Entire issue of Post Graduate Medical Journal (11/1978) devoted to ME

(my bold)

Edwards had a particular interest in DMD. He was also the person ME patients saw in Liverpool before Dr Nye's time. He diagnosed a friend of mine (now deceased) with ME, some 20 or so years later she had a scan privately and it was discovered she actually had MS. This misdiagnosis certainly had profound effects on her finances, as she was refused DLA up until the MS diagnosis when she was immediately granted it. I don't know enough about MS to say that the misdiagnosis prevented any possible treatment. Anyway, he was certainly involved in ME research and he was seeing ME patients, so I think it probably was in his area.

Oddly enough a few months before I ended up with ME I applied for a lab tech job at the Department of Medicine, and Edwards was one of the people who interviewed me. I didn't get the job, but hadn't really expected to. It was the beginning of an effort to get back into full time work from the half time I was doing at the regional cytogenetics unit at the time. And then Life Happened.

 

I don't want to comment on diagnostic decisions but I would say that MS is very easy to miss in the early stages and every physician including myself has made that mistake. ME patients tend to get referred locally to someone fairly arbitrary who has agreed to take referrals. In some areas it is infectious disease physicians, in some areas psychiatrists. I think the problem often comes when specialists think the illness is in their area when it probably isn't! My understanding is that Edwards saw his job as to assess whether people really had muscle disease and he decided they did not, and very likely correctly. I think his research was useful in establishing certain negative findings. There may be more to the clinical story but I am not in a position to say.

 

Thankyou for those comments re Behan research and biopsy usage @Jonathan Edwards

 

On the basis that it is only when people are off guard that they reveal their beliefs here is Richards at page 328.

Probably ln CFS more than any other condition we have a good example of dis-ease. These people are lacking ease. They are uncomfortable in their own skin as the French would say. How do we convey that we have a new paradigm of disease, afeeling of things not being right? This challenges us to develop a new concept of our role as doctors, and of the role of medical education, to allow patients to maintain control and self respect and a sense of proportion in interpreting body signals to provide an adaptive coping strategy, so that they are not dismayed by such a life physical experience. It may be that there is such a thing as a midlife crisis where people are faced with disease, and gradually have to come to terms with it, as with bereavement. I would like to hear a more formal psychological description of this, but it the kind of homegrown philosophy that I find constructive with patients.



Decide for yourselves.

Edit. I have twice used full stops in place of semicolons in the original, solely because my phone seems not to provide the option.

 

@chrisb if he came to those conclusions it makes me think he wasn’t actually studying ME patients and the muscle abnormality consistencies that he didn’t find could potentially be there if studied on a group of ME patients.

 

That was the thought that occurrd to me when reading the barely civil exchanges between Edwards and Behan. We can be reasonably sure of what Behan was researching.

 

@chrisb and although biopsy carries the risk of sampling error finding 39 of 50 with type II atrophy (and very few with Type I atrophy) and now knowing that inflammatory and metabolic problems can cause type II atrophy sounds more than interesting and certainly cause for urgent exploration with a well defined ME group to see if Behans findings stand up. Hopefully NIH study does this...

 

Isn't there also the issue that if you only examine patients with fatigue and an absence of any physical signs, you won't find any physical signs?

Obviously post-1988 definitions of CFS primarily look for unexplained fatigue. Some of the older studies focused on muscle fatigability and neurological signs instead, which is a different beast.

The Oxford criteria were created in the early 1990s, weren't they? So it would make sense things after that point would contradict evidence before then.

I really wish any negative findings were published instead of being hidden. Lots of activists point to the early studies to illustrate their points, which is a problem if they were later on disproved. It means we can't know the specifics of how we're wrong and how to move forward.

 

I want to comment on this specifically ... I think some patients with ME might be anaemic and it NOT show up on full blood count. This is because a full blood count is based on concentration of cells. That is, the number per unit volume. The problem in ME is that many of us have lower blood volume. Those people might be anaemic and still look fine. Its the total numbers that are low.

The issue here is tests have contexts, or bounds. There are limits to what can be said. Now if a test does not find something, then that is valid for a specific context. If the context is not standard then it may not be valid.

In any case we are awaiting the publication of the second large metabolomics study. Its expected to establish that 77% of the earlier study's findings are correct. In other words, there might have been as much as 23% false positives.

I am not trying to defend old findings that were not replicated, but just pointing out issues.

