Input wanted from people who consider ME to be different from SEID

[Snowdrop]

Take someone a little like me for instance: I meet ICC-ME. I also meet IOM-SEID. Now, I think SEID is more accurate than the ME label,

I take this to mean that you find the SEID criteria to be more accurate than the ICC-ME. Can you expand on this?

Also, the criteria I meet for this disease has changed over time (decades). How does one capture progression and severity with these criteria?

 

[SOC]

I fit both criteria too. That is a tough one. I would worry about it making me worse, as I don't do well with drugs in general. Of course, my doctor's opinion would weigh in there too.

So if you fit both criteria for two (supposedly) entirely different conditions, how to you explain that? I assume, in that case, that you don't consider the two diseases mutually exclusive. Do you see it like having both cancer and diabetes -- just an unfortunate confluence of events that you have two entirely different conditions? Or do you see ME and SEID in some kind of subset situation. In other words, do you think ME is a subset of SEID, or the other way around?

 

[SOC]

But things could change, especially if people believing ME is a seperate disease really push for that to be recognised seperately.

I was assuming that the "ME is not SEID" population would be pushing for ME to be considered a separate disease long before any research-based treatment was available.

It's a completely different story if ME, SEID, and CFS were all considered variations of the same illness, but that's not my impression of the stance of those who believe ME is not SEID. Perhaps I'm not reading them correctly.

 

[snowathlete]

I take this to mean that you find the SEID criteria to be more accurate than the ICC-ME. Can you expand on this?

As the IOM criteria are evidence based, I think they are more solid than the ICC. Among other benefits, I think that is important for getting clinicians to adopt the criteria and makes it harder to disprove and deny the disease.
I also think it is much clearer and simpler than ICC, without jeopardizing accuracy, and that's a benefit as diagnostic criteria should only be as complex as they need to be. I think the ICC makes the mistake of trying to be not only be a diagnostic criteria but also a description of the disease, and I think this is part of the reason why some people seem to misunderstand the purpose of the IOM criteria and why they have been done the way that they have (not pointing any fingers, that's just a general observation)

But I also think the ICC is useful as well.

The greatest weakness in the ICC, in my view, is the use of the label myalgic encephalomyelitis, as there is not much evidence of spinal cord/brain inflammation. That is why I consider SEID to be a better, more accurate label.

Also, the criteria I meet for this disease has changed over time (decades). How does one capture progression and severity with these criteria?

Likewise, my illness has changes a lot over the period I ahve been ill. Interestingly, I would have still met the IOM criteria 6 months into my illness. I'd be interested to hear from others on that, whether they think they would or wouldn't.
The IOM clinician's guide has a list of measures (wrong word, but can't think of the right one) that clinicians can use and they would give an indication on severity, and I guess comparisions over time might give an indictation of progression too. I doubt there is a great degree of objective measures from research yet though. Was interested that Lipkin's team saw differences in cytokines in the 0-3 year group and the 3+ group.

 

[Kati]

At the risk of going briefly off-topic, that mortality rate looks a lot higher than what I thought the Rituximab mortality rate was. What do you think, @Jonathan Edwards?

The mortality rate is higher for those who are taking prednisone in combination with Rituximab. Prednisone suppresses immunity even further making patients prone to deadly infections such as JC virus.

 

[Jonathan Edwards]

Where might you stand if research into SEID results in a treatment being approved for patients with SEID? As an example, let's consider Rituximab. Let's assume it is found to work well in ~60% of patients, but no solid data on subgroups and why it works in some but not others. With a mortality rate from treatment of between 2.4-10.4% (as in this mortality study).

