Evidence that "Long Covid" is different from ME/CFS?

J

Jaybee00

Senior Member (Voting Rights)
Can folks point out any studies that demonstrate that "Long Covid" at six months with MECFS symptoms is a distinct disease/syndrome/entity from ME/CFS? I remember Nath commenting on this, but I don't remember where I saw this. I'm seeing way too many articles in the popular press that discuss Long Covid with MECFS-type symptoms, that either don't mention MECFS at all, or if they do, they use verbiage like "similar to" MECFS

Thanks.
 
I don't think that's possible without an actual coherent understanding of what they are. It's clearly mostly said by people who don't want it to be true but don't have actual reasons other than that it's just tradition to dismiss us. It's a taboo subject so it remains mostly unspoken.

Everything remains at a completely superficial level, not enough details to compare. It's actually commonly used nowadays, how LC is not well-defined, which is medicine's responsibility and failure but instead it's used as justification not to bother in the first place. Which is how it happened with us, unsurprisingly.
 
Prof. Warren Tate and Dr. Anna Brooks were just interviewed on Radio NZ's 'Nine til Noon'. They are both running studies into LC vs ME vs NC. They are looking at mitochondrial function and epigenetic changes; and cellular immune changes. Hopefully we can post a link in the NZ section of the forum, when RNZ have published it.

ETA: RNZ link
 
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I'm not sure if there are any LC patients on the forum, but if so they may wish to comment further. In the meantime, I might be the closest thing. I'm not confirmed COVID, but I'm looking increasingly likely. I present as something of a classic case - if such a thing exists as I tick all the same boxes from talking to other LC patients.

In the absence of scientific studies (hugs rvallee!) it's possibly useful to review my situation as a reference. I'll present this as if I am LC but to repeat, that is not known.

History
  • Never tested positive on swabs, with multiple opportunities (hospital work, being careful)
  • Sudden "acute" onset, which in hindsight was probably my first recognition of slow deterioration commencing maybe 6-8 weeks following asymptomatic infection.
  • Now 12 months in
  • Initially mild fatigue and POTS and able to work, supported by increasing restriction of off-work life
  • Negative for anti-SARS-CoV-2 nucleocapsid IgG / IgM in March 21
  • Pfizer 1 and 2 in April 21
  • Crash in June, stopped work due to severe disability, including distressing neurological symptoms
  • 70% disabled at that point
  • Slow recovery (with set-backs)
  • Currently mild end of moderate (say 30%)
Currently
  • Officially diagnosed with POTS, with otherwise normal cardiovascular function
  • PEM manageable currently, though mostly housebound
  • Spend over half the day lying flat to manage OI
  • Able to sit at workstation and work a few hours from home most afternoons
  • I think I'm slowly improving despite no offered treatments
  • Definitely had no CBT/GET - thank you to all here !!!!

Research or Informal Investigations
  • Demonstrated reduction in cerebral blood flow on standing (near-infrared spectroscopy)
  • Demonstrated hypercoagulability (thromboelastography, also clotting venous lines)
  • Probable confirmation of micro-clots (repeated, against one normal control, including contemporaneous identical methods: early, but seems promising)
  • Significantly high anti-SARS-CoV-2 antibodies, 8 months post double-vaccination / no booster (compared with normal / recently double-vacc'ed) - to be confirmed
  • Deep immune profiling underway vs NC, ME

ICC
  • PENE - yes
  • Neurocognitive - maybe slowed speech, possibly just energy related (well recovered)
  • Pain - headaches (mostly recovered)
  • Sleep disturbance - was bad (now resolved)
  • Unrefreshed sleep - yes (improving)
  • Neurosensory - noise hypersensitivity (now resolved)
  • Motor - extreme weakness, twitching (resolved)
  • Flu-like symptoms - no
  • Viral infection susceptibility - no
  • GIT - nausea, pain, irritable bowel (now seemingly resolved)
  • GU - PUing but maybe due to increased fluid intake
  • Sensitivities - no
  • Cardiovascular - OI / POTS
  • Respiratory - mild air hunger (nearly completely resolved)
  • Thermostasis - yes: initially night sweats (resolved)
  • Temperature intolerance - yes: very cold during winter, unable to tolerate summer heat currently
(So I don't qualify as ME, but do qualify as atypical ME)

