Helping to make the UK a better place for people with ME/CFS. ME/CFS is hard to accept. And those who do not accept their illness rarely recover. So we help people understand and come to terms with their illness.
Human blood contains red cells, white cells, platelets and
Red blood cells carry oxygen around the body – so a deficiency or abnormality here will probably cause anaemia.
White blood cells help the body to fight off infections and respond to allergies. White cells are sub-divided into cells called basophils, eosinophils, lymphocytes and neutrophils. Each cell has a slightly different function and an increase in a specific cell type can indicate than an allergic or infective reaction is taking place.
Platelets help to form blood clots and prevent bleeding. So, a platelet deficiency can cause excessive or prolonged bleeding from a wound site.
Plasma is the fluid component that contains a wide variety of substances produced by the immune system (e.g. antibodies, cytokines, natural killer cells) as well as enzymes, hormones and proteins that are made by or excreted by various organs and tissues in the body. The plasma also contains all the other chemicals and substances – vitamins, minerals, sugars and fats – that are carried around the body.
The use of new investigative technologies means that
scientists can now also look at specific proteins (proteomics), metabolites –
the remains of chemical reactions that have taken place (metabolomics) – and genetic
factors that may predispose people to developing specific diseases (genomics).
These tests are increasingly being employed by researchers
who are looking for the cause of ME/CFS. They are also being used to try and
find diagnostic blood markers (biomarkers), or markers for sub-groups, such as people
with severe ME/CFS.
Laboratory analysis of a small sample of blood can,
therefore, reveal a great deal of basic information about your state of health
and the function of various organ systems.
Is there a diagnostic blood test for ME/CFS?
While minor blood test abnormalities can occur in ME/CFS, none of them are sufficiently consistent or robust enough to turn them into diagnostic markers in our current state of knowledge.
So, the simple answer here is ‘no’ and a diagnostic ‘ME blood test’ seems unlikely to be made available in the near future.
The search for a diagnostic biomarker for ME/CFS
Significant progress is however being made in the search for
potential diagnostic biomarkers and a number of research groups have been
reporting some interesting preliminary findings.
The UK ME/CFS Biobank (which is funded by the MEA Ramsay
Research Fund) has found that some people with severe ME/CFS have a lower than normal
level of a muscle enzyme called creatine kinase.
They have also published results from a big study on the
immunology of ME/CFS that was funded by the National Institutes of Health in
America. This study found that some people with ME/CFS have an increased
proportion of an immune system component called MAIT cells (mucosal associated
invariant T cells).
This is an interesting abnormality that is being linked to
neurological and autoimmune conditions such as multiple sclerosis and
inflammatory bowel disease, where these cells appear at sites of inflammation
in the nervous system and gut lining.
The Stanford research group in America have reported on
changes in the shape of red blood cells and more recently observed that when a
specific type of immune cell is stressed to increase its energy requirements it
reacts in a different way to immune cells from healthy controls.
Before drawing any firm conclusions about these findings,
they need to be repeated in larger numbers of people with ME/CFS, and by other
independent research groups, and compared to findings in people with
autoimmune, infective and neurological conditions, as well as people with
unexplained chronic fatigue.
Summaries and reviews of all these recent research studies can be found in the Research section of the MEA website.
Which blood tests should be checked before a diagnosis of ME/CFS is
Everyone should have a number of routine blood tests before
a diagnosis of ME/CFS is confirmed. The results of all of these tests should be
within normal limits. So, the main purpose of arranging all these blood tests
is to help the doctor to rule out medical conditions that can also produce
fatigue and other ME/CFS-like symptoms.
with a list of appropriate blood tests to aid diagnosis, blood tests for
children, when to repeat blood tests, and a detailed explanation of what each
blood test means.
many years, a leading theory of causation in ME/CFS has been problems with the
mitochondria (the part of the cell responsible for generating energy).
However, researchers are now suggesting that this is less likely and that we should be looking for something that is impacting the mitochondria’s ability to function properly – rather than at the mitochondria themselves.
light of this, we have created an overview of mitochondrial research to date;
explaining what mitochondria are, exploring the possibility of mitochondrial
dysfunction as the cause of ME/CFS and offering other possible explanations if
the mitochondria are not to blame.
Mitochondria are the part of the cell responsible for producing most of the body’s energy.
Problems with energy production have been found in ME/CFS and have been primarily linked to mitochondrial dysfunction.
No ‘faulty genes’ or mutations have been discovered in the mitochondria of people with ME/CFS, suggesting it is not a form of classic mitochondrial disease.
There is conflicting research on the role of mitochondrial function in ME/CFS; some studies have found increased mitochondrial activity, some have found reduced activity, and some have found no differences between ME/CFS and healthy controls.
Recent research is now indicating that there is a problem with something ‘upstream’ of the mitochondria that is impacting their ability to function i.e. it is not a problem with the mitochondria themselves.
More research is needed on larger cohorts to identify this upstream factor, but there are already a few theories (and these are discussed in this review).
are small structures inside our cells that generate energy and are often
referred to as ‘the powerhouse of the cell’.
are responsible for converting chemical energy from food into a form that’s
readily available for use by the cell, called ATP (adenosine triphosphate).
energy-rich ATP molecules are the fuel for all of the different functions of
the body. Mitochondria allow the cell to produce up to 15x more ATP then they
would without them (Davidson, 2015).
are found in every cell in the body, except red blood cells, and there can be
up to 2000 mitochondria per cell! There are more of them in parts of the body
that use a lot of energy, such as the brain, the heart, the muscles and the liver.
But producing energy is not all these ‘powerhouses’ do; they are also involved in a range of other processes, such as cellular defence mechanisms, immune response signalling, cell signalling, cell growth and cell death (McBride et al., 2006).
mitochondria are responsible for around 90% of the cell’s energy production,
there are other methods of energy production that the cell can use that don’t
these are a lot less efficient processes that either use a limited fuel supply,
produce harmful by-products or are a lot slower.
are 4 main types of energy production. The first two use glucose as the ‘fuel’
source, whereas the second two use fat and protein:
Aerobic (requires oxygen). The classic form of respiration that the mitochondria adopt, as described above. It is the main form of energy production the body uses to carry out basic functions and low-intensity activities. On average, 36 molecules of ATP (energy molecules) are produced from 1 molecule of glucose.
Anaerobic (doesn’t require oxygen). This is what the body switches to during vigorous activity, where your oxygen supply can’t keep up with the energy demand. This reaction produces lactic acid as a by-product, which is harmful and causes muscle fatigue and aching. Only 2 molecules of ATP are produced from 1 molecule of glucose.
Gluconeogenesis (or fat burning!). This is the slowest form of energy production and can’t be used to supply energy for exercise. The body uses this when glucose is not available and fatty acids become the source of fuel. 1 small fatty acid chain can be used to produce 48 ATP molecules!