This is complete nonsense put out by a small group who treat pemphigus or pemphigoid who have not bothered to look at the vast literature on use of rituximab in autoimmunity. God knows how something like this gets published. There are proper figures on file under the trials that have been conducted. We have treated something like 200 cases at UCL for RA and I am not aware of any death attributable to rituximab. Of course there have been deaths - from stroke, cancer, heart disease, because we followed quite a lot of elderly people for fifteen years. In the phase 2 proof of concept trial of 160 patients there was one death from infection in a patient who was already in very poor health. I do not have figures to hand but death attributable to rituximab with extended (several years) therapy cannot be more than 1% and I suspect it is less than 0.1%. That is much better than total hip replacement for instance. It may be better than aspirin. Patients with blistering diseases are often very old and very frail and susceptible to infection. The authors do not seem to assess (in the abstract) whether or not they have any evidence to link death to the drug.

 

[Jonathan Edwards]

The mortality rate is higher for those who are taking prednisone in combination with Rituximab. Prednisone suppresses immunity even further making patients prone to deadly infections such as JC virus.

The incidence of JC infection in patients using rituximab who have no other more plausible reason for JC infection (like lupus or multiple cytotoxic therapy) is really tiny. When I last knew about this there was one single unexplained case amongst hundreds of thousands in RA - and even without rituximab there are a very tiny number of unexplained cases. In the context of lymphoma and combination chemotherapy there is a significant issue but that is different.
The real problem with rituximab is unexplained pneumonitis in fact.

I doubt prednisolone makes that much difference in RA, although it does not tend to get used long term if patients respond well. I don;t think we have any evidence that prednisolone as a premed once off is a problem.

 

[SOC]

Likewise, my illness has changes a lot over the period I ahve been ill. Interestingly, I would have still met the IOM criteria 6 months into my illness. I'd be interested to hear from others on that, whether they think they would or wouldn't.

My disease has changed over time, mostly with more symptoms developing, but with some disappearing with treatment. I'm not sure I would have met the ICC criteria in the earliest stages where some of my symptoms were so mild I wouldn't have reported them -- particularly neurological ones.

I have met the ICC criteria for many years now and see it as a good description of my illness. The question is: which definition, ICC, CCC, or SEID would catch the most true (as far as we can tell) patients at all stages of the illness? That would be be best clinical diagnosis criteria. It looks like the SEID criteria would catch more patients across the range and progression of the condition, which is what is needed in a clinical diagnostic criteria. Eliminating patients in the early stages, or who have mild versions, from a clinical diagnosis would be extremely unjust. They don't deserve treatment until they're so sick they're housebound or bedbound? I don't think so.

So how do we catch, for clinical treatment, patients at all stages of the illness? We identify the smallest set of features that uniquely defines the condition. Sure, patients will have all kinds of other symptoms -- many changing over time -- but what makes the illness what it is and not depression, or primary OI, or overtraining syndrome, or any of the other conditions previously misdiagnosed as "CFS"? It's PEM -- the unique feature of our condition. We have PEM with other symptoms at milder or more severe levels, but we all have PEM.

 

[Jonathan Edwards]

As a doctor it seems to me that the name business is a storm in a teacup. Diagnostic names are by and large decided on by doctors and doctors are very free and easy about what names they want to use on any particular occasion. I might refer to a patient of mine as having 'RA' or 'inflammatory arthritis' or 'seropositive disease' or 'small immune complex arthritis', depending on what conversation I was having. SImilarly, a plumber might refer to 'my van' or 'my vehicle' or 'my motor' or 'my truck' depending on all sorts of things. ICD classifications are for statisticians, not doctors and patients. SEID is not a different disease, just a new way of categorising. I am not sure if it is better than ME or even if it will catch on, but there is no reason why it should cause anyone any grief. Reiter's syndrome got changed to reactive arthritis and then seronegative oligoarthritis and then about nine other things and it made no difference except that doctors could be more precise in particular contexts by choosing the best term for the context.

 

[Nielk]

So if you fit both criteria for two (supposedly) entirely different conditions, how to you explain that? I assume, in that case, that you don't consider the two diseases mutually exclusive. Do you see it like having both cancer and diabetes -- just an unfortunate confluence of events that you have two entirely different conditions? Or do you see ME and SEID in some kind of subset situation. In other words, do you think ME is a subset of SEID, or the other way around?