The problem with metabolic tests is that, if from simple blood draws, they capture a moment in time. They tell you little about flux through the pathways. A controlled metabolic study with many tests might find issues. Not finding standard and expected metabolic problems does not rule out the unexpected.

I had my first metabolic rate test in about 1993, as a mild patient. It was low. I then had a brain metabolic test, looking for glucose consumed. It was also low. I think this is common in ME, but it tells us nothing about what is causing the issues. Right now metabolic issues are about pathology and markers, not causation. We need to know much more to establish causation, and multiple theories are being looked at.

 

The thought occurred to me too, but for both Edwards and Behan. Some of Behan's case studies were weird and almost half his patients were medical personnel in the 1985 paper.
The disease Behan thought he was studying has not been found by any of the researchers I have got to know recently.

I would not put much faith on muscle samples from a few cases. What I think is needed is a non-invasive test with little or no sampling problems, that can be repeated serially with exertion, like MR spectroscopy of the thigh muscles, looking at a full range of metabolites, water content for inflammation and whatever. I have a feeling that David Jones has probably done this but I have not come across him for about five years now and he does not seem to come to ME meetings.

 

I agree - muscle biopsy from the little I understand is unpleasant to undergo. Maybe not as bad as bone marrow aspiration for testing (been the tech making the slides at that many years ago), but still not something you'd want to undergo!

 

@ladycatlover i had a biopsy last year and it is not something I would agree to again given my current state.

My finding was severe Type II selective atrophy. I have since gone online and asked on various ME groups if anyone else has had biopsies and what was the finding... I have had about 10 people report selective type II atrophy and 0 report type I selective atrophy.

I see Dr John Whiting in Australia who has been a dedicated ME clinician for decades. At first he and I were confused as we thought that Me should be more likely to cause atrophy to aerobic Type I fibers. But then he found the research on inflammatory and metabolic problems causing type II atrophy and also figured out that sinc it takes 3-4 times as much energy for a type II exertion as type I do it would make sense in an energy production disorder to sacrifice the muscle fiber that requires the most atp to exert.

In any case along with muscle biopsy problems already discussed there are several other causes of Type II specific atrophy so couldn’t be used as a specific bio marker.

 

interesting. is this known in medicine? what parts of a cbc/cmp require knowledge of blood volume to interpret correctly?

ignorant questions: can drinking a lot [maybe salt too?] before blood tests help this particular problem? when does homeostasis kick in?

 

His range of interests may have expanded over the years...

______________________________

Br J Psychiatry. 2002 Sep;181:248-52.

Predictors of response to treatment for chronic fatigue syndrome.
Bentall RP, Powell P, Nye FJ, Edwards RH
. . .
RESULTS:
Poor outcome was predicted by membership of a self-help group, being in receipt of sickness benefit at the start of treatment, and dysphoria as measured by the Hospital Anxiety and Depression scale. Severity of symptoms and duration of illness were not predictors of response.

CONCLUSIONS:
Poor outcome in the psychological treatment of chronic fatigue syndrome is predicted by variables that indicate resistance to accepting the therapeutic rationale, poor motivation to treatment adherence or secondary gains from illness.

https://www.ncbi.nlm.nih.gov/pubmed/12204931

 

I hate it when they say "is predicted by" when they mean "is correlated with". The former seems to imply causation; the latter is the neutral way to report what was observed without adding an unwarranted inference.

 

Low blood volume is in the medical literature but very few docs seem to know about it. Dosing with extra water might help correct the issue so that blood counts are closer to the actual numbers. However the inverse is true too ... taking too much water might alter other test readings. Its hard to say what impact that might have.

 

I believe you can measure the blood volume by injecting a measured dose of a radioactive marker into the blood stream. After the marker has thoroughly mixed with the blood supply, you can then remove some blood and the amount of marker and its ratio to the amount of blood taken will tell you what the total blood volume is. (I think.)

ETA: Then you have to consider that volume in relation the to the patient's size to determine if it is within a normal range.

 

Yes, but most docs don't order this test or even think to do it.

 

Is that actually the case, @alex3619 ?

Streeten and Bell say:

Similarly, the total blood volume in our 15 female subjects (Mean 57.49, SD 20.47) was not significantly different from the values found in the same 20 normal females (58.9+/-4.9 mL/Kg).

 

I will run a search and hope to get back to you. Low blood volume is known in individual patients who have been tested for it, I am not sure its been the subject of a formal study, at least in the context of ME. In the general literature its called hypovolemia, which I am sure you are aware of, and usually caused by blood loss or dehydration. I will need to check in relation to ME or CFS specifically.