Myalgic Encephalomyelitis (ME) or What? An Operational Definition, 2018, Frank Twisk

It may be like insulin and diabetes but whatever it is does not look likely to be something like lactate. And the problem is not so much that findings are inconsistent. As far as I know measurements are just normal.



Maybe finding it impossible to do any significant activity, feeling ill, and sensitivity to stimuli including light and sound and standing up. I don't think there is anything very complicated in those terms. People without ME may not be able to understand quite what it feels like but we know enough to see that the problems PWME have do not seem to fit with the usual sorts of metabolic problems involving things like lactate. If they did I am pretty sure that MR spectroscopy study sin the 1980s would have picked them up.

I think it is a pity that certain doctors with an interest in ME have focused on metabolic issues or mitochondria without really knowing much about those. A couple of years ago Mike Murphy came to talk at IiME. He is a mitochondrial biochemist. His view was that the symptoms of ME do not sound at all like sings of mitochondrial malfunction, unless they are due to some sort of danger signalling.

I guess you have to start somewhere with unpicking the whole mess. I have to say ME people are the most abnormal, normal people.

I do wonder how we would have found diabetes if Oskar Minkowski and Joseph Von Mering had not witnesses what happened to that poor dog? Would we have found out about the pancreas and then insulin if that had not happened?
 
3.1.4. Not Just Like Other Post-Viral Fatigue States

ME should be distinguished from other forms of “post-viral debility following Epstein–Barr mononucleosis, influenza and other common fevers” [3] since ME has “an unique clinical and epidemiological pattern” [3] and these other post-viral states “lack the dramatic effect of exercise upon muscle function, the multisystem involvement, diurnal variability of symptoms and prolonged relapsing course” [3]. This is also one of the many reasons why ME [1–4] should not be confused with CFS [11], an ill-defined syndrome which can be initiated by various infections, e.g., the Epstein–Barr virus (mononucleosis), Coxiella burnetii (Q fever), or Ross River virus infections [23].

I previously thought that the postinfectious syndromes following bacterial infections might be different. However, reading descriptions of those who had Giardia l., they sound very ME-like to me , e.g. as discussed in this paper
Factors impacting the illness trajectory of post-infectious fatigue syndrome: a qualitative study of adults' experiences (2017) Jason et al
https://www.s4me.info/threads/facto...-of-adults-experiences-2017-jason-et-al.1535/
 
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If something is going to be a mandatory test, I hope the test is good especially at an individual level. Average differences don't necessarily mean that there are thresholds that have good sensitivity and specificity.

For example, it is not argued that men on average are taller than women. But there are not necessarily good thresholds that can be chosen to say that above a certain threshold somebody is male and below it they are female.
3.2.1. Muscle Fatigability/Prolonged Muscle Weakness after Exertion is a Mandatory Feature of ME

“ME is [..] distinguished by severe muscle fatigue following trivial exertion” [3]. “Muscle fatigability is the dominant and most persistent feature of the disease and [..] a diagnosis should not be made without it. Restoration of muscle power after exertion can take three to five days or even longer.” [1]. This implies that muscle fatigability/prolonged muscle weakness after exertion is a discriminative feature of ME. Long-lasting muscle weakness after exertion can be validated objectively by measuring muscle power of the arms, hands [24,25], legs [26,27], etc., during repeated muscle contractions on two consecutive days using dynamometers [28,29].