I would see it as someone who is diagnosed with O.I. as opposed to one diagnosed with SEID. Certainly someone who has SEID also fits a O.I. diagnosis. They have O.I and more.

I think that one that has ME-ICC encompasses SEID and more the same way.

 

[SOC]

I would see it as someone who is diagnosed with O.I. as opposed to one diagnosed with SEID. Certainly someone who has SEID also fits a O.I. diagnosis. They have O.I and more.

I think that one that has ME-ICC encompasses SEID and more the same way.

So you're now saying that SEID is a subset of ME-ICC ("ME-ICC encompasses SEID")? What happened to them being two different diseases? This is really confusing. Can you explain in more detail? At the moment, the whole picture isn't making sense to me.

Most of all, I'd like to hear a clear position statement from MEAdvocacy. Is their position that SEID and ME are two different diseases? That ME and SEID are "mutually exclusive"? Or is their position that ME is a subset of SEID, or SEID is a subset of ME? Or (this just seems to go on and on), is MEAdvocacy saying the ME=SEID but they just don't like the name and diagnostic criteria? Or is it something else entirely? Clarity and conciseness would be beneficial.

 

[Nielk]

Most of all, I'd like to hear a clear position statement from MEAdvocacy.

Here is their position statement -http://www.meadvocacy.org/now_is_the_time_to_stand_up_for_m_e

Now Is the Time to Stand Up For M.E.
POSTED BY MARY KINDEL 55.80SC ON FEBRUARY 24, 2015 · FLAG

It may seem like things have been a bit quiet on our end since the Institute of Medicine (IOM) Diagnostic Criteria for ME/CFS committee’s release meeting, but I would like to assure all of you that we’ve been working as hard as we can on your behalf. Because of your generosity and support, we are still here and focused on bringing our demands to fruition.

We have grown quite a lot over the past few months. I have organized what was previously an informal group of advocates, into a formalized MEAdvocacy.org Working Group. There are over a dozen volunteer patient members of this group including myself, Joni Comstock, Anne Keith, Kathryn Stephens, Gabby Klein, Robin Funk, Tom Jarrett, Colleen Steckel, Lisa Petrison, Tracey Ann-Tempel Smith, Polly Gilreath, and Mindy Kitei. We plan on adding more.

After much consideration of the IOM report, and listening to the ME community, we have decided that our plan going forward is to stay the course with our original goals and focus on getting myalgic encephalomyelitis (ME) officially recognized as its own distinct disease (separate from chronic fatigue syndrome/systemic exertion intolerance disease (CFS/SEID)), with a true ME definition, (the International Consensus Criteria or better), under the ICD-10-CM code G93.3. Note that we are no longer asking for the Canadian Consensus Criteria - we believe we should be advocating for the most current and best definition that is available.

We are also advocating for the use of the International Consensus Primer - already in use by doctors across the country as a working set of clinical guidelines to diagnose and treat ME patients.

Over time, it has become clearer that there are major flaws with the IOM report, such as not including pain in the criteria, and not excluding other diseases, which creates a disastrously loose definition, just like the 1994 Fukuda-CFS criteria. In addition, while the compulsory symptom of post exertional malaise (PEM) is a plus, we don’t have confidence that general practitioners unfamiliar with the disease will be able to diagnose post exertional malaise (PEM) correctly. They may instead confuse PEM with fatigue, resulting in the over-diagnosis of SEID.

Although the criteria are technically for diagnosis only, it is also possible that SEID could be used for research. This would replicate the same problems as the loosely defined Fukuda criteria, which resulted in hundreds of skewed studies which may have turned out positively if the study cohort included the correct patients.

Many patients also have concerns over the name SEID, believing it implies to doctors and the public that we are lazy instead of extremely sick with a biomedical disease. This would create the same problems as the name chronic fatigue syndrome has for many years.