ATP Phosphocreatine (Protein breakdown). This is the quickest, most immediate source of energy, used for short quick bursts, such as sprinting. Lots of ATP are produced from a component of muscle called ‘Creatine phosphate’, until the stores of it run out. This is not a good form of energy to be using often as it breaks down muscle.
In 1999 I was working and living in Jersey and had been on
the island for about two years following a transfer from the UK. I was in my
element and twelve years into a career. My role in Jersey was still new and
exciting, and any periods of stress were short-lived and resolved without
My health was good, I was exercising regularly, working hard, socialising perhaps too much, and surrounded by people I liked.
We all lived together in a former hotel that my employers had bought and turned into a kind of hostel that housed people around my own age – I was thirty.
Some friends were taking a short break in Greece to relax
and play beach volleyball (something we did fairly regularly in Jersey). One of
their number dropped out unexpectedly and I took his place.
Unfortunately for me, during the course of the holiday I
picked up a nasty infection, but we all expected it would clear-up quickly once
I was back home. The infection did pass but not for some time – time I felt I
could not afford – and the symptoms I was experiencing never seemed to resolve.
I tried several times to return to work but each time I
struggled and was sent home. Remember, I was surrounded by people who also
worked, so being at home and off sick became quite stressful and in ways I had
not experienced before.
As the symptoms continued to wear me down and my health
deteriorated, I was diagnosed first with PVFS and then M.E. These followed
extensive testing, more worry – particularly I recall when a brain tumour was
suspected – more waiting… and the only advice from doctors and consultants was
to, rest, rest, rest.
I know that for some people with M.E., hearing this advice would
be welcome news indeed. How many doctors do we hear about who advise, exercise,
But for me and at that time, hearing that repeated advice to
rest was more stressful than almost anything else. I was not the sort of person
to give up and resting seemed a form of surrender.
Surely there were drugs I could be taking or something other
than convalescing? Resting seemed to make not a jot of difference although trying
to do more was counterproductive as well. I remember that being asked how I was
feeling became a question that I would dread.
There was something particularly difficult about having a
medical condition that sapped my vitality. And not knowing what might be
causing the symptoms of M.E. further undermined my confidence.
Don’t ask how I feel
I even stopped my parents from asking how I was feeling
because the answer was always the same – unless I pretended it wasn’t which was
something I often did just to sound positive.
As the stress and uncertainty built, my mental health began
to spiral. I had a career to get back to and while Lloyds Private Banking were
nothing if not supportive, it was harrowing to keep reporting no positive
In the end my physical and mental health became too much and
I couldn’t look after myself. I returned home to Cornwall and my parents.
There is something special about having familial support and
understanding. It’s good, don’t get me wrong and I couldn’t have survived
without it. But I’d been independent since I was seventeen, and at the time I
returned, I saw this as further evidence that I was weak and a failure.
My parents could see how much the combination of M.E.
symptoms and mental health problems were crippling me, and we decided that if
we couldn’t do very much about the former, we would try to work on improving
In 2000 getting a referral to a mental health specialist on
the NHS was next to impossible. I remember Mum having to pull out all the stops
to get me in to see someone.
At the time we knew I was suffering from depression, but we
also thought I might be bipolar. My emotions were yo-yoing – one moment I was
too positive and the next too negative and suicidal (it transpired that I
Never for a moment did I consider that speaking to a mental
health professional would be unmanly or contribute to my feelings of failure.
Things had become so desperate, I needed help and support from someone who knew
what they were doing and could relieve some of the pressure from me and from my
While the professionals I saw initially and again some months later, did help me through immediate crises, they didn’t instil in me the ability or confidence to cope with a long-term neurological condition or help me deal with acceptance and with the grieving process.
It was almost a year later, and I’d managed to return to
work in the UK. It was tough-going – I had a day-bed set-up in the office, car
service to my hotel, and set my own hours – but I thought I had achieved a
semblance of control and had learned how to manage M.E. and my mental health.
At the end of nine months and the successful conclusion of
the project, I was offered a posting anywhere I wanted. I chose to return to
Jersey so that I might vanquish the ghosts of my past. It was to prove a bad
The nine-month project was too much. I was kidding myself
that I was coping. And this only became apparent when I got back to Jersey and
started a new nine-to-five job. My M.E. came on with a vengeance and was soon
followed by worsening mental health.
I think some of my problems in general related to
embarrassment and in the grip of depression I would imagine that people had
very negative impressions of me and of M.E. I always said that if I could have
chosen any medical condition, then M.E. would be my very last choice. It was
incredibly hard to explain at the time, and it came with a terrible stigma
The occasional stress I experienced at work before I become
ill, was nothing compared to the stress I felt living with M.E.
Getting the right tools
In Jersey while trying to hold down my job once again, I was
put in touch with a private counsellor. He happened to also be an actor who had
co-starred in a famous and long-running Jersey-based detective show on TV – and
he had M.E. Although I didn’t know that before I met him.
He was able to provide me with tools necessary to
self-manage my mental health but more importantly for me, he provided a safe
space where I could offload, and we could begin to work through my issues and
He was also blunt and honest. And I needed blunt and honest.
His own experiences trying to work and manage M.E. were useful, although he was
more hippy-dippy than I cared to be, and he helped me to express some of the
mess that was constantly occupying my thoughts.
I coped better I think when I finally returned to the UK and
my parents in 2002. I was offered, and I accepted, ill-health retirement from
the Bank because of M.E. In fact, by then the end of my career brought with it
a sense of relief and I felt better able to cope.
I have had good and bad experiences of mental health professionals just as I have GPs and specialist consultants. When things were really bleak in the early years, I remember having a blazing row with a psychiatrist who claimed that I can’t have been trying hard enough to get better. What a jerk he was!
I still had cause to call on the services of counsellors and
a psychologist in later years. And I had a really positive experience from my
local NHS ME/CFS specialist service here in Cornwall who provided help in terms
of validation, acceptance and illness management.
We all I think need a break at times and whether you can
attend in person, by phone or Skype, talking to a professional who is removed
from your immediate support network, can bring relief – even if it is just a
way to get things off your chest.
It is often a slow process and one you need to keep chipping
away at. It’s not a cure for your problems – rather good therapy I think equips
you with the right tools to cope better. I learned that I needed to give myself
permission to feel sad on occasion and that it was OK to do so. That living
with M.E. was difficult, that I did need to adjust but that my life wasn’t over
because of it.
It can take some time and effort to find the right
counsellor or therapist. Rather like the huge range of antidepressants that
your GP might choose from, choosing a therapist can also be rather
hit-and-miss. But you have to stick with it until you find the right one for
you and at the right dose.