24. Siemionow, V.; Fang, Y.; Calabrese, L.; Sahgal, V.; Yue, G.H. Altered central nervous system signal during motor performance in chronic fatigue syndrome. Clin. Neurophysiol. 2004, 115, 2372–2381. [CrossRef] [PubMed]

25. Lawrie, S.M.; MacHale, S.M.; Cavanagh, J.T.; O0Carroll, R.E.; Goodwin, G.M. The difference in patterns of motor and cognitive function in chronic fatigue syndrome and severe depressive illness. Psychol. Med. 2000, 30, 433–442. [CrossRef] [PubMed]

26. Paul, L.; Wood, L.; Behan, W.M.; Maclaren, W.M. Demonstration of delayed recovery from fatiguing exercise in chronic fatigue syndrome. Eur. J. Neurol. 1999, 6, 63–69. [CrossRef] [PubMed]

27. Fulcher, K.Y.; White, P.D. Strength and physiological response to exercise in patients with chronic fatigue syndrome. J. Neurol. Neurosurg. Psychiatry 2000, 69, 302–307. [CrossRef] [PubMed]

28. McKay, M.J.; Baldwin, J.N.; Ferreira, P.; Simic, M.; Vanicek, N.; Burns, J. For the 1000 Norms Project Consortium. Normative reference values for strength and flexibility of 1000 children and adults. Neurology 2017, 88, 36–43. [CrossRef] [PubMed]

29. Douma, R.K.; Soer, R.; Krijnen,W.P.; Reneman, M.; van der Schans, C.P. Reference values for isometric muscle force among workers for the Netherlands: A comparison of reference values. BMC Sports Sci. Med. Rehabil. 2014, 6, 10. [CrossRef] [PubMed]
 
This is a continuation of the last post with more information on the citations:

The full text for this is available at: https://sci-hub.tw/https://doi.org/10.1016/j.clinph.2004.05.012


Clin Neurophysiol. 2004 Oct;115(10):2372-81.
Altered central nervous system signal during motor performance in chronic fatigue syndrome.
Siemionow V1, Fang Y, Calabrese L, Sahgal V, Yue GH.
Author information
1
Department of Biomedical Engineering, The Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
Abstract
OBJECTIVE:
The purpose of this study was to determine whether brain activity of chronic fatigue syndrome (CFS) patients during voluntary motor actions differs from that of healthy individuals.

METHODS:
Eight CFS patients and 8 age- and gender-matched healthy volunteers performed isometric handgrip contractions at 50% maximal voluntary contraction level. They first performed 50 contractions with a 10 s rest between adjacent trials--'Non-Fatigue' (NFT) task. Subsequently, the same number of contractions was performed with only a 5 s rest between trials--'Fatigue' (FT) task. Fifty-eight channels of surface EEG were recorded simultaneously from the scalp. Spectrum analysis was performed to estimate power of EEG frequency in different tasks. Motor activity-related cortical potential (MRCP) was derived by triggered averaging of EEG signals associated with the muscle contractions.

RESULTS:
Major findings include: (i) Motor performance of the CFS patients was poorer than the controls. (ii) Relative power of EEG theta frequency band (4-8 Hz) during performing the NFT and FT tasks was significantly greater in the CFS than control group (P < 0.05). (iii) The amplitude of MRCP negative potential (NP) for the combined NFT and FT tasks was higher in the CFS than control group (P < 0.05) (iv) Within the CFS group, the NP was greater for the FT than NFT task (P<0.01), whereas no such difference between the two tasks was found in the control group.

CONCLUSIONS:
These results clearly show that CFS involves altered central nervous system signals in controlling voluntary muscle activities, especially when the activities induce fatigue.

SIGNIFICANCE:
Physical activity-induced EEG signal changes may serve as physiological markers for more objective diagnosis of CFS.

PMID:
15351380
DOI:
10.1016/j.clinph.2004.05.012
[Indexed for MEDLINE]

The full text is available for free here:

http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.858.3532&rep=rep1&type=pdf

Psychol Med. 2000 Mar;30(2):433-42.
The difference in patterns of motor and cognitive function in chronic fatigue syndrome and severe depressive illness.
Lawrie SM1, MacHale SM, Cavanagh JT, O'Carroll RE, Goodwin GM.
Author information

Abstract
BACKGROUND:
Chronic fatigue syndrome (CFS) and major depressive disorder (MDD) share many symptoms and aetiological factors but may have different neurobiological underpinnings. We wished to determine the profile of the biological variables disturbed in CFS and MDD, and identify any critical factors that differentiate the disorders.