We also observe that the report overlooks the needs of our most vulnerable population, severe ME patients, despite this letter from nine severe ME patients to the IOM committee on December 16, 2014.

The needs of these patients are especially urgent. Furthermore, they are key to future research as they are most likely to show biomarkers and other consistent key features of this disease.

Along with getting ME recognized, we will also be lobbying for the establishment of a federal research budget for ME as a distinct disease on par with similar diseases such as multiple sclerosis. Because the institutional bias against ME has been a huge roadblock for decades, we will also lobby for Congressional oversight of the Department of Health and Human Services (DHHS) as we work to get ME established.

We have been working hard to get public awareness for the plight of ME patients (especially severe ME), and also to get MEadvocacy.org widely mentioned. This is starting to pay off.

We have interest from several health reporters – including the Washington Post, NBC Philadelphia, and NBC Cincinnati. Our goal is to get stories done in as many cities as possible.

Also, we have a Day of Action proposed for mid-March in Washington DC, with a demonstration and lobbying of Congress. Assuming we have the funding in place, the PR firm will be organizing and assisting with both of these.

The “Tell HHS What You Think - SEID Survey” and the demonstration are both newsworthy items for interested reporters, and will hopefully generate even more publicity for MEadvocacy.org and our cause.

We will have a list of demands, which will be shared with both the media and Congress.

We believe with the national media attention of the IOM and the upcoming P2P release, the “Tell HHS What You Think - SEID Survey,” and the March Day of Action, that we have the best chance in many years to get some widespread attention for ME patients.

A final goal from these actions is to get enough publicity to drive the public to our website, where we will further educate them on our cause and suggest that they donate. This will hopefully start to take the financial pressure off ME patients.

Until then, we still need your help to get us over the hump. Now is the time to stand up for ME!

We are currently fundraising for March. Our goal is an additional $4100 for a total of $15,000 on the leaderboard by February 27. Please donate!

Click here to donate.

https://meadvocacy.nationbuilder.com/donatepr

 

[SOC]

Thanks, @Nielk. I think that is as much as I need to know. In particular,

...we have decided that our plan going forward is to stay the course with our original goals and focus on getting myalgic encephalomyelitis (ME) officially recognized as its own distinct disease (separate from chronic fatigue syndrome/systemic exertion intolerance disease (CFS/SEID))

[my bolding]

I cannot support dividing the patient population in this way. United we stand, divided we fall. Pushing for support and funding for two distinct diseases with very similar symptom profiles seems counterproductive to me.

The donation to MEAdvocacy just got cut from my March budget. The money can be better used for something that benefits the entire patient population like research or advocacy efforts aimed at getting more funding for that research.

I will watch your efforts to define yourselves a distinct disease and funding for it with interest. But please, DO NOT claim to be representing me.

 

[oceiv]

Although the criteria are technically for diagnosis only, it is also possible that SEID could be used for research. This would replicate the same problems as the loosely defined Fukuda criteria, which resulted in hundreds of skewed studies which may have turned out positively if the study cohort included the correct patients.

Over time, it has become clearer that there are major flaws with the IOM report, such as not including pain in the criteria

We also observe that the report overlooks the needs of our most vulnerable population, severe ME patients, despite this letter from nine severe ME patients to the IOM committee on December 16, 2014.

The needs of these patients are especially urgent. Furthermore, they are key to future research as they are most likely to show biomarkers and other consistent key features of this disease.

I share the above concerns with MeAdvocacy. I also have many other concerns about the definition. However, I don't think these are different illnesses. To me, ME is on the severe side of the illness continuum and SEID as currently defined, is on the "mild" or moderate part of this illnesses' continuum. I believe that the IOM committee failed to represent the severely-ill ME/CFS patients. i suspect the omission was due to the lack of research on severe patients. For me, I don't know that these new criteria would have helped me get a diagnoses. They might have hurt. I tried to articulate these concerns in The Questions to an IOM Committee Member thread. Unfortunately, I can't chime in to all of these discussions as much as I'd like, because I'm just too ill.

