Is it worth explaining the difference between ME and CFS to the public??

[insearchof]

Last year I was fortunate enough to meet Dr Hyde in a small group setting. My story is not typical ME as far as I can tell, unless I take a second infectious incident as being the one that triggered the illness. WHen I tell my story I usually use an earlier incident which involved primarily a bacterial infection. Certainly after a brief discussion and look at some results Dr Hyde said I had obvious central nervous system dysfunction. I also have the body type he often finds and I have since been dx with EDS. What is not clear to me is whether I am an atypical ME type and if this is related to the EDS. He mentions them specifically in his definition but it is not clear to me whether he is saying that this type is different from the epidemic type. Hope that makes sense.
Sandgroper

Hi Sandgroper

I am no Dr Hyde, so take what I have to say with a grain of salt. However, this is how I would see you fitting into my understanding of the historic literature. Others might disagree, which is fine - this is only my view for what its worth and is based on the information you have reported above.

You report two illness episodes: the first an earlier bacterial infection, and the second was an infectious episode that may have triggered your illness.

The second event might be the accute onset trigger of ME with the former possibly amounting to an unrelated illness episode that may have set you up for ME (an immune system assault) and made you much more susceptible to ME, in my view. I dont think that is uncommon. There is support for this in what I have read with regard to ME and Polio.

If Hyde says you have obvious CNS dysfunction and other features associated with historic ME, then in the absence of you acquiring it in the context of an infectious outbreak, then it sounds like you would be a sporadic case of ME.

I used the term typical' loosely in my prior post to Bob, in reference to the cases Hyde briefly mentioned relating to toxic chemical exposure and or vaccines - to signify that the main literature focuses on enteroviral infection as the associated trigger for ME (mostly seen in the context of epidemics when it was easier to diagnose)

But your post raises a good point in reference to the term ''primary ME' and the term ''atypical ME'. I cannot quite recall whether primary ME extends to both epidemic and sporadic cases and the rest might be termed atypical or whether primary ME only applies to ME as diagnosed within the context of epidemics.

Someone else here might known the answer and save me the trouble of looking it up.

 

[Bob]

OK, as an introduction for myself, I've been reading the Ramsay 1990 paper: "Myalgic encephalomyelitis a persistent enteroviral infection?"
http://pmj.bmj.com/content/66/777/526.full.pdf

This is the only paper that I've studied closely so far, so I can't yet make any conclusions of my own about historical 'ME' from this one paper, but I've picked out some points that I find interesting in helping me to try to distinguish the historic 'ME' from the current 'ME/CFS' or 'CFS'...

First, here's some information about having mononucleosis, which compares fatigue due to mononucleosis with fatigue due to ME (i.e. due to enterovirus):

"First, there has been a failure to distinguish the syndrome [ME] from post-viral debility following Epstein-Barr mononucleosis, influenza and other common fevers. Compared with ME, these lack the dramatic effect of exercise upon muscle function, the multisystem involvement, diurnal variability of symptoms and prolonged relapsing course."

Then it goes on to say that mononucleosis can co-exist with ME:

"Laboratory tests can distinguish chronic mononucleosis and other infections which, as our results show, may occasionally co-exist with ME and, by their immunosuppressive effect, precipitate relapse."

Then it talks about the relapsing/remitting nature of ME, and the variation in intensity of symptoms:

"Other characteristics include ... a prolonged relapsing course and variation in intensity of symptoms within and between episodes, tending to chronicity."

Here's a description of the clinical criteria that they used for 'ME' in this paper. Fatigue does seem to be a prominent factor in the illness:

"We adopted the following clinical criteria for investigation of ME: a syndrome commonly initiated by respiratory and/or gastro-intestinal infection but an insidious or more dramatic onset following neurological, cardiac or endocrine disability occurs. The pathognomonic features are: a complaint of general or local muscular fatigue following minimal exertion with prolonged recovery time; neurological disturbance, especially of cognitive, autonomic and sensory functions; variable involvement of cardiac and other systems; a prolonged relapsing course."

So far this doesn't look any different to the ME/CFS that I'm familiar with.

Here, it talks a bit about Polio viruses, which are enteroviruses, and also about non-polio enteroviruses (NPEVs):

"Polio viruses (Types 1-3) are the best known examples of a group of 69 enteroviruses which, by faecal/oral spread, commonly lead to asymptomatic childhood infection. The epidemiology of poliomyelitis remained enigmatic until virus isolation from carriers demonstrated the link between paralytic cases. In 1948, the non-polio enteroviruses (NPEV) were shown to be causative agents of illness previously designated as 'non-paralytic poliomyelitis'. Reports of NPEV isolation from individual cases" 2"' or serological evidence of NPEV infection5'2,13 occur in many published accounts of ME. Our study also supports association of the ME syndrome with NPEV. Thirty three per cent of 205 patients tested had CBV NTs indicative of infection - a figure comparable with that for enterovirus - associated myocarditis.'4
Seasonal distortion was excluded by the observation that 37/75 (49%) of those attending in winter and spring had significant CBV NT compared with 66/130 (51%) of those attending in summer and autumn. Moreover, 31 % of our patients tested had
positive enteroviral IgM tests compared with 12% of normal blood donors tested simultaneously in South London by the same technique.'"

