Poll on myalgia (muscle pain)

[MeSci]

But can anybody speculate on how intracellular non-lytic viral RNA would result in easier muscle tearing? How would contractile proteins in myofibrils be easier to break? If the structure is defective, the muscle should presumably be weaker, too, since it wouldn't be doing its proper job -- unless there is only a small number of weak links. Do people find that a muscle prone to tearing is also weaker?

Or alternately, how would the sarcolemma (the membrane of muscle cells that needs to be able to get shorter or longer) be more likely to rupture? A ruptured sarcolemma would presumably result in more inflammation than damage to myofibrils as cellular contents might spill out.

Has increased (susceptibility to) muscle tearing been reported in ME/CFS?

 

[Sherlock]

Has increased (susceptibility to) muscle tearing been reported in ME/CFS?

Yes. In this thread

 

[MeSci]

Yes. In this thread

I mean in a scientific study.

 

[Sherlock]

I mean in a scientific study.

Not that I'm aware of, but then I don't think that researchers necessarily zero in on the right things.

E.g. the increased expression of pain receptors found by Alan Light in CFS might be a protective measure, not just an unfortunate anomaly.

 

[Mij]

@GracieJ yes, I see that they've changed the diagnostic criteria for FM and it's now considered neurological. I was not aware of this.

 

[Hip]

But can anybody speculate on how intracellular non-lytic viral RNA would result in easier muscle tearing?

I am not aware of muscle tearing being present in ME/CFS, or being the cause of the myalgia of myalgic encephalomyelitis. I suspect the muscle pain in ME/CFS might conceivably be connected to virally-induced muscle inflammation. Or might conceivably be connected to electrolyte abnormalities.

If you have a spasm in a muscle, that may be caused by muscle inflammation, which is why anti-inflammatories such as aspirin or ibuprofen can help with muscle spasms and the pain they can cause. (Note: a muscle spasm is an involuntary contraction of a muscle; and a muscle cramp is spasm which causes pain). Muscle spasm may also be caused by electrolyte abnormalities.

Myositis (muscle inflammation) and myalgia (muscle pain) appear to arise in a wide range of infections, judging by this article on myositis: Infectious Myositis Clinical Presentation.

If you have a chronic intracellular infection in your muscles from non-cytolytic enteroviral RNA, this can lead to chronic muscle inflammation.

Indeed, chronic coxsackievirus B myocarditis involves precisely that: the chronic intracellular infection of the heart muscle by non-cytolytic enteroviral RNA leads to chronic inflammation of this heart muscle. Chronic coxsackievirus B myocarditis has been proposed as a good disease to study if you want to better understand the chronic non-cytolytic enterovirus infections found in ME/CFS patients.




I don't generally get myalgia much as a symptom of my ME/CFS, except in the lower back muscles, where sometimes I can get excruciating pains so sharp that I can sometimes fall to the ground in agony. But I don't get these lower back muscle pains all the time, just for short periods of a week or two, then remission for many months. These lower back muscle pains/spasms are much improved once I take ibuprofen.

Interestingly, many of my friends and family who caught exactly the same enterovirus as me (the enterovirus that triggered my ME/CFS), also started to suffer from these occasional lower back muscle cramps and stabbing lower back pains. This perhaps hints that even in non-ME/CFS patients, enteroviruses can infect muscles and cause spasm and pain.

 

[Vic]

I had always thought that my start was from an ordinary virus, but because of enormous stress the virus had somehow gotten in really deep, so to speak. I didn't know what that meant mechanistically, but this idea sure seems to fit.

But can anybody speculate on how intracellular non-lytic viral RNA would result in easier muscle tearing? How would contractile proteins in myofibrils be easier to break? If the structure is defective, the muscle should presumably be weaker, too, since it wouldn't be doing its proper job -- unless there is only a small number of weak links. Do people find that a muscle prone to tearing is also weaker?

