I think more generel now, it´s a breakdown of synaptical conjunctions of these structures which typically invovle dopamine (though not restricted to dopamine), i.e. basal ganglia and thalamus. I don´t know if this could be made visible say by PET.
Moreover I think this breakdown consists of a hypothetical silencing of some cells (say like in hibernating) or synaptical directions, and the back-foreward direction does not take place. If this inlolved a lesser amount of nerve actions, it could well made visible by PET, but if the same amount of actions took place, probably not.
I still think that this breakdown would say that the being would be in an wound healing process or something like this, and this would cause downstream actions.
Of difficulty should be, that such breakdown might cause some changes on the immunesystem which in turn would induce this breakdown, somehow a somersault for nothing.
Possible might be the breakdown only in humans, because a) the brain is bigger (than in our close relatives, and has not completly adapt to these new mightyness) - and here if I remember rightly, woman´s basal ganglia are bigger than those of men; b) humans are sweating with a concomittant loss of amino acids and with an altering of their homeostasis - and here women do sweat more.
Concrete, the cells would have switched into a silence, rejecting uptake of normal needed stuff (some vitamins), therefore this stuff would be needed to refeed more pronounced concomittantly to:
There are a lot of different metals in the brain which their tasks probably not are already known, however, they would needed to get reconfigurated, because actions should take pace where the metals are.
I also think that the structurers basal ganglia and thalamus allow for the relative wide range of symptoms, which ask for explanations.
CAUSES of a breakdown.
Here I think that an alteration of an initial pathway would have taken place. I prefer a double hit hypothesis, two impacts would have altered one first pathway with a following breakdown of that structres. Viruses, chemicals, maybe even by sudden calcium influx by whatever.
In my case the pathway is the inducible nitric oxide synthases: manganese + arginine = nitric oxide, with changes on all nerves, and especially pronounced in that structures (t-type-ca-channel, many NMDR´s).
I still would like to think that manganese is one good possibility for a dysregulation, because it´s comparable low but used for few tasks all of which seem to be able to be related to a wound healing or more generel to any defense of the body.
This would especially easily go along with the interpretation that our disease is an exaggerated sickness behaviour.
It´s needed to make plausible how a sickness behaviour is possible, and I think it would be easily possible to relate it, in high organsims, to basal ganglia and thalamus which have a lot of NMDR and t-type-ca-channels:
I think a sickness feeling can be made undestandable and deductionable by an initial learning mechanism. Such a mechanism could be compared to a movie where pictures come and go.
Now, when too much have come and wouldn´t go anymore, the being would feel exhausted (and enough is leaerned for today), thereafter a tiredness would take place, the pictures which are too much would go. Now, if the being is acute ill, being tired is a bad idea, instead it needs to be aware, but without wanting to concentrate in interesting things, being aware not to get eaten.
Additionally, too much "pictures" without building up any senseful movie could be interpreted as pain or at least as feeling bad. It also would allow to referre on first physical entities like waves, which can match up harmonically, but could also work against each other (pain). Furthermore, it is thinkable that such a chaos is "willingly" transmitted into an smaller amount of actions, saving some energy (say in higher organisms).
[Finally, the involvement of the learning mechanism would easily explain delayed PEM, because the brain needs to compare up all its experiences again and again, probably best in different time frames. Interestingly, delayed PEM would also imply that the proposed silencing and its concomittant distribution of metals and vitamins is virulent under "somersault for nothing" circumstances, which matches up with experiences that a sudden but usually not lasting good influence (say on the immunesystem) can give all relief. (And the question is how to downregulate the somersault for nothing effectively.)]
For this in first order (in my case):
1) looking at the first pathway if existing, I know that lower manganese diet helps.
2) reconfigurating (some) metals
3) intake of some vitamines, which must not contradict 1), of course
4) patience and trying to do espcially 2) and 3) adroitly, being careful with 1)
finally) not overdoing, because - after this approach - the involved learning mechanism would lead to more chaos again, and the metals might get wrongly placed once again.
I hope it will hold the water (at least in my case).