I'm not quite sure what to conclude from the above yet, but it seems to me that enteroviruses were not found in anywhere near 100% of ME patients, confirmed as follows:

"CBV serology The sera of 205 patients with diagnostic features of ME seen before 1985, were tested by NT: 68/205 (33%) had titres indicative and 35/205 (17%) suggestive of recent CBV infection. Subsequently, 124 patients were additionally tested by the enteroviral IgM ELISA system. Applying the diagnostic criteria established by McCartney et al.,7 38/124 (31%) had evidence of recent/active enteroviral infection. Sixteen patients in our study, who were retested annually for three years, showed persistently raised CBV NTs and intermittently positive enteroviral IgM."


Here's a helpful list of symptoms and signs found in the ME patients in the study, along with the percentage of patients in whom they were found. The list starts with the most common symptoms, descending to the least common symptoms. 'Muscle fatigue' is the most common complaint, in 100% of patients:

Symptoms and signs in 420 patients with ME

Commonly found (> 50%):

SYMPTOM NO. %
Muscle fatigue 420 100
Emotional lability 411 98
Myalgia 336 80
Cognitive disturbance 323 77
Headache 310 74
Giddiness, disequelibrium 302 72
Autonomic dysfunction 289 69
Auditory disturbances 289 69
Reversal of sleep rhythm 268 64
Visual disturbances 260 62
Parasthaesia, hypo & hyperasthaesia 256 61
Intercostal myalgia/weakness 247 59
Clumsiness 235 56

less commonly found (< 50%):

Gastrointestinal symptoms 205 49
Disturbance of micturition 160 38
Recurrent lymphadenopathy 152 36
Arthralgia 118 28
Orthostatic tachycardia 88 21
Recurrent abacterial conjunctivitis 68 16
Orchitis/prostatism in young males 15/113 13
Seronegative polyarthritis 42 10
Vasculitic skin lesions 42 10
Myo/pericarditis 34 8
Positive Romberg sign 25 6
Thyroiditis in female patients 15/307 5
Fasciculation, spasm, myoclonus 239 57 Mesenteric adenitis 5 1
Paresis and muscle wasting 3 1

 

[Bob]

Here are extracts from:

MYALGIC ENCEPHALOMYELITIS:
A Baffling Syndrome With a Tragic Aftermath
by A. Melvin Ramsay M.D., Hon Consultant Physician,
Infectious Diseases Dept., Royal Free Hospital
(Pub. 1986)

http://www.meactionuk.org.uk/ramsey.html

The syndrome which is currently known as Myalgic Encephalomyelitis in the UK and Epidemic Neuromyasthenia in the USA leaves a chronic aftermath of debility in a large number of cases.

The degree of physical incapacity varies greatly, but the dominant clinical feature of profound fatigue is directly related to the length of time the patient persists in physical effort after its onset; put in another way, those patients who are given a period of enforced rest from the onset have the best prognosis.

Although the onset of the disease may be sudden and without apparent cause, as in those whose first intimation of illness is an alarming attack of acute vertigo, there is practically always a history of recent virus infection associated with upper respiratory tract symptoms though occasionally there is gastro-intestinal upset with nausea and vomiting.

Instead of making a normal recovery, the patient is dogged by persistent profound fatigue accompanied by a medley of symptoms such as headache, attacks of giddiness, neck pain, muscle weakness, parasthesiae, frequency of micturition or retention, blurred vision and/or diplopia and a general sense of 'feeling awful'.

There is usually a low-grade pyrexia [fever] which quickly subsides. Respiratory symptoms such as sore throat tend to persist or recur at intervals.

Routine physical examination and the ordinary run of laboratory investigations usually prove negative and the patient is then often referred for psychiatric opinion. In my experience this seldom proves helpful is often harmful; it is a fact that a few psychiatrists have referred the patient back with a note saying 'this patient's problem does not come within my field'. Nevertheless, by this time the unfortunate patient has acquired the label of 'neurosis' or 'personality disorder' and may be regarded by both doctor and relatives as a chronic nuisance. We have records of three patients in whom the disbelief of their doctors and relatives led to suicide; one of these was a young man of 22 years of age.

It is fully accepted that viruses such as herpes simplex and varicella-zoster remain in the tissues from the time of the initial invasion and can be isolated from nerve ganglia post-mortem; to these may be added measles virus, the persistence of which is responsible for subacute sclerosing panencephalitis that may appear several years after the attack and there is a considerable body of circumstantial evidence associating the virus with multiple sclerosis. There should surely be no difficulty in considering the possibility that other viruses may also persist in the tissues. In recent years routine antibody tests on patients suffering from myalgic encephalomyelitis have shown raised titres to Cocksackie B Group viruses. It is fully established that these viruses are the aetiological agents of 'Epidemic Myalgia' or 'Bornholm's Disease' and that, together with ECHO viruses, they comprise the commonest known virus invaders of the central nervous system. This must not be taken to imply that Cocksackie viruses are the sole agents of myalgic encephalomyelitis since any generalised virus infection may be followed by a period of post-viral debility. Indeed, the particular invading microbial agent is probably not the most important factor. Recent work suggests that the key to the problem is likely to be found in the abnormal immunological response of the patient to the organism.