I would like to go forward with the IOM report, but amend it to reflect experiences and symptoms of severely-ill patients, like me. My question to people who support the IOM report is will you include the concerns of severely-ill patients in your advocacy? So that we can all work together, while acknowledging that different sets of patients have legitimate concerns and those concerns should be addressed as the IOM report and future advocacy go forward? This is one way we can stay united, perhaps.

I also endorse the idea stated by @alex3619 (in another thread) that a study should be done to compare patients who fit the SEID and ME definitions. Like the study done by Leonard Jason to compare CFS and ME patients. This could also unite patients who could then see a scientific representation of what needs to be added to the IOM report. We could have common goals, if we choose this route. We are stronger together.

 

[taniaaust1]

Your post assumes those who have SEID cant have ME too. Many people will meet both defintions so can say they have both things, it isnt a case that it needs to be one or another, they can chose to call their illness either to suit themselves when it suits themselves as long as they meet the definitions of whatever illness they declare themselves with.

As I understand it, some people believe that ME is a different disease from SEID.

In my case it is as I dont even meet the SEID definition well but I do meet the CCC and the International ME one no problems.

Believing (as I understand it) that myalgic encephalomyelitis is an accurate term describing their disease pathology and that the description of SEID in the IOM report is an inaccurate description of their disease.

Not all of us who meet the ME definition and see ourselves with ME may not thou necessarily believe the name with the "encephalmyelitis" is the correct one scientifically for all with it. I do have what is termed ME or even myalgic encephalomyelitis due to meeting the defintions of it (not cause I believe the name is correct). There is a certain disease which has certain manifestations to it which is called ME when I seem to meet based on its definition and my own illness resonates very well with.

I'm interested firstly in how you arrived at the conclusion, personally, that you have ME and not SEID? Particularly, I am thinking about encephalomyelitis (brain and/or spinal cord inflammation) here.

Well in my case the SEID by its very own defintion says that my illness should be questioned according to that definition cause I dont fit it well. I do not have unrelieved sleep 50% of time and in fact can go weeks without that symptom if Im not crashed worst or crashing.

I came to conclusion years ago that I had ME .. the illness which appears in outbreaks!! (where is the evidence that SEID as its defined appears in outbreaks? If there is another big outbreak.. you may want to think about if they will probably call it SEID or if they will call it an ME outbreak)

My illness is just like those ME specialists who have dealt or studied ME outbreaks describe. I was in awe of how well it fit me when I read things like Dr Cheney's progression of ME info.. it was path my illness did take. Dr David Bells info sits extremely well with my illness (I even have every one of the 5 testable autonomic dysfunctions he speaks of he sees in ME ). So does the info from others on ME outbreaks highly resonates to my own illness.. its like they are speaking about my illness!!

If a person is reading stuff written by specialists who have dealt with those from the ME outbreaks and it isnt resonating, you probably do not have ME

Another thing..

Primary Infection Phase
: The first phase is an epidemic or endemic (sporadic) infectious disease generally with an

incubation period of 4 to 7 days; in most, but not all cases, an infection or infectious process is evident.

My ME beginning lasted 5-7 days... it was sudden/acute. (the only thing a bit different from my primary infection phase is I recovered from it and got well.. but from there I was getting crashes which were like viral flares .. lasting same kind of time.. over time it became a full time thing).

I stil wasnt thou happy to classify myself with probably having ME even matching symptoms and descriptions till I got enough tests done showing I also had several well known ME abnormalities eg postive Rombergs, the non specific abnormalities found in ME EEGs etc etc. ME to me is a testable illness.. if you have no abnormalites when the right tests are done.. you are doubtful to have ME.

Is SEID seen as an infectious illness???? Well ME is.. Anyway who wants to say they are the same thing.. then should be saying SEID is infectious. Others have been made sick throu me.... my sister developed ME/CFS after she drank out of my glass, my ex.. I made ill throu kissing him.