Learning to cope
I have struggled with acceptance of my new life away from
the Bank. I struggled accepting disability. I struggled accepting the loss of
earnings and with budgeting. And I struggled with the loss of my fiancé and the
realisation that I am likely to live alone without any children of my own. But
most of all I really struggled finding positivity in my life with M.E.
When anxiety and nerves keep coming at you. When negative
thoughts are whirring in your head and preventing sleep. When life seems
pointless. When you are constantly battling fear. When you feel you are letting
everyone down. When you are still trying to do too much. When you still want to
please everyone. When you simply cannot cope. Then I think it’s time to
consider reaching out to a professional for help.
I can’t say my mental health problems don’t return whenever something freaks me out – it can be relatively minor like a phone call, or major like a PIP reassessment or a bad-patch of M.E.
But I am better able to cope and have come to accept my life as a disabled person.
I also know that any periods of acute stress, uncertainty or anxiety will pass – even if they don’t seem like it at the time.
I no longer feel worthless or unable to contribute even if
the things I can do might seem small or sporadic. And I know I can re-refer to
a counsellor or psychologist if I have the need to talk outside of my immediate
My name is Russell, I am now fifty years old, I have occasional mental health issues and I have M.E.
This three-part guide is intended for those making both new claims for ESA or for Universal Credit based on health grounds. People making a renewal claim will also find it helpful.
The rules governing benefits are complex and ever-changing. This guide does not pretend to provide a full list of all them. It’s a general overview only. It is always sensible to seek detailed advice from a welfare rights specialist.
There are three types of ESA: New Style ESA, contribution-based ESA and income-related ESA.
In order to claim any of these, you must be of working age (aged 16 or over but under state pension age) and have an illness or impairment that affects your ability to work.
Part 2: The Work Capability Assessment Questionnaire
The ESA50 / UC50 Questionnaire allows the DWP to score you on a variety of different physical and cognitive tasks to assess your degree of functional impairment and how it affects your ability to work or undertake work-related activity with a view to moving towards work.
These tasks are called descriptors. Each descriptor has a variety of scores, depending on your level of difficulty carrying out that descriptor. In order to pass the Work Capability Assessment at all, you must score at least 15 points across all the descriptors.
To qualify for the “limited capability for work related activity” you must score a full 15 points on any of the “limited capability for work related activity” descriptors, which we will list below.
General Advice on Completing the Questionnaire
Get help to complete the ESA50 / UC50 as this plays an important role in the assessment process. People often answer incorrectly unless they are aware of the assessment criteria, which this guide aims to shed some light on.
When completing the form, think about the questions in the context of a work setting – working 16 hours or more a week. Remember, the DWP are assessing your ability to carry out any type of work, not just your previous job. In such a context, you would be expected to carry out each descriptor regularly, reliably, repeatedly and safely, within a reasonable timescale, without significant discomfort and to an acceptable standard. It must also apply for either most of the time, or the majority of the occasions that someone attempts that descriptor.
Do not complete the form as though it is your worst day. Yes, you do need to focus on what you can’t do rather than what you can do, but explain the variability. The reason I say this is that I have seen clients over the years omit to talk about variability, so that when they either are at their face-to-face assessment or in front of a tribunal panel, they seem “fine” – they can communicate, walk to the assessment room, handle their papers, etc – yet when someone looks at the form it sounds as though they are permanently bedridden and can never communicate. The first thing someone assessing you will think is that you are not credible, or that you have exaggerated your condition.
Continues with further advice about completing the questionnaire and with examples of how to respond to the descriptors…
Part 3 – The Face-to-Face Assessment
Preparing for the assessment
Try to take someone with you and for someone to support you to get there and back. You will be asked at the assessment how you got there and assumptions will be made if you got there yourself. Don’t forget, you not only have to deal with getting to an assessment centre, but also a potential wait of an hour or more to be seen sat upright in a straight backed chair, possibly without arms, in a potentially busy and noisy assessment centre with strip lighting. You then have to get through the assessment itself, which can last up to an hour (although typically it is usually around half an hour). You then have the journey home.
Ask for your assessment to be recorded.This should be done on your claim form but again over the telephone as soon as you receive your appointment. Call the number on your appointment letter to check this is in place.
You can change your face-to-face assessment appointment once only.If your request for a home visit is denied, back it up with medical evidence and ask for your request to be looked at again. An experienced welfare rights adviser may be able to assist you in changing the decision.
Continues with further advice about what to do in preparation and while at the assessment…
Pippa Stacey, Social Media Manager, ME Association.
In the run-up to Severe M.E. Day (8th August), we’re looking for people with Severe M.E. who would like to tell their stories.
We want to talk about the key
issues that affect arguably the most neglected section of our community, and
plan on raising awareness throughout the week commencing Monday, 5th August.
interested in hearing from people with Severe M.E. and their experiences of the
UK benefits system, which might include any problems encountered while trying
to obtain the help they deserve.
We’re also keen to share
stories of how benefit awards have positively influenced people’s lives or
helped them to better manage their condition, to show how much of a lifeline
these payments can be.
If you or your carer would
like to be involved, you must be comfortable sharing your identity
and photographs in either the news-media (newspapers) and on the ME Association
website and social media platforms.
If interested, please get in touch by Wednesday 24th July, and provide the following information:
Your name, age, where you live, and confirm that you have or have had Severe M.E.
A short summary of your story and experiences: in no more than 200 words.
Attach good quality photographs of yourself that you feel best represents your current circumstances.
Even if your story is not selected as a case study for the press, we hope to be able to share it on our website and social media, in a similar way to the successful Real M.E. campaign and reach beyond our immediate community.
Jen Taylor is very kindly raising money for the ME Association by selling her fabulous limited edition animal prints. Here she explains all about her M.E. and how she completes her art mainly from bed.
This lovely squirrel, striking a pose for my camera, is my favourite visitor to my garden, even though he’s only here to raid my bird feeders! I see him through my window while I’m resting and sometimes it seems like I inspire him to have a rest himself as he has taken to falling asleep on the tree or curling up in the hanging basket.
It took over a year to get my official diagnosis and this was a worrying and lonely time, not understanding what was going wrong with my body and why I couldn’t recover.
When I finally got my diagnosis, the ME Association were there for me with information and support.
Now I want to both give something back to this charity and to support others with ME.
I don’t have any artistic training – it’s only since having ME and needing to give up work that I started getting into art.
So that’s one of the positive things that has come out of my illness. I sketch my designs in bed and then carve a little whenever I have the energy.
It’s really helped me to release some of the frustration of being stuck indoors for so much of my time.
Very Limited Editions
I want to raise money for the ME association by selling some of my lino-cut prints. I make original prints based on my own drawings and photos. I’ve just a few prints as yet but I’m really excited to keep learning and printing.
