I have seen some discussions here and there around the puzzling fact of muscle pain being a consequence of neural exhaustion, whatever that actually means in pathophysiology, but not within a formal thread. It's not quite clear how much distinction there is between PEM and PENE. Maybe they are the same, just brought about by different mechanisms. For the purpose of this discussion I differentiate between effort (physically doing too much) for PEM and stimuli (here being noise) for PENE. Maybe they all mean the same, but it's the difference between doing something leading to a crash and being subjected to stimuli leading to a crash. I am coming down one such episode, a complete neural exhaustion brought about by excessive noise. It was a relatively typical crash, although when noise is the cause I always find a more pronounced increased noise sensitivity then when it comes from physical effort. But it's distinct in the fact that I did not personally make particular physical effort at all, which is the usual cause of a PEM crash for me. And in that relapse, I had high muscle pain, particularly in the legs, thighs and calves mostly, as well as the damn hanger coat pain and at the base of the skull. It's remarkable that in recovering from that crash (to my previous baseline, not an improvement) the muscle pain has come down pretty much along with noise sensitivity. The muscle pain was relieved a bit by massaging several times a day. Not great but it definitely helped a bit. Muscle pain and noise sensitivity are both still present, but their intensity followed remarkably well. And this is quite a puzzle. How can something like neural exhaustion (again a hard concept to define but one most here would be familiar with) lead to muscle pain? I had many of the usual increase in other symptoms as well, especially difficulty with movement. I was basically moving like a sloth, very calculated, strained, in order to do the most basic things. As if I was a rusted out metal machine. I also had high neck, spine, head and facial pain, especially the trigeminal nerve and base of the skull. Pain that is hard to relieve with normal painkillers. It all came down along with. Still there, just back to their usual self 2-4/10 instead of being a 7-8/10 on the pain scale during the relapse. I don't know how we can make something useful out of it but this is clearly a thing that isn't subject to much research and frankly only we can make some sense of it. I just don't know how but discussion is always a good start.