Some other people consider themselves to have the disease described in the IOM report, yet disliking the name SEID, will continue to use the label ME to describe their disease. How will you distinguish yourselves from these other people with "ME"?

Why would those people even need to be distinguishing themselves.. if they meet both defintions.. they rightfully can be said to have both things.

Where might you stand if research into SEID results in findings of brain and/or spinal cord inflammation in SEID patients? Perhaps, or perhaps not, resulting in the name SEID being dropped in favour of ME, once backed by this evidence. Specifically I'm wondering whether you would then consider the two diseases (ME and SEID) to be the same disease after all? Or still different?

As SEID is going to be a more mixed group then the ME itself group..any findings will be weakened and may be missed... the same question could be asked with the ME and SEID parts of what you said switched around.

Just cause America may take on SEID, it doesnt mean at all other countries in the world will.. (I heard yesterday my states ME/CFS society thinks the whole SEID thing is a bit of a joke so they wont be supporting SEID here where I are).

So this means research using definitions of either the international ME one or the CCC which would be mostly ME people will be continuing even if not in America. (Some good research into ME is being done in Australia. The participates in studies here tend to meet at least the CCC as well as other lesser definitions)

Where might you stand if research into SEID results in a treatment being approved for patients with SEID?

What will people in America do if ME research shows something and a treatment... if ME is now gone from there as its became SEID and the criteria not as strict??? (as not all SEID people do meet ME definitions so that will probably cause the American system not to recommend the treatment shown benefical for me esp if its a risky one).

 

[taniaaust1]

At the risk of going briefly off-topic, that mortality rate looks a lot higher than what I thought the Rituximab mortality rate was. What do you think, @Jonathan Edwards?

I didnt look at the study but seeing its used to treat cancer.. if the study people had cancer.. maybe some died from that and not the Rituximab?

 

[taniaaust1]

The IC Primer on p. 5 states re. Neurological impairments -



My spect scan showed this exact abnormality.

In addition:



My qeeg shows elevated delta and beta frequencies.

Yeah, mine shows that too...

 

[taniaaust1]

This is one of my tests.. fast beta... typical ME finding.. 2 out of 3 of my EEGs over the years have shown this and I wasnt even on any meds at all (and had stopped supplements too) when I had the fast beta so it wasnt due to that. (I havent had many of the ME tests done but the ones I have, most of them show up ME abnormalities).

What they've done with SEID is like taking everyone with cancer "symptoms" or feeling this or that way.. and lumping them into the same group without doing tests or even recommending them. What kind of medicine is that?

IOM should of worked up from the CCC. I think the CCC almost has world wide acceptance too and if the IOM thing hadnt been done, I think it would of been accepted in America in the end (maybe that is exactly the reason why in America ones in high places decided to do the IOM thing?).. instead things have gone way backwards there, towards UK CFS definitions...and we all know just how much good that has done there.

 

[taniaaust1]

Take someone a little like me for instance: I meet ICC-ME. I also meet IOM-SEID. Now, I think SEID is more accurate than the ME label, .

Explain it then when I have fairly clearly ME why I dont meet the SEID well if its a good match for ME?

 

[Ecoclimber]

Explain it then when I have fairly clearly ME why I dont meet the SEID well if its a good match for ME?

Can't explain any better than Charles Shepard
http://forums.phoenixrising.me/inde...-myalgic-encephalomyelitis.35504/#post-557267

I suspect that you may have missed one of my fairly regular responses in relation to neuroinflammation and the relationship to a diagnosis of encephalomyelitis

Neuroinflammation occurs in a number of inflammatory and infective diseases. Examples include hepatitis C, HIV and lupus.

The presence of neuroinflammation in the well publicised Japanese study does NOT mean that these patients have what neurologists and neuropathologists would recognise or define as an encephalomyelitis.

Encephalomyelitis refers to widespread and significant inflammation involving both the brain and spinal cord.