A second group of clinical features found in patients suffering from myalgic encephalomyelitis would seem to indicate circulatory disorder.

The third component of the diagnostic triad of myalgic encephalomyelitis relates to cerebral activity. Impairment of memory and inability to concentrate are features in every case. Many report difficulty in saying the right word and are conscious of the fact that they continue to say the wrong one, for example 'cold' when they mean 'hot'. Others find that they start a sentence but cannot complete it, while some others have difficulty compre- hending the written or spoken word.

After moderate excercise, from which a normal person would recover with nothing more than a good night's rest, an ME patient will require at least 2 to 3 days while after more strenuous excercise the period can be prolonged to 2 or 3 weeks or more. Moreover, if during this recovery phase, there is a further expenditure of energy the effect is cumulative and this is responsible for the unrelieved sense of exhaustion and depression which characterises the chronic case.

The clinical picture of myalgic encephalomyelitis has much in common with that of multiple sclerosis but, unlike the latter, the disease is not progressive and the prognosis should therefore be relatively good. However, this is largely dependent on the management of the patient in the early stages of the illness. Those who are given complete rest from the onset do well and this was illustrated by the aforementioned three patients admitted to hospital in an unconscious state; all three recovered completely.

 

[floydguy]

OK, as an introduction for myself, I've been reading the Ramsay 1990 paper: "Myalgic encephalomyelitis a persistent enteroviral infection?"
http://pmj.bmj.com/content/66/777/526.full.pdf

This is the only paper that I've studied closely so far, so I can't yet make any conclusions of my own about historical 'ME' from this one paper, but I've picked out some points that I find interesting in helping me to try to distinguish the historic 'ME' from the current 'ME/CFS' or 'CFS'...

First, here's some information about having mononucleosis, which compares fatigue due to mononucleosis with fatigue due to ME (i.e. due to enterovirus):

"First, there has been a failure to distinguish the syndrome [ME] from post-viral debility following Epstein-Barr mononucleosis, influenza and other common fevers. Compared with ME, these lack the dramatic effect of exercise upon muscle function, the multisystem involvement, diurnal variability of symptoms and prolonged relapsing course."

Then it goes on to say that mononucleosis can co-exist with ME:

"Laboratory tests can distinguish chronic mononucleosis and other infections which, as our results show, may occasionally co-exist with ME and, by their immunosuppressive effect, precipitate relapse."

Then it talks about the relapsing/remitting nature of ME, and the variation in intensity of symptoms:

"Other characteristics include ... a prolonged relapsing course and variation in intensity of symptoms within and between episodes, tending to chronicity."

Here's a description of the clinical criteria that they used for 'ME' in this paper. Fatigue does seem to be a prominent factor in the illness:

"We adopted the following clinical criteria for investigation of ME: a syndrome commonly initiated by respiratory and/or gastro-intestinal infection but an insidious or more dramatic onset following neurological, cardiac or endocrine disability occurs. The pathognomonic features are: a complaint of general or local muscular fatigue following minimal exertion with prolonged recovery time; neurological disturbance, especially of cognitive, autonomic and sensory functions; variable involvement of cardiac and other systems; a prolonged relapsing course."

So far this doesn't look any different to the ME/CFS that I'm familiar with.

Here, it talks a bit about Polio viruses, which are enteroviruses, and also about non-polio enteroviruses (NPEVs):

"Polio viruses (Types 1-3) are the best known examples of a group of 69 enteroviruses which, by faecal/oral spread, commonly lead to asymptomatic childhood infection. The epidemiology of poliomyelitis remained enigmatic until virus isolation from carriers demonstrated the link between paralytic cases. In 1948, the non-polio enteroviruses (NPEV) were shown to be causative agents of illness previously designated as 'non-paralytic poliomyelitis'. Reports of NPEV isolation from individual cases" 2"' or serological evidence of NPEV infection5'2,13 occur in many published accounts of ME. Our study also supports association of the ME syndrome with NPEV. Thirty three per cent of 205 patients tested had CBV NTs indicative of infection - a figure comparable with that for enterovirus - associated myocarditis.'4
Seasonal distortion was excluded by the observation that 37/75 (49%) of those attending in winter and spring had significant CBV NT compared with 66/130 (51%) of those attending in summer and autumn. Moreover, 31 % of our patients tested had
positive enteroviral IgM tests compared with 12% of normal blood donors tested simultaneously in South London by the same technique.'"

I'm not quite sure what to conclude from the above yet, but it seems to me that enteroviruses were not found in anywhere near 100% of ME patients, confirmed as follows:

"CBV serology The sera of 205 patients with diagnostic features of ME seen before 1985, were tested by NT: 68/205 (33%) had titres indicative and 35/205 (17%) suggestive of recent CBV infection. Subsequently, 124 patients were additionally tested by the enteroviral IgM ELISA system. Applying the diagnostic criteria established by McCartney et al.,7 38/124 (31%) had evidence of recent/active enteroviral infection. Sixteen patients in our study, who were retested annually for three years, showed persistently raised CBV NTs and intermittently positive enteroviral IgM."