Most muscle pain and and tears are actually caused by dysfunction elsewhere. Like almost all idiopathic knee pain is caused by tight hips and/or ankle muscles (calves), which have reduced flexibility/ROM, so the knee has to make up for more of its normal share, causing pain.

So if it is the case that these enteroviruses are causing damage, I think the body's response would then be to build scar tissue, maybe even biofilm-fibrosis like mesh, and then restrict the muscle fibers wherever those are formed. Then that tightness and reduced ROM causes excessive strain on other muscles that have to pick up the slack. For me, my tears definitely were far removed from the tighter areas of my body.

What I think is an even more interesting idea, though, is that fibrosis actually "invites" viruses and bacteria to the sites. As the muscle fibers collapse and cellular chaos ensues it's probably a very opportune time for infections to take advantage of moments of weakness. What might be even MORE interesting is they might even be somewhat symbiotic relationships, infections actually helping to stabilize tissue during intense periods of out of control stress/muscle collapse. This isn't based on studies, just some experiences I've had.

 

[Woolie]

As for anti-inflammatories, I think that could have merit (as well as anti-oxidants) but would be less important than using anti-acid such as bicarb. However, @Woolie recently reported "I do still seem able to get PEM" despite a medium dose of prednisone, which would be much more powerful than herbs or NSAIDS. http://forums.phoenixrising.me/inde...ed-should-i-continue.35521/page-2#post-559020

Yes, @Sherlock, but it probably all depends on how much inflammation you have and how much pred you're taking. I'm thinking some of us here might have massive inflammation/immune activity (whatever you want to call it). After some breakthrough symptoms after light exercise last week, my doc upped my pred dose to 40mg, and now they're gone (but 40mg is a big does and its gonna be huge tapering off in the next few days).

 

[Woolie]

This is maybe a bit of the track, but relates to something @Hip said above. I was reading about Lupus the other day, and apparently these patients have high antibody titres to common herpes viruses like EBV. But this is never considered a cause of the lupus, but rather an effect.

http://www.direct-ms.org/pdf/MolecularMimicryOther/Lupis EBV Mole Mimic 06.pdf

I wonder if this is the same for us? Perhaps the high markers for pathogens are symptoms of the illness not the cause?

 

[GracieJ]

@Sherlock I am intrigued by what you have described.

One of my clients was telling me about her husband's misfortune. All he did was turn over in bed one night - and his rotator cuff tore, requiring surgery. I do not know his full medical profile. They were religiously telling everyone they met to be careful - odd things can happen.

 

[SOC]

Myalgia was one of the first symptoms I recognized. I no longer have myalgia when I am managing my condition well, but it is one of the first things to show up when I PEM. I get muscle pain, and substantial stiffness. I move like a 90 yo during a PEM episode.

 

[wastwater]

I've never had any muscle pain at all

 

[Gingergrrl]

All he did was turn over in bed one night - and his rotator cuff tore, requiring surgery. I do not know his full medical profile. They were religiously telling everyone they met to be careful - odd things can happen.

@GracieJ If all he did was turn over in bed and his rotator cuff tore, there is a good chance that he had taken a fluoroquinolone antibiotic in the last year (such as Levaquin, Avelox or Cipro) which have FDA black box warnings for spontaneous tendon rupture. Many people never make the connection when this happens to them.

 

[lansbergen]

Myalgia was one of the first symptoms I recognized. I no longer have myalgia when I am managing my condition well, but it is one of the first things to show up when I PEM. I get muscle pain, and substantial stiffness. I move like a 90 yo during a PEM episode.

There is a typical ME gait even laymen can see.

 

[MeSci]

BTW, I have found that two things relieve my muscle tension/cramps/spasms and occasional tremor - sedating (anticholinergic) antihistamines and cannabis. They also relieve nausea, and the cannabis relieves weakness. The fact that anticholinergic drugs relieve these symptoms is one reason that I suspect inhibition of acetylcholinesterase, but I also strongly suspect electrolyte deficiency because these and other PEM symptoms occur after solute/osmotic polyuria.