METHODS:
Thirty patients with CFS, 20 with MDD and 15 healthy controls matched group-wise for age and sex were recruited. Subjects were given a detailed battery of motor and cognitive tests, including measures of psychomotor speed, memory and maximal voluntary muscle contraction in both the morning and evening that were balanced to avoid order effects.

RESULTS:
CFS patients generally performed worse on cognitive tests than healthy controls, but better than patients with MDD. Both patient groups had markedly impaired motor function compared with healthy controls. MDD subjects showed a significantly greater diurnal improvement in maximal voluntary contraction than healthy controls.

CONCLUSIONS:
Patients with CFS and MDD show similarly substantial motor impairment, but cognitive deficits are generally more marked in MDD. Diurnal changes in some functions in MDD may differentiate the disorder from CFS.

PMID:

10824663
[Indexed for MEDLINE]

I have attached the full text:

Eur J Neurol. 1999 Jan;6(1):63-9.
Demonstration of delayed recovery from fatiguing exercise in chronic fatigue syndrome.
Paul L1, Wood L, Behan WM, Maclaren WM.
Author information

Abstract
Patients with the chronic fatigue syndrome (CFS) complain consistently of delay in recovery of peripheral muscle function after exercise. The purpose of this study was to try to confirm this observation. A fatiguing exercise test was carried out on the quadriceps muscle group of ten patients and ten control subjects. The test consisted of 18 maximum voluntary contractions (MVCs) with a 50% duty cycle (10 s contraction, 10 s rest), and the force generated by each contraction was recorded using a KinCom dynamometer. This was followed by a recovery phase lasting 200 min in which quadriceps strength was evaluated at increasing intervals, and a follow-up session at 24 h post-exercise involving three 10 s MVCs. Throughout the exercise period, the MVCs obtained from the control group were significantly higher than those of the patient group (P = 0.006), but both groups showed a parallel decline in force over the 18 contractions, in keeping with a similar endurance capacity. Recovery was prolonged in the patient group, however, with a significant difference compared to initial MVCs being evident during the recovery phase after exercise (P = 0.001) and also at 24 h (P < 0.001). In contrast, the control group achieved MVCs which were not significantly different from initial values during the recovery phase, and maintained these at 24 h. These findings support the clinical complaint of delayed recovery after exercise in patients with CFS.

PMID:

10209352
[Indexed for MEDLINE]

The full text is available for free here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1737090/pdf/v069p00302.pdf
J Neurol Neurosurg Psychiatry. 2000 Sep; 69(3): 302–307.
doi: 10.1136/jnnp.69.3.302


PMCID: PMC1737090
PMID: 10945803
Strength and physiological response to exercise in patients with chronic fatigue syndrome
K. Fulcher and P. White

Abstract
OBJECTIVE—To measure strength, aerobic exercise capacity and efficiency, and functional incapacity in patients with chronic fatigue syndrome (CFS) who do not have a current psychiatric disorder.
METHODS—Sixty six patients with CFS without a current psychiatric disorder, 30 healthy but sedentary controls, and 15 patients with a current major depressive disorder were recruited into the study. Exercise capacity and efficiency were assessed by monitoring peak and submaximal oxygen uptake, heart rate, blood lactate, duration of exercise, and perceived exertion during a treadmill walking test. Strength was measured using twitch interpolated voluntary isometric quadriceps contractions. Symptomatic measures included physical and mental fatigue, mood, sleep, somatic amplification, and functional incapacity.
RESULTS—Compared with sedentary controls, patients with CFS were physically weaker, had a significantly reduced exercise capacity, and perceived greater effort during exercise, but were equally unfit. Compared with depressed controls, patients with CFS had significantly higher submaximal oxygen uptakes during exercise, were weaker, and perceived greater physical fatigue and incapacity. Multiple regression models suggested that exercise incapacity in CFS was related to quadriceps muscle weakness, increased cardiovascular response to exercise, and body mass index. The best model of the increased exercise capacity found after graded exercise therapy consisted of a reduction in submaximal heart rate response to exercise.
CONCLUSIONS
Patients with CFS were weaker than sedentary and depressed controls and as unfit as sedentary controls. Low exercise capacity in patients with CFS was related to quadriceps muscle weakness, low physical fitness, and a high body mass ratio. Improved physical fitness after treatment was associated with increased exercise capacity. These data imply that physical deconditioning helps to maintain physical disability in CFS and that a treatment designed to reverse deconditioning helps to improve physical function.