Here's a helpful list of symptoms and signs found in the ME patients in the study, along with the percentage of patients in whom they were found. The list starts with the most common symptoms, descending to the least common symptoms. 'Muscle fatigue' is the most common complaint, in 100% of patients:

Symptoms and signs in 420 patients with ME

Commonly found (> 50%):

SYMPTOM NO. %
Muscle fatigue 420 100
Emotional lability 411 98
Myalgia 336 80
Cognitive disturbance 323 77
Headache 310 74
Giddiness, disequelibrium 302 72
Autonomic dysfunction 289 69
Auditory disturbances 289 69
Reversal of sleep rhythm 268 64
Visual disturbances 260 62
Parasthaesia, hypo & hyperasthaesia 256 61
Intercostal myalgia/weakness 247 59
Clumsiness 235 56

less commonly found (< 50%):

Gastrointestinal symptoms 205 49
Disturbance of micturition 160 38
Recurrent lymphadenopathy 152 36
Arthralgia 118 28
Orthostatic tachycardia 88 21
Recurrent abacterial conjunctivitis 68 16
Orchitis/prostatism in young males 15/113 13
Seronegative polyarthritis 42 10
Vasculitic skin lesions 42 10
Myo/pericarditis 34 8
Positive Romberg sign 25 6
Thyroiditis in female patients 15/307 5
Fasciculation, spasm, myoclonus 239 57 Mesenteric adenitis 5 1
Paresis and muscle wasting 3 1

I could certainly be wrong but I think there is a differentiation between muscular fatigue and the can't get out of bed fatigue described in CFS.

 

[Bob]

Well, looking at the 1986 and 1990 Ramsay papers, it seems to me that they give a significantly different picture to the historical 'ME' that has been painted on this thread. I've yet to study the Nightingale definition paper closely, or the rest of the historic literature on ME, but seeing as Ramsay is said to be such an authority on ME, then I think this is a good place to start.

Unless I've made a big mistake somewhere here, then much of what has been said on this thread about the nature of historical 'ME' seems to contradict what Ramsay actually has to say about ME...

These are the main contradictions that I've noticed so far...

Unless I've misread the info, Ramsay says:

It is possible to completely recover from ME.
ME is not necessarily progressive.
ME does not have to be caused or precipitated only by enteroviruses.
The dominant feature of ME is fatigue.
All other specific signs and symptoms associated with ME, other than fatigue, are variable between patients and in each patient.


Ramsay seems to paint a picture of exactly the same disease that I am familiar with.
It seems to me that it's exactly the same disease that everyone, who is familiar with the organic disease ME/CFS, describes.

Next, I will look at the Hummingbird and Nightingale literature.

 

[Boule de feu]

What a great find!

Way too sick to be able to read all of this, BOB (boy Oh boy - LOL) does it look interesting! When my brain is back, I will have a look.

I know I said that I would not participate anymore (some of the posts are way too complicated for my little head - who could imagine I have a degree in microbiology and in medical biology???) but I just wanted to let you know that when I got my diagnosis in 2006, I read two great books on this subject. I read several books but I can't remember which ones. It will eventually come back to me.

The Polio Paradox

and

Dr Hyde's encyclopedia

Some wonderful literature!

 

[Tulip]

Bob, the difference is the definition for CFS is chronic fatigue, hence its name. PEM is quite different. Chronic fatigue is not a defining feature of M.E.. And yes for some people M.E. IS progressive, it depends on how much damage has been done to the CNS. That is why people are dieing. As for M.E., not being lifelong, much has been learnt since 1986, history and the thousands of patients that have been sick for over 20, 30, and 40 years indicates that it is.

 

[Bob]

More...

"The Myalgic Encephalomyelitis Syndrome"
A. Melvin Ramsay M.A. M.D.

http://myalgic-encephalomyelitis.com/Melvin-Ramsay.html#mono
http://www.hfme.org/wramsay.htm

The clinical identity of the Myalgic Encephalomyelitis syndrome rests on three distinct features, namely:

A :- A unique form of muscle fatiguability whereby, even after a minor degree of physical effort, 3, 4, 5 days or longer elapse before full muscle power is restored.

B :- Variability and fluctuation of both symptoms and physical findings in the course of a day. And,

C :- An alarming tendency to become chronic.

The unique form of muscle fatiguability described above is virtually a sheet-anchor in the diagnosis of Myalgic Encephalomyelitis and without it a diagnosis should not be made.

I am informed of two families who are said to have all the conditions conforming to the clinical picture but lacking the muscle fatiguability. These cases should be very carefully reviewed. It is quite common to find that muscle power is normal during a remission and in such cases tests for muscle power should be repeated after exercise.

 

[Bob]

Bob, the difference is the definition for CFS is chronic fatigue, hence its name. PEM is quite different. Chronic fatigue is not a defining feature of M.E.. And yes for some people M.E. IS progressive, it depends on how much damage has been done to the CNS. That is why people are dieing. As for M.E., not being lifelong, much has been learnt since 1986, history and the thousands of patients that have been sick for over 20, 30, and 40 years indicates that it is.