Each of my prints is limited edition – VERY limited – there will be just 10 prints of each edition for this sale.
Each of the prints I’m selling is hand carved and printed. Please understand due to the handmade nature – each print may look a little different from these images here.
The illness now
called myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) was first
described in the mid-1980s. At that time, nothing was known about its
Indeed, because many standard laboratory test results were normal, some clinicians explained to patients that “there is nothing wrong.”
There was, of course, an alternative explanation: the standard laboratory tests might not have been the right tests to identify the underlying abnormalities.
Over the past 35
years, thousands of studies from laboratories in many countries have documented
underlying biological abnormalities involving many organ systems in patients
with ME/CFS, compared with healthy controls: in short, there is something
wrong. Moreover, most of the abnormalities are not detected by standard
In 2015, the Institute of Medicine of the National Academy of Sciences concluded that ME/CFS “is a serious, chronic, complex systemic disease that often can profoundly affect the lives of patients,” affects up to an estimated 2.5 million people in the United States, and generates direct and indirect expenses of approximately $17 billion to $24 billion annually (1).
Over the past several years, the National Institutes of Health (NIH) has expanded its research efforts directed toward this disease. It has initiated an unusually comprehensive multisystem study at the NIH Clinical Center, funded 3 extramural ME/CFS research centers and 1 data coordinating center, awarded supplemental support to 7 existing grants, and held regular telebriefings on the illness (as has the Centers for Disease Control and Prevention) (2).
A 2-day conference at the NIH in April 2019 highlighted recent progress. New research was presented that both reinforced and expanded on previous reports. Equally important, several plausible models were proposed that could explain many of the abnormalities that have been described.
Since the early 1990s, multiple studies have compared patients with ME/CFS with healthy age- and sex-matched controls and found abnormalities of the central and autonomic nervous system (3).
Neuroendocrine abnormalities were among the first evidence reported and involve impairment of several limbic-hypothalamic-pituitary axes (involving cortisol, prolactin, and growth hormone end products). A general downregulation of the hypothalamic-pituitary-adrenal axis is seen in patients with ME/CFS, in contrast to the upregulation of the hypothalamic-pituitary-adrenal axis seen in major depression.
Impaired cognition has been found by many investigators, including slowed information processing speed and impaired memory and attention that are not explained by concomitant psychiatric disorders.
Magnetic resonance imaging has revealed increased numbers of punctate areas of high signal in white matter. Functional magnetic resonance imaging has demonstrated different responses to auditory and visual challenges and to tests of working memory, as well as altered connectivity between different brain regions.
Positron emission tomography and magnetic resonance spectroscopy recently have demonstrated that patients with ME/CFS have a widespread state of neuroinflammation (particularly activation of microglial cells) as well as increased ratios of choline-creatinine and increased levels of lactate that correlate with levels of fatigue (4). Spinal fluid contains increased levels of proteins involved in tissue injury and repair.
Autonomic nervous system abnormalities have been repeatedly demonstrated in ME/CFS, particularly altered systemic and cerebral hemodynamics that correlate with symptoms (5). At the NIH conference, it was reported that with prolonged upright posture, abnormal increases in heart rate and decreases in blood pressure are common; even when heart rate and blood pressure responses are normal, substantial cerebral blood flow reductions are noted.
Recently, it has become possible to measure simultaneously thousands of metabolites in a sample of blood or other fluid. Several such metabolomic studies have revealed that in patients with ME/CFS, levels of many metabolites are lower than normal, as occurs in hibernation (6).
generation from all sources is impaired, including energy from oxygen, sugars,
lipids, and amino acids. In other words, the human organism may feel that it
lacks “energy” because its cells have a problem generating (and possibly using)
In addition, many
studies have reported markers of both oxidative stress and nitrosative stress (e.g.
increased levels of inducible nitric oxide synthase).
Many phenotypic and
functional abnormalities have been reported in lymphocytes. The most
consistently reported are increased numbers of activated cytotoxic CD8+ T
cells and poorly functioning natural killer cells.
Blood levels of
many cytokines are significantly higher in patients with ME/CFS, especially in
the first 3 years of illness. Moreover, the levels of many of the circulating
cytokines correlate positively with the severity of symptoms. Abnormal levels
of several cytokines in spinal fluid also have been reported.
At the NIH
conference, new HLA associations with both presence and severity of ME/CFS were
reported. In addition, investigators performing single T-cell receptor
sequencing reported expansion of CD8+ T-cell clones;
characterization of the antigenic targets is under way.
In patients with
ME/CFS, physical, postural (orthostatic), and cognitive challenges often
produce a flare of symptoms, typically after a 12- to 48-hour delay, a
condition called postexertional malaise.
seek to clarify whether challenges that make people with ME/CFS feel worse also
make a biological abnormality worse. If so, it becomes more likely that the
abnormality may be causally connected to the symptoms of the illness.
The NIH conference summarized evidence from multiple studies demonstrating that during exercise, the tissues of patients with ME/CFS have difficulty extracting oxygen, leading to a lower anaerobic threshold; with exercise, patients also have lower heart rate, blood pressure, and preload, several of which become much more prominent during a second exercise test repeated 24 hours after the first (7, 8).
Potential Unifying Models
What if ME/CFS
reflects the activation of biologically ancient, evolutionarily conserved
responses to injury or potential injury, a pathological inability to turn these
responses off, or both?
presentations at the NIH conference, citing work in animal models, indicated
that low-grade neuroinflammation triggers protective behavioral changes,
including reduced activity and appetite and increased sleep; this helps to
focus the available energy on preventing or healing the injury.
behavior change is likely triggered by a “fatigue nucleus” (a group of
neurons); the nucleus is triggered, in turn, by the cytokines produced by
neuroinflammation could have different triggers in different individuals. In
some, it could be induced by brain infection (such as by chronic herpesvirus
infection), autoantibodies, neurotoxins, or chronic stress.
inflammation outside the brain may be activating the innate
immune system inside the brain, both through humoral signals
that breach a porous blood-brain barrier and by retrograde signals sent up the
presentations included evidence that gut inflammation may be one peripheral
trigger of neuroinflammation: the gut microbiota of patients with ME/CFS often
include high numbers of proinflammatory species and low numbers of
hypometabolic state seen in patients with ME/CFS might also reflect a second
and possibly related biologically ancient response to injury. Such
hypometabolism is seen during the state of dauer (i.e. a developmental larval
stage) in the worm Caenorhabditis elegans and during
hibernation in more complex animals.
hibernation allow animals that perceive a vital threat (such as crowding in
worms or winter in bears) to throttle down nonessential, energy-consuming
metabolic processes to preserve the energy needed for vital functions; i.e. the
animal is temporarily sacrificing its ability to function in order to remain
initiate (and end) dauer and hibernation are known; investigators are pursuing
whether they have been activated (or not deactivated) in patients with ME/CFS.