From a clinical point of view, encephalomyelitis presents with severe neurological symptoms and signs, which may be life threatening.

There is, at present, no pathological or neuroradiological evidence to show that people with ME/CFS have an encephalomyelitis, and that incudes the findings from the post mortem research group that I am a member of.

Like everyone else, I want to establish what the neuropathology of ME actually is - but there is no point in coming to flawed conclusions about cause unless there is sound scientific evidence to demonstrate what you are claiming.

Abstract from our paper in the Journal of Neurological Sciences on post-mortem findings which have also demonstatred neuroinflammation in the form of dorsal root ganglionitis:

Pathology of Chronic Fatigue Syndrome: Pilot Study of Four Autopsy Cases

DG O’Donovan1, 2, T Harrower3, S Cader2, LJ Findley2, C Shepherd4, A Chaudhuri2
1Addenbrooke’s Hospital Cambridge UK
2Queen’s Hospital Romford Essex UK
3Royal Devon & Exeter Hospitals UK
4Honorary Medical Advisor to ME Association UK

Chronic Fatigue Syndrome / Myalgic Encephalomyelitis is a disorder characterised by chronic exercise induced fatigue, cognitive dysfunction, sensory disturbances and often pain. The aetiology and pathogenesis are not understood.

We report the post mortem pathology of four cases of CFS diagnosed by specialists.

The causes of death were all unnatural and included: suicidal overdose, renal failure due to lack of food and water, assisted suicide and probable poisoning.

Selected portions of tissue were made available by the various Coroners in the UK and with the assent of the persons in a qualifying relationship.

The cases were 1 male, and 3 female. Ages (years) M32, F32, F43 & F31.

One case showed a vast excess of corpora amylacea in spinal cord and brain of unknown significance but Polyglucosan Body Disease was not supported by clinicopathologial review. No ganglionitis was identified.
One case showed a marked dorsal root ganglionitis and two other cases showed mild excess of lymphocytes with nodules of nageotte in the dorsal root ganglia.

This raises the hypothesis that dysfunction of the sensory and probably also the autonomic nervous system may lead to abnormal neural activity eg hyperalgesia & allodynia rather than anaesthesia and may explain some of the symptoms of CFS / ME such as pain, hypotension, hyperacusis and photophobia. However, the syndrome may be heterogeneous.

Nevertheless, the precise relationship of fatigue, which may be either peripheral or central, to abnormalities in the peripheral nervous system (PNS) needs to be studied.

The differential diagnosis of ganglionitis should be investigated in CFS / ME patients hence Varicella Zoster, Lyme disease, HIV, Sjogren’s disease, paraneoplastic sensory ganglionopathy should be excluded by appropriate history and tests.

Thorough histopathological study of cases coming to autopsy may help to confirm or refute the hypothesis, that CFS is a disease process, and whether the symptomatology may be explained by inflammation of the sensory and autonomic divisions of the PNS.

A specific CFS / ME brain and tissue bank in the UK is proposed.

Further CS notes:

The dorsal root ganglia (DRG) are, in very simple terms, minute bundles of nerve cell bodies that lie outside the spinal cord - and so form part of the peripheral nervous system.

So inflammation of the DRG is not the same as myelitis in ME. Myelitis refers to inflammation of the spinal cord.

The DRG appear to be involved in the transmission of sensory information, and so disturbances in function may result in sensory disturbances and pain

Dorsal root ganglionitis, inflammation of the DRG, can be caused by infection such as chickenpox

But it can be associated with specific conditions such as Sjogren's Syndrome - which has some interesting overlaps with ME/CFS, including debilitating fatigue.

In the case of SS, the presence of DRG-itis has been linked to the sensory neuropathy that occurs.

As far as ME/CFS is concerned, we just don't know at this stage whether DRG-itis is part of the disease process, or whether it could just be the result of a triggering infection such as herpes

As we do more post mortems the position may become more clear.

Dr Charles Shepherd Hon Medical Adviser, MEA