Thanks Tuliip, I've added the word 'necessarily' in my earlier post, so it now reads accurately that, according to Ramsay, "ME is not necessarily progressive".

I was only comparing what I've now read by Ramsay, in relation to ME, to what has been said about ME on this thread.

Ramsay does say that ME can be life-long, but not necessarily.

About the chronic forms of ME, he says this:

"The chronic case of M.E. can take two different forms. In the first there is a recurring cycle of remission and relapse. In three doctors who contracted the infection between 1955 and 1958 the endless alternation of remission and relapse, still continues. In my experience a remission can last as long as 3 years. Marinacci and Von Hagen record one of seven years. The second form of chronic M.E. is more tragic in that no remission occurs. The patient lives a very restricted existence, unable to walk more than a short distance and that with considerable difficulty, unable to read for any length of time and in many cases subject to disturbance of sleep rhythm and/or vivid dreams and always the almost invariable frequency of micturition, hyperacusis and dizzy spells. A few of these chronic cases are compelled to sleep upright as a result of permanent weakness of the intercostal and abdominal recti musculature."

 

[Tulip]

Bob, I'm not really seeing any real difference in what Ramsey says to what has been said in this thread. I have read all of his info and it is still how I have described it in this thread. As I said historic M.E. does not mention "chronic fatigue" which is different to post exertional fatigue. The updated definitions included chronic fatigue, that is one of the symptoms that has led to it becoming a "catch all" name for anything with fatigue in it.

I was told that I would be better in 2-5yrs and to rest, which is what I did. Nearly 20yrs later i'm still sick. What I have wanted to know is did he follow up the one's that made a "full recovery"? were they still well 10 yrs later?, did they really have M.E.. I have never met someone with real M.E. that has recovered, gone into remission and led an almost normal life for years at a time, yes. Most doctors will tell you the same thing. Is it possible that is what happened to those patients? Remission, not recovery. I really do wonder..

 

[Boule de feu]

Bob, I'm not really seeing any real difference in what Ramsey says to what has been said in this thread. I have read all of his info and it is still how I have described it in this thread.

I was told that I would be better in 2-5yrs and to rest, which is what I did. Nearly 20yrs later i'm still sick. What I have wanted to know is did he follow up the one's that made a "full recovery"? were they still well 10 yrs later?, did they really have M.E.. I have never met someone with real M.E. that has recovered, gone into remission and led almost a normal life for years at a time, yes. Is it possible that is what happened to those patients? Remission, not recovery. I really do wonder..

Wasn't there a boy named Ryan something? He received some of Wesseley's bad medicine. There are actually a few children who did make a come back.
Maybe we don't here about them.

 

[Tulip]

Wasn't there a boy named Ryan something? He received some of Wesseley's bad medicine. There are actually a few children who did make a come back.
Maybe we don't here about them.

But it still comes down to recovery or remission, remissions of 10 years are not unheard of.

I should say my personal view that it is lifelong has only been developed in the last few years and relates to observing the history of the last 16 yrs of this disease, and the changing view amongst M.E. specialists. It is not related to historical literature. Most M.E. specialists now agree that "recovery" is rare. But that does not mean your health can't improve to the point of being able to be almost normal, it just means you will always have the disease.

 

[insearchof]

Copyright Protected Materials

CAUTIONARY NOTE

I would be careful doing a cut and paste of large slabs of information from copyright protected materials out of scientific journals. It may amount to a copyright infringement and would be in breach of forum rules (Additional Information Pt 4). Publication of the material would put PR at fault.

 

[insearchof]

Hi Bob

The Dowsett Ramsay paper published in 1990 is an interesting paper.

I see you have also referred to little bits of the paper that you have found personally interesting, which I agree with you they are. But context is important both with respect to how those little bits of information sit within the overall document, its focus and intent - as well as a more extensive body of work.


The opening paragraph of that study makes it clear, that purpose of this study was two fold:


(a) one to demonstrate the association bewteeen ME and enteroviral infection and

(b) two that unique clinical and epidemiological patterns associated with enteroviral infection distinguish ME from PVF states.


The study co hort was selected from 6.000 of Dr Ramasays patients he had seen over a period of 12 years from 1975-87. 77% came from general practice and 23% were referred from hospital specialists.

From this large group, 402 were chosen for the purposes of this further study.

I refer to my earlier post to Bob discussing the difficulty detection enteroviruses outside of an epidemic setting (due to serology limitations and the flux of time). I suggest this was one reason for the need to identify a co hort that was likely to return a positive enteroviral finding for the purposes of the study.

Hence, a specific criteria was designed to select such patients - but again, it was for the purposes of this study. I view this in the same context as what the WPI did when they went looking for XMRV. They selected patients that were presenting with certain clinical features, which suggested to them that this would give them the best chances of finding XMRV in that group.


The criteria they used for the purposes of selecting a study co hort:

*illness initiation by respiratory and or gastro intestinal infection (common trait of enteroviral infection)
*neurological (CNS) disability and
*cardiac disability or
*endocrine disability

Signs of ME selected for

*neurological CNS disturbance - especially cognitive, autonomic nervous system dysfunction and sensory dysfunction
*cardiac and other system involvement (of a varible nature)
*general or local muscle fatigue following minimal exertion with prolonged recovery time.