 

[MeSci]

There is a typical ME gait even laymen can see.

I call mine the 'ME trudge'. I can hardly lift my feet and am dragging them along. That was one of the things I recognised in an Open University video of a woman with ME - she walked like I did.

EDIT - but that is due to weakness rather than stiffness.

 

[Sidereal]

This is maybe a bit of the track, but relates to something @Hip said above. I was reading about Lupus the other day, and apparently these patients have high antibody titres to common herpes viruses like EBV. But this is never considered a cause of the lupus, but rather an effect.

http://www.direct-ms.org/pdf/MolecularMimicryOther/Lupis EBV Mole Mimic 06.pdf

I wonder if this is the same for us? Perhaps the high markers for pathogens are symptoms of the illness not the cause?

I came across a study recently (don't have a link handy) done before widespread knowledge/acceptance of H. pylori that investigated acyclovir as a treatment for stomach ulcers because they found reactivation of herpes simplex in those patients. I have seen several papers talking about increased prevalence of shingles and other herpes viruses in lupus, not just EBV. I bet lots of chronic illnesses have these reactivations it's just that no one focuses on them because there are other more salient findings on blood tests whereas some ME/CFS clinicians and researchers have been hyper-focused on herpes virus titres due to absence of other obvious measurable abnormalities in the blood.

I personally think herpes viruses do not play a causal role in ME/CFS; they can trigger the illness but I view our inability to keep them in check as a consequence of whatever is causing our energy metabolism breakdown and immune dysregulation. That's not to say antivirals can't help. If I didn't take acyclovir, I'd be in big trouble.

 

[MeSci]

This is maybe a bit of the track, but relates to something @Hip said above. I was reading about Lupus the other day, and apparently these patients have high antibody titres to common herpes viruses like EBV. But this is never considered a cause of the lupus, but rather an effect.

http://www.direct-ms.org/pdf/MolecularMimicryOther/Lupis EBV Mole Mimic 06.pdf

I wonder if this is the same for us? Perhaps the high markers for pathogens are symptoms of the illness not the cause?

I wonder what @Jonathan Edwards thinks of this. He is sceptical about molecular mimicry.

 

[lansbergen]

I call mine the 'ME trudge'. I can hardly lift my feet and am dragging them along. That was one of the things I recognised in an Open University video of a woman with ME - she walked like I did. .

I describe it as shambling with feet more apart than normal.

 

[Jonathan Edwards]

This is maybe a bit of the track, but relates to something @Hip said above. I was reading about Lupus the other day, and apparently these patients have high antibody titres to common herpes viruses like EBV. But this is never considered a cause of the lupus, but rather an effect.

http://www.direct-ms.org/pdf/MolecularMimicryOther/Lupis EBV Mole Mimic 06.pdf

I wonder if this is the same for us? Perhaps the high markers for pathogens are symptoms of the illness not the cause?

I wonder what @Jonathan Edwards thinks of this. He is sceptical about molecular mimicry.

Yes, I think molecular mimicry is both unsubstantiated and pretty nonsensical if you look at the mechanisms properly. It is just an idea from the 1960s that everybody has come to believe like the Bible despite there being no miracles yet!
The paper Woolie quotes seems to me to be very naive and simpleminded.

In fact lupus patients have antibodies to everything - because they have lost the ability to select B cells. They have antibodies to lots of self antigens, and infections and drugs they have never met. And because there is no fine tuning the antibodies to infections tend not to work very well in getting rid of the infection so lupus patients get lots of infections.

It could be that antibodies to viruses in ME are results of the ME process rather than the cause. But I am not sure we have evidence for increased antibodies in ME patients. My memory is that Carmen Scheibenbogen, who is probably the key authority on EBV responses in ME, actually found reduced antibody responses as a whole. I think we need hard epidemiological data on this. I don;t think results from isolated commercial labs are any good.