IoM / NAM
  • Fatigue / substantial impairment - YES
  • PEM - YES
  • Unrefreshing sleep - YES
  • Cognitive impairment - NO
  • Orthostatic Intolerance - YES
(Qualifies as ME)

Comment
I'm an n=1 and I'm still across "both worlds" as I don't know if I'm ME or LC. I think LC is ME with a known inciting agent and a starting-to-be-understood mechanism. Likely this is only a minority of ME. Judging from what we've seen described of adverse vaccine responses, I wonder if the figure will be end up being around 20% - but that's looking a long way ahead of what the data can support at the moment.

ETA:
The above is n=1 so of course doesn't count for much in the grand scheme. As Hutan wrote here, we need others to replicate this with larger numbers.
 
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What I'm noticing is that while many with Long Covid don't meet ME/CFS diagnostic criteria initially, those that have remained unwell for a longer period are developing more ME/CFS-like symptoms over time. Subsequently many who have been ill for longer than 12 months are now being diagnosed with ME/CFS.

This phenomenon was apparently noticed in the Dubbo studies according to Cort:

They tracked an extensive cohort of people (n=253) who’d experienced various infectious events (Ross River virus, Epstein-Barr virus, Q fever (Coxiella burnetii ) over the course of year in the mid-2000’s.
...
They found, though, that 35% of people still had “post-infectious illness” (e.g. chronic fatigue syndrome) at 6 weeks, 27% did so at three months, and 9% were still sick at 12 months. The studies also found that while the initial symptom set was different in all three infections, it evolved over time to a general pattern characterized by fatigue, musculoskeletal pain, and neurocognitive issues.
Click to expand...

The symptoms that are more specific to Covid (eg, dyspnea, loss of smell/taste) seem to be less significant over time while other ME/CFS symptoms appear or become more prominent.
 
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I was diagnosed with PVFS 'atypical ME' during the first 2-4 years. I didn't have PEM or orthostatic impairment. I didn't hae to lie down most of the day.

Understanding the pathophysiology of PEM will determine whether we are all dealing with the same pathology. I think we will see many similarities with pwLC.
 
Art Vandelay said:
What I'm noticing is that while many with Long Covid don't meet ME/CFS diagnostic criteria initially, those that have remained unwell for a longer period are developing more ME/CFS-like symptoms over time. Subsequently many who have been ill for longer than 12 months are now being diagnosed with ME/CFS.
Click to expand...

Further to this, this study attempted to track LC symptoms over 7 months. It's interesting to note that symptoms specific to covid such as shortness of breath, fever and coughing diminished over time, while PEM developed over the first few months.

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The weight of numbers.
I don't think those with SARS were ever offered any distinction.

The initial trigger virus may have some idiosyncrasies ( which may exist with different viral ME onset anyway - has this really been seriously studied in any depth )

The degree of symptom overlap and timescale for symptom development and PEM manifestation may offer important clues re pathophysiology.

We already know that many things trigger this end state- we just have not seen this happen so openly in real time.

Epigenetic info would be interesting over time. I don't know of any research is looking at this.
 
Amw66 said:
The weight of numbers.
I don't think those with SARS were ever offered any distinction.

The initial trigger virus may have some idiosyncrasies ( which may exist with different viral ME onset anyway - has this really been seriously studied in any depth )

The degree of symptom overlap and timescale for symptom development and PEM manifestation may offer important clues re pathophysiology.

We already know that many things trigger this end state- we just have not seen this happen so openly in real time.

Epigenetic info would be interesting over time. I don't know of any research is looking at this.
Click to expand...


