confident that the NICE guideline development group are determined to get the new ME/CFS guideline right. I suspect that when this is published much will change for people with ME.
Telegraph: I want to go out on a high’: Meet Parliament’s last Countess, 4 May 2020
…yet it was only after she suffered a catastrophic accident in 1989 that she fully realised the power of her peerage. The couple were ‘dipping’ sheep on their farm in the Malvern Hills when some of the organophosphate liquid splashed inside her Wellington boot. ‘Three weeks later it was as though I’d been poleaxed,’ she recalls.
The poisoning sparked 18 months of chronic fatigue syndrome (ME), which affected the Countess’s memory and speech. The experience prompted her to embark on a lifelong campaign for better awareness of the condition, dismissed by many at the time as ‘yuppy flu’. ‘Psychiatrists would say – it’s all in your head. They’d been working on the principle that everybody was a shirker or could be cured by a bit of cognitive behaviour therapy and exercise,’ she recalls.
It took nearly 30 years of campaigning but in 2018, NICE (the National Institute for Health and Care Excellence) agreed to rewrite the outdated guidelines around ME.
ME Association: Stalwart champion of the ME community retires after distinguished parliamentary career 1 May 2020
Action for ME: Countess of Mar retires: share your message of thanks, 4 may 2020
BACKGROUND:
Myalgic encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS) is a multi-system illness characterised by a diverse range of debilitating symptoms including autonomic and cognitive dysfunction.
The pathomechanism remains elusive, however, neurological and cognitive aberrations are consistently described. This systematic review is the first to collect and appraise the literature related to the structural and functional neurological changes in ME/CFS patients as measured by neuroimaging techniques and to investigate how these changes may influence onset, symptom presentation and severity of the illness.
METHODS:
A systematic search of databases Pubmed, Embase, MEDLINE (via EBSCOhost) and Web of Science (via Clarivate Analytics) was performed for articles dating between December 1994 and August 2019. Included publications report on neurological differences in ME/CFS patients compared with healthy controls identified using neuroimaging techniques such as magnetic resonance imaging, positron emission tomography and electroencephalography. Article selection was further refined based on specific inclusion and exclusion criteria. A quality assessment of included publications was completed using the Joanna Briggs Institute checklist.
RESULTS:
A total of 55 studies were included in this review. All papers assessed neurological or cognitive differences in adult ME/CFS patients compared with healthy controls using neuroimaging techniques.
The outcomes from the articles include changes in gray and white matter volumes, cerebral blood flow, brain structure, sleep, EEG activity, functional connectivity and cognitive function. Secondary measures including symptom severity were also reported in most studies.
CONCLUSIONS:
The results suggest widespread disruption of the autonomic nervous system network including morphological changes, white matter abnormalities and aberrations in functional connectivity. However, these findings are not consistent across studies and the origins of these anomalies remain unknown. Future studies are required confirm the potential neurological contribution to the pathology of ME/CFS.
1. Introduction
ME/CFS is a complex disease of unknown aetiology, but there is an increasing evidence which suggests an autoimmune component after a viral infection [1]. In the quest of understanding disease pathogenesis, Gherardi et al provided a thorough review of the role of adjuvants in the development of ME/CFS after vaccination [2]. As highlighted by the authors, many cases of vaccination-induced macrophagic myofasciitis could be alternatively classified as patients with ME/CFS using the 1994 CDC criteria [3].
In addition, vaccination against the human papillomavirus (HPV) seems to have the capacity of triggering different autonomic dysfunctions including ME/CFS [4]. Under the concept of Autoimmunity/Inflammation Syndrome Induced by Adjuvants (ASIA) [5], Gherardi et al [2] suggested that ME/CFS after vaccination results from a chronic and systemic inflammation triggered by a persistence and diffusion of adjuvants in the body.
As a general principle, vaccination uses attenuated versions of natural infections in order to generate immunological memory against a specific harmful microorganism. However, vaccination as well as a natural infection has also the potential to trigger an autoimmune response via molecular mimicry, as recently discovered for Pandemrix (a vaccine against H1N1 influenza A virus) and type 1 narcolepsy [6]. Another important example of molecular mimicry with potential devastating adverse events for vaccinated individuals has been discussed for the L1 proteins included in the bivalent Cervarix and the quadrivalent Gardasil [7,8], two vaccines against HPV discussed in Gherardi at el [2].
Antigen mimicry has also been hypothesized as the cause of a case suffering from pancreatitis after HPV immunization [9]. We revisited this topic in the context of ME/CFS by performing a stringent bioinformatic analysis of these vaccine proteins.
3. Discussion
In summary, our bioinformatic analysis identified a potential antigenic mimicry between HPV L1 and different human proteins. Two of our candidate epitopes are included in a long list pentapeptides and hexapeptides from HPV L1 proteins already identified in previous studies [7–9]. The first one is the pentapeptide KFLLQAG from HPV16_L1, which has a high sequence homology with ANKDR16 human protein [7]. The second one is the hexapeptide ASSSRLL found in HPV6_L1 and HPV11_L1 proteins [9], which has already been validated experimentally as a strong inducer of virus-specific CD4+ T-cell responses [14]. The remaining epitopes identified here are novel and possibly so because of sequence variations in the L1 proteins used in this and previous studies.
From a standpoint of human genetics, HPV-vaccinated individuals who are carriers of either HLA-DRB1*01:01, HLA-DRB1*07:01, or HLA-DRB5*01:01 alleles might be at a higher risk of ME/CFS due to the suggested molecular mimicry. This genetic specificity is in line with several disparate associations between ME/CFS and different HLA genes reported in the literature [15,16]. However, given the numerous infection triggers of the disease [17], we foresee a problem of irreproducibility in future studies investigating these genetic associations. To overcome this problem, we suggest that researchers should make the effort of routinely collecting data and reporting on infection triggers of the disease in their study participants.
… In conclusion, the suggested molecular mimicry as a trigger of ME/CFS in HPV-vaccinated individuals is another piece of evidence supporting an autoimmune origin of the disease [1]. A fundamental question should be then addressed: what is the difference between ME/CFS and known autoimmune diseases? In this regard, Tregs might hold the answer to this question since these cells are thought to be key players in supressing deleterious autoreactive immune responses [27].
In addition, several studies reported an increased percentage of these cells in patients with ME/CFS when compared to healthy controls or autoimmune patients [28–30]. The overlooked role of these cells in ME/CFS will be discussed elsewhere [34].