A great deal more
is known today than 35 years ago about the underlying biology of ME/CFS. It is
clear that many biological measurements clearly distinguish patients with
ME/CFS from healthy control individuals.
At the same time,
some areas of ME/CFS research remain a challenge, and research has not yet
given practicing physicians 2 important tools.
First, there are as
yet no US Food and Drug Administration–approved treatments. Second, although
various biological measurements distinguish patients with ME/CFS from healthy
controls, none yet have demonstrated the high sensitivity and specificity
required for a good diagnostic test.
However, 1 small study (20 cases and 20 controls) described at the NIH conference (and recently published (9)) reported perfect sensitivity; the specificity of the test in individuals with other fatiguing illnesses remains to be shown.
international interest in the illness, and increased research support from the
NIH, the day is coming when physicians will be able to explain to patients not
only that there is something wrong but also that advances in understanding the
pathophysiology have led to effective therapy.
Corresponding Author: Anthony L. Komaroff, MD, Brigham and Women’s Hospital, 1620 Tremont St, Boston, MA 02120 (firstname.lastname@example.org).
3. Komaroff AL, Cho TA. Role of infection and neurologic dysfunction in chronic fatigue syndrome. Semin Neurol. 2011;31(3):325-337. doi: 10.1055/s-0031-1287654
4. Mueller C, Lin JC, Sheriff S, Maudsley AA, Younger JW. Evidence of widespread metabolite abnormalities in myalgic encephalomyelitis/chronic fatigue syndrome: assessment with whole-brain magnetic resonance spectroscopy. Brain Imaging Behav. 2019. doi: 10.1007/s11682-018-0029-4
5. van Campen CLMC, Rowe PC, Visser FC. Blood volume status in ME/CFS correlates with the presence or absence of orthostatic symptoms: preliminary results. Front Pediatr. 2018;6:352. doi: 10.3389/fped.2018.00352
6. Naviaux RK, Naviaux JC, Li K, et al. Metabolic features of chronic fatigue syndrome. Proc Natl Acad Sci U S A. 2016;113(37):E5472-E5480. doi: 10.1073/pnas.1607571113
7. Stevens S, Snell C, Stevens J, Keller B, VanNess JM. Cardiopulmonary exercise test methodology for assessing exertion intolerance in myalgic encephalomyelitis/chronic fatigue syndrome. Front Pediatr. 2018;6:242. doi: 10.3389/fped.2018.00242
8. Nelson MJ, Buckley JD, Thomson RL, Clark D, Kwiatek R, Davison K. Diagnostic sensitivity of 2-day cardiopulmonary exercise testing in myalgic encephalomyelitis/chronic fatigue syndrome. J Transl Med. 2019;17(1):80. doi: 10.1186/s12967-019-1836-0
9. Esfandyarpour R, Kashi A, Nemat-Gorgani M, Wilhelmy J, Davis RW. A nanoelectronics-blood-based diagnostic biomarker for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Proc Natl Acad Sci U S A. 2019;116(21):10250-10257. doi: 10.1073/pnas.1901274116
The ME Association
Real People. Real Disease. Real M.E.
We are a national charity working hard to make the UK a better place for people whose lives have been devastated by an often-misunderstood neurological disease.
I have no diagnosed mental health condition, but in the same way that we all have a physical health, every single one of us has a mental health too. And recently my mental health hasn’t been as good as it once was.
put it simply, I have been unwell every single day since September 2010 and no
human being can endure what we endure as M.E. sufferers and come away
have experienced incredible ignorance, disbelief, battled with the DWP, and
missed out on a lot of life since being ill, but it was the realisation that
motherhood would not be something I would experience that ended up being the
straw that broke the camel’s back.
to the severity of my M.E. and the all-encompassing effects that my health has
on my life, I will not be having children (it is not something I am wishing to
discuss or justify at this time).
Having reached this devastating conclusion some time ago, I steeled myself for the day my siblings or cousins made a pregnancy announcement.
But I still wasn’t quite ready for it. I will be an aunty for the first time later this month.
‘The Baby Thing’
every friend that announced that they were having a baby, there was a huge
internal conflict. I was overjoyed for them, but heartbroken for myself.
birth announcement left me torn between elation and despair. These feelings
were amplified when my sister announced her pregnancy late last year. I have
missed out on a lot since being ill, but this sacrifice seemed too cruel a
thing to endure.
have never viewed seeking help for one’s mental health as something to be
ashamed of, but I also genuinely never saw myself needing such help.
nearly nine years I have been okay. More than okay. Happy. Content. Grateful. But
it seems you can be all those things and still be sad, angry, frustrated and
lost. And feel this searing pain and despair over what I feel is an ultimate
loss; not becoming a mother.
conflicting emotions became overwhelming. I sought help. It took over six
months to find the courage to send that first email to my counsellor.
The breaking point came one evening after speaking to my pregnant sister. It was clearly deeply unhealthy to come away from each phone call and cry inconsolably.
I started to look for a local counsellor online, I became incredibly angry and
frustrated to see CFS/ME listed amongst the issues that a counsellor claimed
they could offer support with.
despised the implication that my very physical health condition was something
that talking therapy could help. When my appointment came around, I endeavoured
to mention my physical health condition as little as possible and just
concentrate on The Baby Thing.
can’t tell you how hard it was to go to that first appointment; to put myself
out there when I am so incredibly vulnerable and not nearly as thick-skinned as
M.E. sufferers need to be.
put myself in a situation where another’s views on M.E. could have done such
damage to me was a huge risk. But I was desperate. Perhaps the fact that I went
highlights how much of a struggle missing out of this milestone has been.
the optimist I though 6-8 sessions, as initially recommended, would be enough.
But now, 4 months on, I realise it is more of an ongoing commitment.
It’s opened a can of worms. It’s not that I kept everything in, or hidden away, or bottled up. I have had an incredible support system to lean on. It’s that now I have someone to offload to who has no emotional response to my struggles, and over 8 years of tales to tell.
it was The Baby Thing that led to me seeking help, it is the overall subject of
long-term illness that has been the main topic of discussion. Afterall, it is
M.E. and only M.E. that is the reason behind my husband and I facing a
childless future. A condition like M.E. has an incredibly far-reaching effect
on the sufferer and those in the sufferer’s life.
too many medical professionals have inaccurate and outdated views about M.E.
being psychological, my person-centred counsellor is in no way trying to cure
or help me recover. She is simply supporting me through the emotional impact
that M.E. has had. There is a difference.
think it’s important to note that it is a privilege to be able to seek this
help, from both a financial and a health point of view. Just a couple of years
ago I would have been too unwell to even contemplate starting this process.