There is this study here that is funded by the Hungarian National Academy of Sciences (google translate):

Follow-up study of the discovery of immune (epi) genetic components that play a key role in long-term COVID syndrome in children

The research of Gábor Kovács and his colleagues at Semmelweis University on the follow-up of the discovery of immune (epi) genetic components that play a key role in long-term COVID syndrome in children is based on the fact that new types of coronavirus infection the children. Symptoms following an infection or new onset as a complication of COVID known as long-COVID syndrome (long-COVID syndrome).

The molecular background of long-COVID is currently unknown. The aim of the research is to map the T-cell-mediated immune response of children with long-term COVID syndrome by examining circulating immune cells, anti-coronavirus memory T-cells, T-cells at the protein, RNA and DNA levels -cryptomy of cell subgroups and relevant genes of immune cells. Complex characterization of cells involved in the antiviral immune response may aid in the early diagnosis of long-COVID syndrome, differential diagnosis, phenotyping, and prognosis estimation.
Click to expand...

If someone is interested they can check out some of the other long covid studies funded by the Academy in this post: News from the Visegrád Countries - Czech Republic, Poland, Slovakia and Hungary
 
Wyva said:
There is this study here that is funded by the Hungarian National Academy of Sciences (google translate):



If someone is interested they can check out some of the other long covid studies funded by the Academy in this post: News from the Visegrád Countries - Czech Republic, Poland, Slovakia and Hungary
Click to expand...
Thanks @Wyva .
Looks interesting. It would be good to have more international coordination to maximise what can be done.

Children are different: the prognosis for recovery from ME is noted as better.

How much of this is due to misdiagnosis or is simply mildly affected adjusting to a new " normal" is unclear .
Rowe did find on follow up that adjustment was pretty common in mildly affected

Relapse later in life seems little more than an acknowledgement . Having data on this would also be interesting and very pertinent now.
 
The description of a typical patient with ME given by Dr Ramsay was a colleague who managed to work for a few weeks then became ill again. The idea of ME as something where patients never recovered form the initial infection but remained weak and very fatigued for months came with the invention of CFS. (Not that it never happened)

Many longcovid patients are describing the yoyo illness that matches Ramsay better than most. He also described an illness where the symptoms were variable and that seems to be happening in longcovid as well.

What made it ME was the abnormal response to exercise that was excessive, prolonged and often delayed. There was pain, neurological symptoms and autonomic symptoms that not only included POTS and OI but also the other types of homeostatis such as temperature control, water balance and blood sugar control.

Moving fatigue to the main symptom lost these things.

The tweets from longcovid patient match my own illness progression much better than many things I have read.

It may all be a superficial resemblance of a few symptoms and, like the types of diabetes, turn out to be completely different diseases as may ME as it stands just now. It is too soon to know.
 
Mithriel said:
but also the other types of homeostatis such as temperature control, water balance and blood sugar control.
Click to expand...
Are there any sources about this available online? These are quite prominent symptoms for me and I'd love to read more, especially about the water balance issue that badly affects me but only seems to affect a very small number of patients otherwise (and thus I struggle to find decent info about it).
 
Mithriel said:
The description of a typical patient with ME given by Dr Ramsay was a colleague who managed to work for a few weeks then became ill again. The idea of ME as something where patients never recovered form the initial infection but remained weak and very fatigued for months came with the invention of CFS. (Not that it never happened)

Many longcovid patients are describing the yoyo illness that matches Ramsay better than most. He also described an illness where the symptoms were variable and that seems to be happening in longcovid as well.

What made it ME was the abnormal response to exercise that was excessive, prolonged and often delayed. There was pain, neurological symptoms and autonomic symptoms that not only included POTS and OI but also the other types of homeostatis such as temperature control, water balance and blood sugar control.

Moving fatigue to the main symptom lost these things.
Click to expand...

This only describes mild & moderate PwME though, surely? I think I’ve seen you mention this elsewhere too when talking about Ramsays disease, and how it was about variability rather than fatigue - and I felt confused then as well. PwME who are severe don’t have variability, I thought? Not huge variability, anyway. I thought they tend to feel very ill and very exhausted / fatigued, day in day out, and then when they exert themselves a little, feel even worse?
 