Results.

One of the first points made is that results show acute or sudden onset in 81% of patients. As previously pointed out, a key feature of historical enteroviral ME.
This is not a feature required in any CFS definition.

The results then go on to discuss clinical characteristics.

The first point discussed is the duration and severity of the illness of the 402 subjects.

At the time of the study, patients reported being ill for the following durations.

9% had been ill for less than 12 months

32% between 1-2 years

47% between 3-10 years

8% 11-20 years

4% 21-60 years

Over this spread, illness was reported to be

improving in 31

fluctuating in 21

stead disability in 25

no remission or worse in 24



Consequently, the table of symptoms table and the symptoms in it (ie muscle fatigue) you posted, must be seen in light of this data.



In the commentary they also suggest that symptoms associated with enteroviral infection also vary due to age, susceptibility of the host, viral strain and virulence.


I would also suggest to you Bob, that 100% muscle fatigue (a very specific type) found in the co hort, although high, is not surprising because it was specifically selected for amongst the co hort in the studies design.


Further, the emphasis on this as a selection criteria, was I beleive, to demonstrate this feature as one of many in ME, that can be easily used to distinguish it from PVF states. That was, after all, one of the intentions of the study - to demonstrate how you could distinguish enteroviral ME from PVFS. It was not and should but be otherwise used to elevate this symptom as the key criteria to be selected for in ME, because it is not. It is not consistent with the general body of ME literature. It is a feature though.

Here's a description of the clinical criteria that they used for 'ME' in this paper. Fatigue does seem to be a prominent factor in the illness.........

Therefore, whilst it might appear from reading the isolated paragraph Bob referred to suggest that fatigue (and I might add, a specific kind of fatigue) is a prominent factor in the illness, this is IMO a mistaken view, that cannot be supported either on the basis of the study itself or within the broader body of literature on historic ME.



Bob, no one has suggested that enteroviral infection must be found 100% of the time. I alluded to the problem with this in the post I made to you regarding epidemics and sporadic cases and the limitations of serology/stool tests which made (and still do so) hard to return a positive finding. Though the literature on epidemics is what has given rise to this very strong enteroviral association. Evidence of enteroviral damage to the CNS has been found in the historic ME literature. This is why emphasis is placed on SPECT, PET, MRI, QEEG, etc is made - and when taken with other evidence ie: acute onset illness etc and other signs and tests - show that this is consistent with ME entroviral infection (even though enteroviral detection might be illusive because of general serology and stool based tests.


The findings of this study with respect to evidence of Coxsackie enteroviral infection - were impressive -given the limitations for detecting enetroviral infections (on this point, Dr John Chia would agree I am sure. You might like to read the interview Cort posted between himself and Dr Chia who, in his own studies, had to run multiple tests over a long period - in order to get a positive test result....which is why he developed stomach tissue biopsy and analysis). On this point, you might also like to note that 91% of the co hort had been ill for more than 12 months. Findings are also difficult to pin point because, as stated by the authors of the study - a variation in the viralence of the strain in individuals, the age and susceptibility of the individual. On that point, I note that 50% of the co hort were improving and or their symptoms fluctuating. This would also explain and be consistent with the results of the stuy with regard to evidence of enteroviral infection in this co hort.

The study however, reminds the scientific community of what they know: that enteroviral infection is common. Most doctors will agree and believe it is trivial. It is in 95% of cases, but for 5% (as historic Polio and Non paralytic polio cases showed) it can be severe and life threatening illness. The study reports that enteroviral infection is common and that this was the rationale for introducing polio vaccines. The study also makes mention of the difficulties associated with testing.

In all, this study outcome produced a very good result.

They are more impressive when you understand that the co hort had been suffering from ME many months and sometimes many years away from the incute onset enteroviral infection.

 

[insearchof]

Hi Floydguy

I could certainly be wrong but I think there is a differentiation between muscular fatigue and the can't get out of bed fatigue described in CFS.

You are correct Floydguy. Perhaps you would like to read my previous post to Bob above which explains how they defined ''muscle fatigue'' as general or local muscle fatigue following minimal exertion with prolonged recovery time.

Such a definition that refers to prolonged recovery time - would be consistent with the 'cant get out bed'' circumstances.

 

[insearchof]

Hi Bob

Well, looking at the 1986 and 1990 Ramsay papers, it seems to me that they give a significantly different picture to the historical 'ME' that has been painted on this thread. I've yet to study the Nightingale definition paper closely, or the rest of the historic literature on ME, but seeing as Ramsay is said to be such an authority on ME, then I think this is a good place to start.

Unless I've made a big mistake somewhere here, then much of what has been said on this thread about the nature of historical 'ME' seems to contradict what Ramsay actually has to say about ME...

These are the main contradictions that I've noticed so far...

Unless I've misread the info, Ramsay says:

It is possible to completely recover from ME.
ME is not necessarily progressive.
ME does not have to be caused or precipitated only by enteroviruses.
The dominant feature of ME is fatigue.
All other specific signs and symptoms associated with ME, other than fatigue, are variable between patients and in each patient.


