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Muscle injections with lidocaine improve resting fatigue and pain in patients with CFS

Londinium

Senior Member
Messages
178
Other than that, I'm in agreement with those above who are sceptical that the fatigue score is really statistically significant.

Having re-read the paper with less brain fog, I'm now thinking I was possibly a little uncharitable in my initial response. However, the relatively modest p-value plus the fact that the two groups appeared to have a fairly different fatigue baseline (if I'm reading the graphs right) means this paper should probably go in the 'interesting but replication strongly needed' category.
 

pattismith

Senior Member
Messages
3,940
For the limited value that anecdotal evidence has:

I've done this twice: once in my early 20s and once in my early thirties. Both times, it reduced my pain and allowed me to resume a schedule of running for fitness after it had become to painful/refractory to do so. In my case, the effect lasted for between 9 and 15 months.

The lidocaine has two effects as I understand it. The first, of course, is short-term pain relief. However, for the second, it seems to relax trigger points for an extended period of time in a very targeted way. Like most interventions, I think it has a temporary effect that will only be seen in some patients, but for those patients it's significant. I'd be interested to see the overlap between PWME who experience some relief from massage therapy and those who gain benefit from lidocaine injections.
Hello,

it's nice to read your testimonial, could you explain to us how the lidocaine injections were performed, was it intra muscle or subcutaneous? How many of them did you received in one time?
Did that treatment was useful against brain fog as well?
 

trishrhymes

Senior Member
Messages
2,158
Thanks, @sdmcvicar, I hadn't realised there could be a long term effect. I guess this might be relevant to people with fibromyalgia if the trigger points are injected and reduce the pain in those muscles. However, in ME, while it might usefully reduce pain, it would have no impact on mitochondrial or immune dysfunction, and therefore on ME symptoms apart from muscle pain.
 
Messages
58
My lidocaine injections were intramuscular, close to the trigger points, though the description of the location for the gluteus maximus injections in the paper puts the ones I received in the same vicinity. Look up trigger point injections for myofascial pain for additional info.
 

valentinelynx

Senior Member
Messages
1,310
Location
Tucson
Read through this fast, so apologies if this has been noted already...
IV lidocaine infusions are used to treat chronic pain, including fibromyalgia.
Did this study in any way control for the effect of giving a large dose of systemic lidocaine vs the local effect? It appears they are attributing the (small) benefit to the peripheral effects of the lidocaine, but it seems to me that any such benefit could have just as likely come from the systemic effect (perhaps on the CNS or even on the cardiovascular system).
 

deleder2k

Senior Member
Messages
1,129
I've received a lidocaine _infusion_ at the hospital. Was terrible. Numbness. Eventually ME symptoms got worse. Couldn't almost move. Luckily it got better after an hour. No reduction in pain. I suffer from joint pain and muscle pain. Lactic acid/cramps in legs
 

Valentijn

Senior Member
Messages
15,786
I've received a lidocaine _infusion_ at the hospital. Was terrible. Numbness. Eventually ME symptoms got worse. Couldn't almost move. Luckily it got better after an hour. No reduction in pain. I suffer from joint pain and muscle pain. Lactic acid/cramps in legs
It sounds like lidocaine does various nasty things to mitochondria.
 

deleder2k

Senior Member
Messages
1,129
I don't know anything about that. I was told that I could feel numbness and experience issues with talking, swallowing and so on. Not sure if it was my ME that got worse, or if it was ME+ side effects since some of the side effects are similar to ME symptoms.
 

deleder2k

Senior Member
Messages
1,129
Strange... I got a massive infusion. Didn't help a tad. I also know of others who has received it without benefit.
 

Kati

Patient in training
Messages
5,497
Strange... I got a massive infusion. Didn't help a tad. I also know of others who has received it without benefit.
I always wonder if this represents the placebo effect, for those who improved. I do not see this paper as a landmark paper, more like a quick fix that is not looking at the real pathology of this disease.
 

deleder2k

Senior Member
Messages
1,129
I think some may have less pain. In combination with placebo that may be enough for a statistical effect.
 

Valentijn

Senior Member
Messages
15,786
I think their theories are pretty much all ass-backwards:
The disorder may cause the body to amplify fatigue signals associated with physical activity, the researchers explained, which is why some patients become worn out just walking across a room.
CPET and heart rate monitors are a good indication that it's not just amplified signals. We can (and often do) push through the pain, but then crash. I've had a major leg muscle stop working entirely. And I consistently have elevated blood lactate levels many hours after mild exertion. All of that suggests to me that I'm not amplifying signals from normal levels of metabolities - my metabolities (and muscles) are the subject of some sort of malfunction.