Every cloud eh…
and friends have offered me support when I have shared my struggles, but there’s
something very powerful about getting sympathy and understanding from a health
professional. I think that’s something all M.E. sufferers can relate to.
have coped in any kind of way with the reality of M.E. is commendable. Kicking,
screaming, crying, full of hope and optimism, at peace…all responses are
valid. I have done them all.
seems I just needed to hear from someone further removed than my own support
network, that it is perfectly okay to be feeling the way I am feeling,
particularly around the subject of parenthood.
I can’t stress enough how valuable the experience has been for me so far. It really is good to talk.
At 39 the Conservative peer Baroness Nicola Blackwood of North Oxford is 30 years younger than the average member of the Lords. But as well as being the youngest member of the second chamber, she has another distinction — last month she made headlines for fainting at the despatch box.
It happened three weeks ago when, in her capacity as junior health minister, she was answering a question on the outbreak of listeria in hospitals. Looking peaky, Blackwood began to repeat the same phrase about food provisions before alerting other members: “I apologise. I’m going to faint. I’m going to faint.”
The collapse wasn’t a clever strategy for avoiding a difficult question. Blackwood suffers from a rare genetic condition called Ehlers-Danlos syndromes (EDS), which has made any sort of political career challenging.
Caused by a collagen-production defect, EDS can result in hypermobility, migraines and chronic muscle and joint pain.
As a result of EDS, Blackwood has also been diagnosed with postural tachycardia syndrome (PoTS), an abnormality of the autonomic nervous system, which controls breathing, digestion and the heartbeat.
This time she was “fighting off flu”. Infections play havoc with her blood pressure, meaning she can get “much sicker than everyone else”, but she has learnt how to anticipate and prevent these collapses. However, with such an urgent problem facing the NHS, she had not wanted to call in sick.
“That’s why I conked in the chamber, because I should have taken time off, and I didn’t, and it’s all my own fault,” Baroness Blackwood.
She experienced her first symptoms at seven, when
she suffered an asthma attack and had to be rushed to hospital at night by her
medic parents. Her father was a consultant cardiologist, her mother a nurse.
She continued to get weaker throughout her childhood, but no one could diagnose the problem. At school she learnt that “you have to have a stiff upper lip because you don’t want to be perceived as weak. You want to make sure you can still achieve”.
By the age of 17 she was barely able to climb
stairs because of severe muscle pain and problems with her heart rate and blood
pressure. One doctor told her parents that she wouldn’t be able to go to
university or hold down a normal job. But home-schooling helped her through her
GCSEs and A levels, and she won a place at St Anne’s College, Oxford, to study
No matter how determined she is, she says: “Mind
over matter only goes so far and you end up in hospital. Psychologically there
were times when I did think, ‘Shall I just give up and accept the fact I shall
lie on a bed of pain and never go forward,’ but I wasn’t really brought up like
“I was trying to manage all those moving parts with a fluctuating health condition and hide it from everybody, except my closest family. I realised it wasn’t working particularly well and my health deteriorated,” Baroness Blackwood.
Having had various wrong diagnoses —
including chronic fatigue syndrome/ME — Blackwood finally found a doctor, who
himself had EDS. Until that point she had always felt “like a hypochondriac”.
But her health “got worse before it got better”. It took a long time to fine-tune her medication and lifestyle regime. At first she was having 32 injections in her head every few months for her migraines.
“You think ‘I’m the unluckiest person in the world’ and then you realise it’s just one thing. It makes perfect sense,” Baroness Blackwood.
She kept the illness secret until she fainted in the presence of Tom Newton Dunn, the political editor of The Sun, in the 2015 general election and was forced to come clean.
She fears that “the trope of weakness” is more readily attached to women. “It’s been instructive how the public have reacted to the prime minister with her diabetes. Some have thought it’s a good thing and others have seen this as a sign of weakness.”
Yet Blackwood is determined to show illness and high-profile jobs are not mutually exclusive. She controls her symptoms with a fine-tuned holistic regime, combining medication, physiotherapy, diet and Pilates (yoga overstretches the ligaments and causes her muscles to go into spasm).
Mercifully, she no longer has to have the injections for her migraines, but she does “titrate” herself daily. She pulls out her phone and shows me the app she uses to monitor her heart rate.
Does she ever get to slow down? After she lost her seat in the last election her Instagram feed was wall-to-wall Mediterranean holidays, trips to Glyndebourne and skiing. However, since she’s been appointed to the Lords, the pictures are of her visiting hospitals.
Westminster, she concedes, is “not a great environment for your mental health or your physical health, especially at the moment. But we are as a government and a parliament trying to solve one of the biggest challenges that we have faced as a nation”.
Nevertheless, she says she couldn’t live with
herself if she didn’t try to make it easier for patients with rare diseases to
get an early diagnosis and help to create a care system that is easier to
“Each day I look at what I have in the diary and make a judgment about whether I really have to do it,” she says. “If the person I’m going to see or the speech I’m going to give is something that needs to be done more than I need to have a rest, then I take the hit. That’s what I signed up for and I did it consciously knowing that sometimes it’s not going to work out perfectly for the good of my health.”
The ME Association
Real People. Real Disease. Real M.E.
We are a national charity working hard to make the UK a better place for people whose lives have been devastated by an often-misunderstood neurological disease.
Abstract Chronic fatigue syndrome/myalgic encephalomyeltis is a condition of complex nature, characterised by unexplained disabling fatigue and a combination of non-specific accompanying symptoms. Individuals with chronic fatigue syndrome/myalgic encephalomyeltis frequently present with debilitating orthostatic symptoms, which may fall under the umbrella of postural tachycardia syndrome. Postural tachycardia syndrome is underpinned by autonomic nervous system dysfunction.
The gravitational deconditioning that occurs in those
severely affected by chronic fatigue syndrome/myalgic encephalomyeltis
alongside postural tachycardia syndrome has been suggested as a key focus for
interventions in this group. This case report documents the evaluation and
rationale behind a novel gravity-induced exercise intervention to improve the
symptoms of a 44-year-old female severely affected by chronic fatigue
syndrome/myalgic encephalomyeltis and postural tachycardia syndrome, who had
been bedbound for 10–15 years.
An exercise intervention was designed to challenge and
therefore improve key areas of autonomic nervous system regulation in the
presence of gravity. It contained seven different exercises conducted once a
month in a class over a 6-month period. Fatigue impact score, activity levels
and heart rate upon standing, as detected by an active stand test, improved
during the exercise intervention and at follow up.
Gravity-induced exercise intervention can have a positive
effect on an individual severely affected by Chronic fatigue syndrome/myalgic
encephalomyeltis alongside postural tachycardia syndrome.