The full text is available for free here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5200854/
Neurology. 2017 Jan 3;88(1):36-43. doi: 10.1212/WNL.0000000000003466. Epub 2016 Nov 23.
Normative reference values for strength and flexibility of 1,000 children and adults.
McKay MJ1, Baldwin JN2, Ferreira P2, Simic M2, Vanicek N2, Burns J2; 1000 Norms Project Consortium.
Collaborators (24)

Author information

Abstract
OBJECTIVE:
To establish reference values for isometric strength of 12 muscle groups and flexibility of 13 joint movements in 1,000 children and adults and investigate the influence of demographic and anthropometric factors.

METHODS:
A standardized reliable protocol of hand-held and fixed dynamometry for isometric strength of ankle, knee, hip, elbow, and shoulder musculature as well as goniometry for flexibility of the ankle, knee, hip, elbow, shoulder, and cervical spine was performed in an observational study investigating 1,000 healthy male and female participants aged 3-101 years. Correlation and multiple regression analyses were performed to identify factors independently associated with strength and flexibility of children, adolescents, adults, and older adults.

RESULTS:
Normative reference values of 25 strength and flexibility measures were generated. Strong linear correlations between age and strength were identified in the first 2 decades of life. Muscle strength significantly decreased with age in older adults. Regression modeling identified increasing height as the most significant predictor of strength in children, higher body mass in adolescents, and male sex in adults and older adults. Joint flexibility gradually decreased with age, with little sex difference. Waist circumference was a significant predictor of variability in joint flexibility in adolescents, adults, and older adults.

CONCLUSIONS:
Reference values and associated age- and sex-stratified z scores generated from this study can be used to determine the presence and extent of impairments associated with neuromuscular and other neurologic disorders, monitor disease progression over time in natural history studies, and evaluate the effect of new treatments in clinical trials.

© 2016 American Academy of Neurology.

PMID:

27881628

PMCID:

PMC5200854

DOI:

10.1212/WNL.0000000000003466
[Indexed for MEDLINE]
Free PMC Article

Free full text:
https://bmcsportsscimedrehabil.biomedcentral.com/articles/10.1186/2052-1847-6-10
Reference values for isometric muscle force among workers for the Netherlands: a comparison of reference values
  • Rob KW DoumaEmail author,
  • Remko Soer,
  • Wim P Krijnen,
  • Michiel Reneman and
  • Cees P van der Schans
BMC Sports Science, Medicine and Rehabilitation20146:10
https://doi.org/10.1186/2052-1847-6-10

© Douma et al.; licensee BioMed Central Ltd. 2014

  • Received: 11 March 2013
  • Accepted: 12 February 2014
  • Published: 25 February 2014
Open Peer Review reports
Abstract
Background
Muscle force is important for daily life and sports and can be measured with a handheld dynamometer. Reference values are employed to quantify a subject’s muscle force. It is not unambiguous whether reference values can be generalized to other populations. Objectives in this study were; first to confirm the reliability of the utilization of hand-held dynamometers for isometric strength measurement; second to determine reference values for a population of Dutch workers; third to compare these values with those of a USA population.