Assuming I have ME/CFS, I think it's a matter of severity.

Initially I had a few bad mornings every month.

Then it became more severe and I had more frequent and longer lasting crashes, but with few symptoms between crashes.

Then it became more severe and turned into feeling unwell most of the time (sometimes badly), but with large variability in symptom severity and occasionally feeling almost normal.

Then for some time it get worse and I developed POTS and it was a torture due to constant severe symptoms.

Then it improved and became more like it was before, with a few more symptoms added.

It's probably mostly all the same illness. I'm not sure if the POTS is a separate disease process or a manifestation of the original illness. It's an unpredictably fluctuating illness so these descriptions are not entirely accurate as reality is more chaotic and hard to summarize. It also depends a lot on how much pacing I'm allowed to do and how well I do it. It's a life destroying illness but it's still possible to maintain quality of life that is good enough to make life worth living.
 
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Mithriel said:
The description of a typical patient with ME given by Dr Ramsay was a colleague who managed to work for a few weeks then became ill again. The idea of ME as something where patients never recovered form the initial infection but remained weak and very fatigued for months came with the invention of CFS. (Not that it never happened)

Many longcovid patients are describing the yoyo illness that matches Ramsay better than most. He also described an illness where the symptoms were variable and that seems to be happening in longcovid as well.

What made it ME was the abnormal response to exercise that was excessive, prolonged and often delayed. There was pain, neurological symptoms and autonomic symptoms that not only included POTS and OI but also the other types of homeostatis such as temperature control, water balance and blood sugar control.

Moving fatigue to the main symptom lost these things.

The tweets from longcovid patient match my own illness progression much better than many things I have read.

It may all be a superficial resemblance of a few symptoms and, like the types of diabetes, turn out to be completely different diseases as may ME as it stands just now. It is too soon to know.
Click to expand...
Out of interest, how many patients did, or could, Ramsay have ever seen? I have no reason to think he wasn't accurately describing the patients he saw but I don't think we should assume that he saw the full range of severity, at least from that description.
 
Ramsay of course is not the only historic authority - it was Acheson who wrote the first systematic review to use the term ME albeit as Benign Myalgic Encephalomyelitis: Acheson, E. D. (1959). The clinical syndrome variously called benign myalgic encephalomyelitis, Iceland disease and epidemic neuromyasthenia.

https://sci-hub.se/10.1016/0002-9343(59)90280-3

from which -

"A period of six weeks convalescence was found necessary for patients who had been in bed for more than a month. Even when this was completed many patients could work only four hours
a day. Four patients still had marked disability at the time of the report, two years after the epidemic. In one patient choreoathetoid movements had developed in her paralysed right hand; two required leg callipers and a fourth crutches."

and

"The Aftermath. Relapses: The majority of patients afflicted in these outbreaks have been discharged from the hospital within two months and have returned to work after a period of convalescence prolonged by fatigue, aches and pains, depression and lack of concentration. However, in a proportion which has varied from outbreak to outbreak, relapses or a chronic state of ill health have developed."

Ramsay and Acheson were writing within the limitations of their time - perception of disease, limited data, limited science etc all of which impacted how and what they wrote and how the thought about ME. How we now see the illness is radically different, and that's not surprising. For example although Ramsay and Acheson formulated their early ideas about ME after Watson and Crick had published their work on DNA, it was nearly two decades before the full extent of what genetics meant for understanding illness was begun to be grasped.

Acheson's paper now seems more like a description of various acute infections that were followed by post infection syndromes that we would recognise as bearing strong resemblance to post COVID, and without necessarily having any certain relationship to ME/CFS. Ramsay's later writings probably more accurately reflect current understanding of ME/CFS but we shouldn't consider his work as tablets of stone - he had a vision of what ME/CFS may be but it was inevitably a limited vision.
 
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