Abstract Systemic Exertion Intolerance Disease (SEID) or myalgic encephalomyelitis (ME) or chronic fatigue syndrome (CFS) has an unknown aetiology, with no known treatment and a prevalence of approximately 22 million individuals (2%) in Western countries. Although strongly suspected, the role of lactate in pathology is unknown, nor has the nature of the two most central symptoms of the condition – post exertional malaise and fatigue.
The proposed mechanism of action of pyruvate dehydrogenase
complex (PDC) plays a central role in maintaining energy production with
cofactors alpha-lipoic acid (LA) and its counterpart dihydrolipoic acid (DHLA),
its regeneration suggested as the new rate limiting factor. Decreased DHLA
regeneration due to impairment of the E3 subunit or crossover of the
swinging arms of the E2 subunit of PDC have been suggested as a cause of
ME/CFS/SEID resulting in instantaneous fluctuations in lactate levels and
instantaneous offset of the DHLA/LA ratio and defining the condition as an LA
deficiency with chronic instantaneous hyperlactataemia with explicit
stratification of symptoms.
While instantaneous hyperlactataemia has been suggested to
account for the PEM, the fatigue was explained by the downregulated throughput
of pyruvate and consequently lower production of ATP with the residual
enzymatic efficacy of the E3 subunit or crossover of the E2 as a
proposed explanation of the fatigue severity.
Functional diagnostics and visualization of instantaneous
elevations of lactate and DHLA has been suggested. Novel treatment strategies
have been implicated to compensate for chronic PDC impairment and
This hypothesis potentially influences the current
understanding and treatment methods for any type of hyperlactataemia, fatigue,
ME/CFS/SEID, and conditions associated with PDC impairment.
Abstract Background: Few reports have examined the association between unemployment and work disability in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME). This study explored the key determinants of work disability in a CFS/ME cohort.
Methods: A community-based prospective study included 1086
CFS/ME patients aged 18–65 years. Demographic and clinical characteristics and
outcome measures were recorded. Multiple linear regression analysis was
performed to identify key risk indicators of work disability.
Results: Four hundred and fifty patients with CFS/ME were
employed (41.4%) and 636 were unemployed (58.6%). Older age at pain onset (OR:
1.44; 95% CI: 1. 12–1.84, autonomic dysfunction (OR: 2.21; 95% CI: 1.71–2.87),
neurological symptom (OR: 1.66; 95% CI: 1. 30–2.13) and higher scores for
fatigue (OR: 2.61; 95% CI: 2.01–3.39), pain (OR: 2.09; 95% CI: 1.47–2.97),
depression (OR: 1.98; 95% CI: 1. 20–3.26), psychopathology (OR: 1.98; 95% CI:
1.51–2.61) and sleep dysfunction (OR: 1.47; 95% CI: 1. 14–1.90) were all
associated with a higher risk of work disability due to illness.
Conclusions: Using an explanatory approach, our findings
suggest that unemployment is consistently associated with an increased risk of
work disability due to CFS/ME, although further more rigorous research is now
needed to help in targeting interventions at the workplace.
Abstract Background: Chronic fatigue syndrome (CFS) is estimated to affect up to 5% of people in Europe and is more common in women than men. It is characterised by unexplained fatigue, post-exertional malaise and a range of other symptoms. Recent studies indicate potential immune dysfunction in CFS, specifically regarding cytokines and the adaptive behavioural response.
Objectives: This study aims to investigate serum
transforming growth factor-beta (TGF-β) and the expression of the TGF-β
Receptor 1 (TGFBR1) and TGF-β Receptor 2 (TGFBR2) genes, in relation to the
fatigue associated with CFS.
Methods: Serum active and total TGF-β concentrations
were measured in 117 CFS patients and 40 HCs using a TGF-β responsive
luciferase bioassay. Expression levels of TGFBR1 and TGFBR2 were analysed using
quantitative PCR. Fatigue was measured using the fatigue impact scale (FIS)1.
FIS was categorised into three groups; ‘mild’ (0-80), ‘moderate’ (81-120) and
‘severe’ (121-160). Linear and ordinal regressions were performed on the
continuous FIS and FIS categories respectively.
Results: Serum TGF-β concentrations in the CFS group
did not differ significantly compared with the HC group (p=0.58). TGF-β
concentrations showed no correlation with disease duration but there was a
trend towards decreased TGF-β with increasing symptom duration. There were no
significant differences between the levels of TGFBR1 and TGFBR2 in any of the
fatigue groups, or between HCs. Active TGF-β concentrations were significantly
elevated in the ‘severe’ FIS group compared to the ‘mild’ FIS group (p=0.04).
Active/total TGF-β levels were significantly higher in the ‘severe’ FIS group
than the ‘mild’ and ‘moderate’ FIS groups (p=0.02, p=0.03 respectively).
Conclusion: These data suggest no differences in serum
concentrations of TGF-β or expression of TGFBR1 and TGFBR2, between the HC and
CFS groups. It also suggests no differences in expression levels of TGFBR1/2
between any of the CFS fatigue groups. However, active/total TGF-β levels were
increased in more severely fatigued patients based on FIS. This finding could
be due to higher levels of circulating TGF-β, or increased amounts of TGF-β
activation. Further work is necessary to confirm this finding in a larger
cohort of CFS patients, and to explore how this increase in TGF-β relates to
Abstract Background: Orthostatic intolerance (OI) is a significant problem for those with chronic fatigue syndrome (CFS). We aimed to characterize orthostatic intolerance in CFS and to study the effects of exercise on OI.
Methods: CFS (n = 39) and control (n = 25) subjects had
recumbent and standing symptoms assessed using the 20-point, anchored, ordinal
Gracely Box Scale before and after submaximal exercise. The change in heart
rate (ΔHR ≥ 30 bpm) identified Postural Orthostatic Tachycardia Syndrome
(POTS) before and after exercise, and the transient, exercise-induced postural
tachycardia Stress Test Activated Reversible Tachycardia (START) phenotype only
Results: Dizziness and lightheadedness were found in 41% of
recumbent CFS subjects and in 72% of standing CFS subjects. Orthostatic
tachycardia did not account for OI symptoms in CFS. ROC analysis with a
threshold ≥ 2/20 on the Gracely Box Scale stratified CFS subjects into three
groups: No OI (symptoms < 2), Postural OI (only standing symptoms ≥ 2), and
Persistent OI (recumbent and standing symptoms ≥ 2).
Conclusions: Dizziness and Lightheadedness symptoms while
recumbent are an underreported finding in CFS and should be measured when doing
a clinical evaluation to diagnose orthostatic intolerance. POTS was found in 6
and START was found in 10 CFS subjects. Persistent OI had symptoms while
recumbent and standing, highest symptom severity, and lability in symptoms
Abstract Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM) are both chronic disorders that have a devastating effect on the lives of the affected patients and their families. Both conditions have overlapping clinical features that partly resemble those of inflammatory disorders. The etiology is still not understood, and it is suggested that the immune system might be a contributing factor. So far, the results are inconclusive.