Ramsay seems to paint a picture of exactly the same disease that I am familiar with.
It seems to me that it's exactly the same disease that everyone, who is familiar with the organic disease ME/CFS, describes.

Next, I will look at Nightingale.

Bob

Unless I've made a big mistake somewhere here, then much of what has been said on this thread about the nature of historical 'ME' seems to contradict what Ramsay actually has to say about ME...

I think you have made a couple of mistakes in your analysis and interpretation of the Ramsay Dowsett paper. I need to address the other Ramsay paper you posted though.

I think it is a little unwise to base your conclusions on two papers - one of which you appear to have taken out of context or viewed through a distorted lens - and then suggest that what has been posted in this thread by others is at direct odds with Historic ME. It is not and in fact, I would hope that my post on the Dowsett and Ramsay paper shows quite the contrary to be true.

 

[insearchof]

Hi Boule de feu

Way too sick to be able to read all of this, BOB (boy Oh boy - LOL) does it look interesting! When my brain is back, I will have a look.

I know I said that I would not participate anymore (some of the posts are way too complicated for my little head - who could imagine I have a degree in microbiology and in medical biology???) but I just wanted to let you know that when I got my diagnosis in 2006, I read two great books on this subject. I read several books but I can't remember which ones. It will eventually come back to me.

The Polio Paradox

and

Dr Hyde's encyclopedia

Some wonderful literature!

Both books are excellent, I agree and make some very useful reading to understanding the subject matter more.

In fact, the Dowsett / Ramsay paper that Bob referred to in this thread, is printed in what you refer to tas Dr Hyde's encyclopedia. So if you still have it, you might like to read the paper there.

 

[insearchof]

Here are extracts from:

MYALGIC ENCEPHALOMYELITIS:
A Baffling Syndrome With a Tragic Aftermath
by A. Melvin Ramsay M.D., Hon Consultant Physician,
Infectious Diseases Dept., Royal Free Hospital
(Pub. 1986)

http://www.meactionuk.org.uk/ramsey.html

The syndrome which is currently known as Myalgic Encephalomyelitis in the UK and Epidemic Neuromyasthenia in the USA leaves a chronic aftermath of debility in a large number of cases.

The degree of physical incapacity varies greatly, but the dominant clinical feature of profound fatigue is directly related to the length of time the patient persists in physical effort after its onset; put in another way, those patients who are given a period of enforced rest from the onset have the best prognosis.

Although the onset of the disease may be sudden and without apparent cause, as in those whose first intimation of illness is an alarming attack of acute vertigo, there is practically always a history of recent virus infection associated with upper respiratory tract symptoms though occasionally there is gastro-intestinal upset with nausea and vomiting.

Instead of making a normal recovery, the patient is dogged by persistent profound fatigue accompanied by a medley of symptoms such as headache, attacks of giddiness, neck pain, muscle weakness, parasthesiae, frequency of micturition or retention, blurred vision and/or diplopia and a general sense of 'feeling awful'.

There is usually a low-grade pyrexia [fever] which quickly subsides. Respiratory symptoms such as sore throat tend to persist or recur at intervals.

Routine physical examination and the ordinary run of laboratory investigations usually prove negative and the patient is then often referred for psychiatric opinion. In my experience this seldom proves helpful is often harmful; it is a fact that a few psychiatrists have referred the patient back with a note saying 'this patient's problem does not come within my field'. Nevertheless, by this time the unfortunate patient has acquired the label of 'neurosis' or 'personality disorder' and may be regarded by both doctor and relatives as a chronic nuisance. We have records of three patients in whom the disbelief of their doctors and relatives led to suicide; one of these was a young man of 22 years of age.

It is fully accepted that viruses such as herpes simplex and varicella-zoster remain in the tissues from the time of the initial invasion and can be isolated from nerve ganglia post-mortem; to these may be added measles virus, the persistence of which is responsible for subacute sclerosing panencephalitis that may appear several years after the attack and there is a considerable body of circumstantial evidence associating the virus with multiple sclerosis. There should surely be no difficulty in considering the possibility that other viruses may also persist in the tissues. In recent years routine antibody tests on patients suffering from myalgic encephalomyelitis have shown raised titres to Cocksackie B Group viruses. It is fully established that these viruses are the aetiological agents of 'Epidemic Myalgia' or 'Bornholm's Disease' and that, together with ECHO viruses, they comprise the commonest known virus invaders of the central nervous system. This must not be taken to imply that Cocksackie viruses are the sole agents of myalgic encephalomyelitis since any generalised virus infection may be followed by a period of post-viral debility. Indeed, the particular invading microbial agent is probably not the most important factor. Recent work suggests that the key to the problem is likely to be found in the abnormal immunological response of the patient to the organism.

A second group of clinical features found in patients suffering from myalgic encephalomyelitis would seem to indicate circulatory disorder.

The third component of the diagnostic triad of myalgic encephalomyelitis relates to cerebral activity. Impairment of memory and inability to concentrate are features in every case. Many report difficulty in saying the right word and are conscious of the fact that they continue to say the wrong one, for example 'cold' when they mean 'hot'. Others find that they start a sentence but cannot complete it, while some others have difficulty compre- hending the written or spoken word.

