The symptom signaling theory of ME/CFS involving neurons and their synapses

leokitten said:
Many of us would disagree somewhat with this belief, because for us the first couple years or so of ME it felt very, very strongly immune system driven, like our immune system was stuck in some strange chronic activation. Many of my lymph nodes were constantly swollen and hard as a rock and I had many other what felt like immune system dysfunction symptoms. All the neurological symptoms really felt like a direct downstream consequence of this immune system activation.

Now yes as the years have gone by the immune activation symptoms have gradually subsided and the neurological symptoms have stayed or gotten worse and now it feels mostly neurological, but I cant help think that the immune system craziness of the first few years still have something really important to do with it
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Understood - and I certainly did not mean to argue against your own experience or to suggest that my experience in any way carries more weight than your own when it comes to figuring any of this out. This is, of course, one of the many frustrating things about even beginning to trace the origins of whatever has ruined us: our experiences are all so very different, sometimes profoundly so. I regularly read of experiences here and elsewhere that leave me questioning whether I could actually have the same condition at all.
 
jnmaciuch said:
Interestingly I didn’t even register it for the first few years of my illness (just bled into the background of general aches and pains)
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jnmaciuch said:
I’ve commented on this elsewhere but one specific symptom which leads me to think something must be occurring in the muscle as well as brain is muscle stiffness—much worse after activity but nearly constantly present to some degree.
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Nor did I. In fact I initially put it down to drastically reducing my usual exercise routine. I thought perhaps that's what happens when you go from exercise 6 days a week to viritually nothing. The stiffness was there but it was the least of my problems so I easily overlooked it.

It wasn't until I started taking TUDCA (off the back of Hwang's study showing ER stress in 2023) that my lactic acid reduced (I measured this with a lactate acid monitor) and my general muscle fatigue and muscle strength reduced drastically. I went from not being able to open a bottle of water to popping them open willingly. I've been taking it for a year and a half now and although it's made a discernible difference with grip strength and muscle endurance unfortunately it hasn't touched the general fatigue.
 
ME/CFS Science Blog said:
ME/CFS patients don’t fall during CPET because their muscles stop working or they don’t quit because they can’t breathe enough.
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I can tell you haven't done a true maximal CPET because it is absolutely the muscles being unable to continue/the heart reaching its limits that causes cessation of CPETs. Treadmill CPETs are not conducted with ME/CFS patients due to the risk of falling. I literally had my vision black out when I knew I had reached a true VO2Max, but some patients cannot get that far because their muscles just cannot do the work.

The main criticism of the hypothesis is that it is disconnected from all of the research we know about how fatigue is sensed and the effects on the brain. Central fatigue is not a mystery, it is not a mistake, it is a carefully tuned feedback system between muscle afferents, spinal efferents and feedback on the motor cortex. Central fatigue signalling mechanisms helps maintain endurance performance of animals. Fact is that peripheral sensitisation mechanisms DO follow the kinetics that matches PEM, whereas central mechanisms don't.

The brain cannot misperceive fatigue out of thin air, because peripheral and central systems are deeply intwined.
 
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