The purpose of this study was to compare the two conditions
and investigate the level of the inflammatory marker high-sensitivity CRP
(hsCRP) in CFS and FM patients compared to healthy controls. Female
participants aged 18–60 years were enrolled in this study. The group consisted
of 49 CFS patients, 57 FM patients, and 54 healthy controls.
hsCRP levels were significantly higher for both the CFS and
the FM groups compared to healthy controls when adjusting for age, smoking, and
BMI (p < .001). There was no difference between the two patient groups. The
level of hsCRP was affected by BMI but not by age and smoking.
Patients with CFS and FM have higher concentrations of hsCRP
compared to healthy controls. This remains significant even after adjusting for
BMI. CFS and FM cannot be distinguished from each other on the basis of hsCRP
in our study.
Abstract Post‐exertional malaise and delayed recovery are hallmark symptoms of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Studies on repeated cardiopulmonary exercise testing (CPET) show that previous exercise negatively affects oxygen uptake (VO2) and power output (PO) in ME/CFS. Whether this affects arterial lactate concentrations ([Laa]) is unknown.
We studied 18 female patients (18–50 years) fulfilling
the Canadian Consensus Criteria for ME/CFS and 15 healthy females
(18–50 years) who underwent repeated CPETs 24 h apart (CPET1 and
CPET2) with [Laa] measured every 30th second.
VO2 at peak exercise (VO2peak) was lower in patients
than in controls on CPET1 (P < 0.001) and decreased in
patients on CPET2 (P < 0.001). However, the difference in
VO2peak between CPETs did not differ significantly between groups. [Laa]
per PO was higher in patients during both CPETs
(Pinteraction < 0.001), but increased in patients and decreased in
controls from CPET1 to CPET2 (Pinteraction < 0.001).
Patients had lower VO2(P = 0.02) and PO (P = 0.002) at the
gas exchange threshold (GET, the point where CO2production increases relative
to VO2), but relative intensity (%VO2peak) and [Laa] at GET did not differ
significantly from controls on CPET1. Patients had a reduction in
VO2 (P = 0.02) and PO (P = 0.01) at GET on CPET2, but
no significant differences in %VO2peak and [Laa] at GET between CPETs.
Controls had no significant differences in VO2, PO or %VO2peak at GET
between CPETs, but [Laa] at GET was reduced on
CPET2 (P = 0.008).
In conclusion, previous exercise deteriorates physical
performance and increases [Laa] during exercise in patients with ME/CFS while
it lowers [Laa] in healthy subjects.
Abstract The use of graded exercise therapy and cognitive behavioural therapy for myalgic encephalomyelitis/chronic fatigue syndrome has attracted considerable controversy. This controversy relates not only to the disputed evidence for treatment efficacy but also to widespread reports from patients that graded exercise therapy, in particular, has caused them harm.
We surveyed the National Health Service-affiliated myalgic
encephalomyelitis/chronic fatigue syndrome specialist clinics in England to
assess how harms following treatment are detected and to examine how patients
are warned about the potential for harms. We sent 57 clinics standardised
information requests under the United Kingdom’s Freedom of Information Act.
Data were received from 38 clinics.
Clinics were highly inconsistent in their approaches to the
issue of treatment-related harm. They placed little or no focus on the
potential for treatment-related harm in their written information for patients
and for staff. Furthermore, no clinic reported any cases of treatment-related
harm, despite acknowledging that many patients dropped out of treatment.
In light of these findings, we recommend that clinics
develop standardised protocols for anticipating, recording, and remedying
harms, and that these protocols allow for therapies to be discontinued
immediately whenever harm is identified.
Abstract Changes in the terminology and diagnostic criteria for chronic fatigue syndrome/myalgic encephalomyelitis are explained in this paper. This syndrome is a complex and controversial entity of unknown origins. It appears in the medical literature in 1988, although clinical pictures of chronic idiopathic fatigue have been identified since the nineteenth century with different names, from neurasthenia, epidemic neuromyasthenia, and benign myalgic encephalomyelitis up to the current proposal of disease of intolerance to effort (post-effort). All of them allude to a chronic state of generalised fatigue of unknown origin, with limitations to physical and mental effort, accompanied by a set of symptoms that compromise diverse organic systems.
The International Classification of Diseases (ICD-10) places
this syndrome in the section on neurological disorders (G93.3), although
histopathological findings have not yet been found to clarify it. Multiple
organic alterations have been documented, but a common biology that clarifies
the mechanisms underlying this disease has not been established. It is defined
as a neuro-immune-endocrine dysfunction, with an exclusively clinical diagnosis
and by exclusion. Several authors have proposed to include CFS/ME within
central sensitivity syndromes, alluding to central sensitisation as the common
pathophysiological substrate for this, and other syndromes.
The role of the family doctor is a key figure in the
disease, from the detection of those patients who present a fatigue of unknown
nature that is continuous or intermittent for more than 6 months, in order to
make an early diagnosis and establish a plan of action against a chronic
disease with high levels of morbidity in the physical and mental sphere.
OBJECTIVE: To carry out a bibliographic review of the
terminology and diagnostic criteria of the chronic fatigue syndrome/myalgic
encephalomyelitis, in order to clarify the pathology conceptually, as a
usefulness in the diagnosis of Primary Care physicians.
Abstract Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a disabling condition that affects 0.4% to 2.4% of adolescents in the UK. Previous studies have reported high levels of anxiety, depression and worry among adolescents with CFS/ME. In adult studies, concerns have been raised about delays in accessing specialist CFS/ME services and the impact of delays on patients’ health and well-being.
In this study, we aimed first to assess the prevalence of
self-reported anxiety/depression, worry and degree of symptom impact among our
patient population of adolescents with CFS/ME. We then investigated whether
longer illness duration was associated with higher prevalence of self-reported
anxiety/depression, worry and symptom impact at initial assessment.
Abstract Chronic Fatigue Syndrome (CFS) and chronic pain syndromes represent major health problems in society. These conditions are disabling and strongly associated with low quality of life. Even though CFS and chronic pain are separate conditions, they have strikingly much in common.
Both pain and fatigue are important sensations
with protective value in an acute situation. It can be life-threatening not to
be aware of them. However, as these symptoms become chronic, their
protective roles decrease and instead they become health problems.
Our understanding of the perception of pain
and fatigue has shifted through the years, from a dualistic
biomedical point of view to a holistic biopsychosocial understanding. This
combined with the increasing evidence of how our brain works in a
predictive/anticipatory manner, gives a deeper understanding of why treatments
like cognitive behavior therapies and stress relief therapies can..