Methods
462 Healthy working subjects (259 male, 203 female) were included in this study. Their age ranged from 20 to 60 years with a mean (sd) of 41 (11) years. Muscle force values from elbow flexion and extension, knee flexion and extension, and shoulder abduction were measured with the break method using a MicroFet 2 hand-held dynamometer. Reliability was analyzed by calculating ICC’s and limits of agreement. Muscle force expressed in Newton, means, and confidence intervals were determined for males and females in age groups ranging from twenty to sixty years old. Regression equations and explained variances were calculated from weight, height, age, and gender. The mean values and 95% CI were compared to the results from other studies.

Results
Reliability was good; the ICC ranged between 0.83 to 0.94. The explained variance ranged from 0.25 to 0.51. Comparison of data for the Dutch population mean muscle force values with those from the USA revealed important differences between muscle force reference values for the American and Dutch populations.

Conclusions
Muscle force measurements demonstrate a sound reliability. Reference values and regressions equations are made available for the Dutch population. Comparison with other studies indicates that reference values differ between countries.
 

Attachments

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These are the results from a 2014 study. Admittedly, only the Fukuda criteria were used. But I tend to believe that by the time one looks at research cohorts which weren't chosen from random digit studies, most of the patients probably have ME. So based on this, I would be cautious about making delayed recovery a mandatory feature.
A proviso is that this was a same-day study rather than a next-day study.


Ickmans Recovery of upper limb muscle function in CFS.png



http://www.meresearch.org.uk/our-research/completed-studies/upper-limb-muscle-function/

Recovery of upper limb muscle function in chronic fatigue syndrome with and without fibromyalgia

Authors
Ickmans K, Meeus M, De Kooning M, Lambrecht L, Nijs J

Institution
Pain in Motion Research Group, Department of Human Physiology and Physiotherapy, Faculty of Physical Education & Physiotherapy, Vrije Universiteit Brussel, Brussel, Belgium

Background
Chronic fatigue syndrome (CFS) patients frequently complain of muscle fatigue and abnormally slow recovery, especially of the upper limb muscles during and after activities of daily living. Furthermore, disease heterogeneity has not yet been studied in relation to recovery of muscle function in CFS. Here, we examine recovery of upper limb muscle function from a fatiguing exercise in CFS patients with (CFS+FM) and without (CFS-only) comorbid fibromyalgia and compare their results with a matched inactive control group.

Design
In this case-control study, 18 CFS-only patients, 30 CFS+FM patients and 30 healthy inactive controls performed a fatiguing upper limb exercise test with subsequent recovery measures.

Results
There was no significant difference among the three groups for maximal handgrip strength of the non-dominant hand. A significant worse recovery of upper limb muscle function was found in the CFS+FM, but not in de CFS-only group compared with the controls (P<0.05).

Conclusions
This study reveals, for the first time, delayed recovery of upper limb muscle function in CFS+FM, but not in CFS-only patients. The results underline that CFS is a heterogeneous disorder suggesting that reducing the heterogeneity of the disorder in future research is important to make progress towards a better understanding and uncovering of mechanisms regarding the nature of divers impairments in these patients.

Publication
Eur J Clin Invest 2014 Feb; 44(2): 153–9

Comment by ME Research UK
The fact that muscles take longer to recover after exertion is a characteristic feature of ME, but experimental studies showing this have been few and far between over the past 30 years. In fact, as Dr Kelly Ickmans (ME Research UK research fellow at Vrije Universiteit Brussel) points out in this paper in European Journal of Clinical Investigation, muscle recovery in the upper limb has never been subjected to research in ME/CFS patients, despite the fact that these muscles are most frequently used for everyday activities, such as combing and washing hair, ironing and cooking.