The researchers noted the findings suggest that the muscles and other peripheral tissues are involved in chronic fatigue. They concluded that lidocaine injections helped block the abnormal signaling of muscle metabolites.
Or a numbing agent simply blocks local pain like it's supposed to?

"It's unlikely the central nervous system creates fatigue out of nothing," Staud said in a university news release. "It uses just very minute fatigue signals that it receives and inappropriately amplifies them, which results in significant impact on the quality of life of these individuals."
Or processing is normal, and there's actually something peripheral causing more pain. If it were central, the signals would be consistently amplified, not fluctuating.
 

RogerBlack

Senior Member
Messages
902
'oversensitisation to normal signals' as a mechanism is pretty obviously broken, if you count those without pain.

I have (for the last several years anyway) had ME/CFS with no global muscle pain other than perhaps a week.
During this time, I've had normal exercise response to overexercised muscled (delayed onset muscle soreness), and paid it as little attention as it deserves, nor has it been particularly painful.

However, also during this period, I've had multiple (>50) episodes of PEM, some triggered by watching too complex emotional TV, some by doing the washing up and some by trying to in-depth concentrate on something for several hours (when in bed). On the severest of these I get global overall pain. Even if it's a cognitive trigger.

Not that pain when it happens 'alone' isn't an important symptom. I had pain as a major symptom when I was first diagnosed.
 

snowathlete

Senior Member
Messages
5,374
Location
UK
I think their theories are pretty much all ass-backwards:

CPET and heart rate monitors are a good indication that it's not just amplified signals. We can (and often do) push through the pain, but then crash. I've had a major leg muscle stop working entirely. And I consistently have elevated blood lactate levels many hours after mild exertion. All of that suggests to me that I'm not amplifying signals from normal levels of metabolities - my metabolities (and muscles) are the subject of some sort of malfunction.


Or a numbing agent simply blocks local pain like it's supposed to?


Or processing is normal, and there's actually something peripheral causing more pain. If it were central, the signals would be consistently amplified, not fluctuating.

Glad it's not just me Val. I haven't read the study - maybe it would change my mind - but from reading the press release quotes from the study authors the idea that it is due to the signals being amplified seems unlikely to me, it annoys me when I read unreasonable conclusions not backed up by the findings, and especially when it is unnecessarily complex and more obvious explanations are rejected/or not talked about. The author's conclusions are just not in keeping with my experience and knowledge of the disease. I can't see any reason to reach this conclusion from the study. Perhaps the authors reached this conclusion because of their possible route to where they are now:
The idea that ME pain is all in the head has been around for ages. It's also an idea put forward for lots of other pain conditions that science has yet to figure out. It looks like these researchers do not believe that idea in ME (a good thing). And so they appear to have set out to test if it is peripheral pain or in the mind and the study idea does that quite well, I think. But having done that they then reach a conclusion that seems closer to the original idea they try to disprove than more likely explanations.

My conclusion would be that the pain is real and correct; there is something causing that pain locally, not that the pain receptors or whatever are amplifying normal signals.

ME causes lots of problems all over the body, immunological etc. And as you point out Val, CPET, heart rate, etc. Lots of things actually. It's not just a pain condition. Some patients don't even get pain but still clearly have ME. The conclusion that normal signals are amplified doesn't explain all the other stuff going on, it doesn't really fit.
 

Valentijn

Senior Member
Messages
15,786
I can't see any reason to reach this conclusion from the study.
I think they're making a typical BPS mistake, and reducing a complicated multi-system disease to a single symptom, albeit pain in this case instead of fatigue. So they attempt to explain the pain of ME in a vacuum where the rest of ME doesn't exist - perhaps it's too complicated for them otherwise.
 

Cinders66

Senior Member
Messages
494
I'm glad there is some experimental treatment research going on.
I'm not qualified to judge in the science or statistics but it does tie in with some research I saw whereby sensations of fatigue after arm muscles were used were substantially reduced in ME subjects by wearing a cuff to block muscle metabolites travelling versus exercise without a cuff. and which I dont think made any difference in healthy people Obviously cuffs aren't practical or useable continually so something blocking the effect of metabolites might theoretically have some impact on some types of ME fatigue?
We need trials of basics like LDN, B12 and IV saline in the severely affected community, astonishing they haven't bern tried, but I'm pleased that aside from the Norwegians there are other people in the world working from a let's see if we can find anything to help Angle.