After moderate excercise, from which a normal person would recover with nothing more than a good night's rest, an ME patient will require at least 2 to 3 days while after more strenuous excercise the period can be prolonged to 2 or 3 weeks or more. Moreover, if during this recovery phase, there is a further expenditure of energy the effect is cumulative and this is responsible for the unrelieved sense of exhaustion and depression which characterises the chronic case.

The clinical picture of myalgic encephalomyelitis has much in common with that of multiple sclerosis but, unlike the latter, the disease is not progressive and the prognosis should therefore be relatively good. However, this is largely dependent on the management of the patient in the early stages of the illness. Those who are given complete rest from the onset do well and this was illustrated by the aforementioned three patients admitted to hospital in an unconscious state; all three recovered completely.

Hi Bob,

This article was written in 1986 when there was much confusion between the terms ME and PVFS and the article needs to be acknowledged in that context. We looked at this earlier in the thread. Please see post #90 here
http://forums.phoenixrising.me/show...erence-between-ME-and-CFS-to-the-public/page9

Without uinderstanding the historical context and historical sequence of events that impacted on historical ME literature and promoting only two papers, it is easy to see ME narrowly and through a distorted lens - which might make it appear as though, there is no difference between ME and CCC and or that ME PVFS and CCC are all the same, when they are not. Again the ICDs attest to this.

As for disease progression, I also note that he states prognosis is ''largely dependent'' on managenet of the patient in the early stages of the illness.

 

[insearchof]

Hi Bob

Unless I've misread the info, Ramsay says:

It is possible to completely recover from ME.
ME is not necessarily progressive.
ME does not have to be caused or precipitated only by enteroviruses.
The dominant feature of ME is fatigue.
All other specific signs and symptoms associated with ME, other than fatigue, are variable between patients and in each patient.
.

Prognosis and Recovery

In the paper you cite, Ramsay states that he does not believe the illness is progressive - at least not in the way that MS is. That is not to say that it is not otherwise progressive, but I wil come back to this point.

He does that as the illness is not progressive in the same way MS is, then prognosis should herefore be relatively good.

I note, he does not say it is. He is careful there, and he also uses the term ''relatively'' good. That is important, because other literature highlight that ''recovery' as understood in ME is not the same as generally understood in other illnesses.


Further, prognosis is subject to and largely dependent on, the management of the patient in the early stages of the illness. Those who are given complete rest from the onset ''do well''. I note he does not say ''completely recover''.

He observes that the three patients that he does state did 'recovered completely'' were unconscious This however is not a common state in ME and most patients advised to rest, are not and are not placed, into an induced coma.

Also, we do not know what follow up over the long term, indicated in these three patients. So whether they did completely recover is questionable also, based on the basis of other ME literature - which questions complete recovery and that it may be more appropriate to say ''remission''.


Other literature would suggest that some do *appear* to recover, but these individuals usually fall subject to a relapse - sometimes years later. That of course is consistent with the notion of enteroviral infection that is left untreated and which exists in the tissues long terem (Chia).

Marinacci et al who treated a lot of patients out of epidemic oeriods said that most of those patients never recovered and were ill 40 years after the illness onset.

So complete recovery is questioned elsewhere, even by Ramsay himself in his own subsequent study you previously quoted (Dowsett and Ramsay) showed that over 50% of patients did not do so and have a cycle of remissions and relapses. 25% of this group never experienced a remission period at all.


Progressive

It is hard to know what he meant here. Progression in MS represents an escalation in symptom severity as it was explained to me. There is fluctuation in symptoms, together with severity. To say anything more, I would need to go back to some papers. So I will leave it there. Someone else might be able to elaborate in the interim.


ME does not have to be caused or precipitated only by enteroviruses.


I refer again, to previous posts (in particular post #90). I dont think that there is general support for this proposition in the general body of historic literature on the matter. It is also why there ME and PVFS are both listed at G93.3 ICDs It being recognised that a particular virus has been associated and found to cause CNS damage in patients diagnosed with ME and other viruses as the cause of PVFS.

As previously stated though, Hyde does refer to this odd group (vaccine and toxic chemical exposures) in ME which I referred to as atypical ME. However these were cases, which lie outside of what is known and accepted as the norm by the historical ME literature. The limitations with serology/stool analysis for enteroviral detection were unable to assist here obviously. It would be interesting to see whether they had such via a tissue stomach biopsy - in accordance with the method used by Dr Chia.


The dominant feature of ME is fatigue.

There is no support for this, either on the basis of the Ramsay literature you quote Bob - and especially when you place them within an historical and wider context of the general body of historic ME literature.

Fatigue is a symptom common to many illnesses. I would even go as far as saying that it is not regarded as a dominant feature in any illness outside of CFS and even then, it is an unremitting fatigue.

 

[Bob]

I think it is a little unwise to base your conclusions on two papers

I agree... This is a work in progress for me, and those were my initial observations based on the Ramsay literature (3 of Ramsay's papers)...

I've got much more reading to do...

I'm slowly working through it all, and will start looking at the Hummingbird literature next.

I'll read through all the responses to my posts as soon as I can. But it will be slowly.