Kelly decided to test muscle function in the upper arm during and after exercise using a simple hand dynamometer which measures force and strength. After an exercise challenge consisting of 18 maximal contractions and a recovery phase of 45 minutes, she found that the muscle recovery was significantly slower in ME/CFS patients than healthy people (muscle strength was still recovering 30-45 minutes after the exercise). Intriguingly, this was only true for patients who also fulfilled the 2010 criteria for fibromyalgia, i.e. who had a high degree of “widespread pain” as well as the symptoms shared with ME/CFS. In fact, it seems that 43–70% of ME/CFS patients also meet the criteria for fibromyalgia, so this test could be a simple, easy-to-perform way of objectively measuring delayed muscle recovery in a substantial number of people.

One take-home message from this investigation is that meaningful experiments don’t have to be complex and expensive, and that even simple ones, like the change in upper arm strength over a short period, can yield useful information. In fact, the results remind us of a study we funded at the University of Dundee in 2004, which showed that a significant number of patients had easily measureable muscle weakness in the lower limbs and absent or abnormal nerve reflexes.
 
I previously thought that the postinfectious syndromes following bacterial infections might be different. However, reading descriptions of those who had Giardia l., they sound very ME-like to me , e.g. as discussed in this paper
My son had post viral fatigue. Our GP now thinks it was CFS/ ME.After 6 months he was very ill. Severe migraines prompted lumbar puncture as it was thought it was a potential brain bleed. Yet he never had PEM.
 
It almost certainly has to do with sites of tensile force in continuous postural muscle action. Most muscles in the body are called on to do specific jobs intermittently. But trapezius and soleus (which is in the same place as gastrocnemius) contract almost constantly just to keep your body upright with slumping. The tennis elbow spot gets tender if you carry something for a long period with the arm slightly bent, and so on. Tender spots in trapezius are something casualty officers and rheumatology trainees get familiar with in their first clinics - and learn to reassure people that they do not mean anything. By the time I got to be a medical student I had already had episodes of tender trapezius and my father, who was a doctor, had reassured me.

So we have cause and effect, but that is normal and although you get bursts of abnormal tenderness with a virus say (mine always flairs up when I get a cold sore) you get to know the difference? You get someone who is constantly looking at these areas you get two outcomes. They get blase and and expect discomfort so just accept it no matter if it has changed and move on, or they get to know when something is wrong. I would say you and Dr Ramsay are/were the latter?

Me with Angus for instance, I would not have a clue, when he complains of stiffness or soreness and his very often in a low sate of cognition at this point that he would not be able to tell me if it was in his shoulder or ankle. I know this sounds funny but we are talking about a poor lad that opens the fridge and asks me the question "What is my name". He had a glass in his hand at the time and wanted to fill it up with water on the outside of the fridge door. We would not be able to tell a Dr the facts they would need to know to find a problem and so these problems are missing. This soreness and stiffness comes on around 3rd to 4th day of recovery after an activity, so it is not part of muscle being used. I don't think Dr Ramsay would just mention this tenderness without having a very good reason to do so? Not that I knew the man, but he is on my dinner party list along with you and few others.

There is something more here? I have been wondering about this since the time of the fridge incident when I first noticed he walked on tip toes and couldn't hold the glass filled with water. He also blacked out going up the stairs.

This is the other thing I noticed early on - he gets cold on the outside of his calf muscles and just below the elbow about four days in from recovery from an activity. I give him body temp salt baths and just warm those areas up and the pain eases. This really is the most bizarre condition.

I have been summoned to the school next Friday where I will be questioned about my son's illness and his inability to get to school for the meeting. The Safeguarding officer of the school won't come to my house and has never met my son. The paediatric thinks the POTS symptoms (even though he has a diagnosis of POTS by that Drs team) are all down to Anxiety. There is no science they would accept on my side to say any different?

It is a strange world we live in.
 
The paediatric thinks the POTS symptoms (even though he has a diagnosis of POTS by that Drs team) are all down to Anxiety. There is no science they would accept on my side to say any different?

I think that is a common error: To think that when there is no" biological" explanation, then there is only a psychological explanation left - or vice versa: A psychological explanation could be disproven by a biological one (like POTS). In my view an anxiety diagnose has to be made based on clear criteria and not on some symptoms which superficially seem similar to anxiety symptoms.

As a matter of fact, the cognitive symptoms we have are the field of expertise of neuropsychiatry or neuropsychology. Thus, in this sense we might have "psychiatric" symptoms, but these I think can be differentiated from anxiety symptoms or other mental illnesses without the need of an alternative proof of a biological cause. (I think we really could benefit from good neuropsychiatrists/ neuropsychologists with regard to be taken serious.)

[Edited to add: The "science" that could support you imo is e.g. that when your son's symptoms have the pattern of ME and he has an ME diagnosis, he does not need an additional POTS diagnosis; it is possible to have ME and an anxiety comorbidity but I think it is also possible to differentiate anxiety from ME related symptoms; there is no evidence that any psychological treatment is effective for ME.]

Best wishes for you and your son, @Tilly ! I hope you will find support.
 
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It is a strange world we live in.

It certainly is and I appreciate the impossibility of your situation.

However, I would query whether one should take too much notice of what Melvin Ramsay said. When I look this account I get the impression that he was not a very rigorous observer. He is popular because his name is associated with the term ME but it was not in fact him that invented the term and the term was really invented to describe an illness that is not the illness that we call ME today. It was a pathological concept with implication of a virus that turned out not to have any identifiable pathology. Everything has become muddled and the more I learn about ME the more I think we should forget what was said fifty years ago and focus on people's problems now. Maybe it is better to think in terms of chronic fatigue syndrome, but I appreciate that the focus on fatigue is not ideal.
 
Fluff I had incorrectly given Melvin Ramsay hero status. Thank you for the history of the name now that makes sense why so many get hung up with the name.

It is more than muddled. Wish we could start again. I know when I was at the NICE meeting this was a sticking point and we decided to move on quickly.

Fatigue is only a bad term due to the way it has been used in some quarters? Though I don't like the term as this is not what I witness or explains what the people experience of those I talk to. America had a good go at changing the name but the less said about that the better.

How about Chronic Post Exertional Malaise? CPEM, Less said about that the better too? I explain it to Angus as Post Activity Increase in New or Severity of Symptoms PAINSS for short and he said it was a pain in more ways than one.

I agree we should focus and get serious about what happens to the people now. The focus should be and always have been an inability to do any activity with feet on the floor standing time for three consecutive days. If this was acknowledge and we started looking at this in detail over a five day period after each activity that produces symptoms - what ever they were, we would no doubt be a lot further forward. Well I can dream.

It does not matter what we call it, it matters how we perceive the condition.
 
Dr Ramsay was popular because he interacted with patients with respect and consideration. If we had had forums then he would have been here answering questions and trying to help. He had no agenda beyond helping people. He fought for us till he died.

Chronic Fatigue Syndrome was a name given to a disease to make it disappear. I think SW was explicit about making ME disappear and the patients with it and let's face it he succeeded.

CFS not only trivialised what was happening - everyone feels fatigue but only wimps and freeloaders give in to it. It makes everyone who struggles out of bed on a Monday morning resent us. We go to a GP who is overworked and struggling and how much sympathy will they have for someone complaining about chronic fatigue?

It also gives a beautiful opportunity to conflate chronic fatigue, tired all the time, fatigue as experienced in other disease (but of course they don't give into it; at one point it was described as fatigue but not the real dreadful kind that people with MS get)

It also opens up CFS research money to researchers looking at their disease interests. Everyone wins except us.

Finally it made fatigue the focus instead of the strange energy problems we have. It misses the things that make us disabled and concentrates on a side issue. Like MS concentrating on fatigue instead of not being able to walk or move. The BPSers could move in on CFS where it was harder with ME.

Call it SEID if ME seems too inaccurate but never CFS, that is letting ourselves down, it is a term of oppression used against us.
 
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