JohnBoy2000
Bluelighter
- Joined
- May 11, 2016
- Messages
- 2,463
Traditionally, it's been one of the three monoamines.
I feel fortunate in that, although I had no response to serotonin - noradrenergic based agents did and do provide relief and remission of symptoms for me.
That being said, it's still very hit and miss and, I would say I've achieved at most 50% remission thus far.
With the modification and augmentation of medication moving forward, I'm hoping to improve that figure but, it also makes me question - is there the possibility that more than one NT could be implicated?
Given limited responsiveness to DA agents, Ritalin, pramipexole - I'm thinking it's not histamine.
Olanzapine would rule out cholinergic NTs.
The one that's on my mind is, GABA.
Implicated by pregabablin and gabapentine.
So - insomnia, fatigue and concentration - the most difficult symptoms to get to go into remission, are the most bothersome.
Now - GABA inhibites DA and NE, right?
I don't know how the aformentioned work but - I know they induce sleep.
Would that suggest they agonize GABA and thus act to promote the inhibition of DA/NE??
If that were the case - it would be counterproductive for my symptoms - but like I said - do those agents act to agonize or block inhibitory GABA??
Oddly - with Bupropion - my sleep was the best it's been, oddly because many people complain that it disturbs their sleep - but that failed to be long term effective unfortunately.
But that occurance would suggest that, with the correction of either noradrenaline imbalances, or NA receptor sensitivity, sleep issues effectively began to go into remission - which would reinforce the idea that perhaps it is solely NE being the implicated receptor in my condition?
In any case - for completeness - I guess the other receptors that would potentially be addressed are - GABA, and NMDA - though the latter might require some innovative thinking.
Any insights?
PS - the other factor to consider is, with too high a dose of desipramine - it actually began to induce fatigue.
I cut the dose to 2/3'rds and, whilst there was an energy improvement, it did also incite the return of some symptoms of irritable bowel syndrome, which had been completely alleviated at high dose desipramine.
My next step in any case, is to attempt to replace mirtazapine, with its analogue, mianserin - to exclude any 5HT effects - and potentiate the NA effects.
I feel fortunate in that, although I had no response to serotonin - noradrenergic based agents did and do provide relief and remission of symptoms for me.
That being said, it's still very hit and miss and, I would say I've achieved at most 50% remission thus far.
With the modification and augmentation of medication moving forward, I'm hoping to improve that figure but, it also makes me question - is there the possibility that more than one NT could be implicated?
Given limited responsiveness to DA agents, Ritalin, pramipexole - I'm thinking it's not histamine.
Olanzapine would rule out cholinergic NTs.
The one that's on my mind is, GABA.
Implicated by pregabablin and gabapentine.
So - insomnia, fatigue and concentration - the most difficult symptoms to get to go into remission, are the most bothersome.
Now - GABA inhibites DA and NE, right?
I don't know how the aformentioned work but - I know they induce sleep.
Would that suggest they agonize GABA and thus act to promote the inhibition of DA/NE??
If that were the case - it would be counterproductive for my symptoms - but like I said - do those agents act to agonize or block inhibitory GABA??
Oddly - with Bupropion - my sleep was the best it's been, oddly because many people complain that it disturbs their sleep - but that failed to be long term effective unfortunately.
But that occurance would suggest that, with the correction of either noradrenaline imbalances, or NA receptor sensitivity, sleep issues effectively began to go into remission - which would reinforce the idea that perhaps it is solely NE being the implicated receptor in my condition?
In any case - for completeness - I guess the other receptors that would potentially be addressed are - GABA, and NMDA - though the latter might require some innovative thinking.
Any insights?
PS - the other factor to consider is, with too high a dose of desipramine - it actually began to induce fatigue.
I cut the dose to 2/3'rds and, whilst there was an energy improvement, it did also incite the return of some symptoms of irritable bowel syndrome, which had been completely alleviated at high dose desipramine.
My next step in any case, is to attempt to replace mirtazapine, with its analogue, mianserin - to exclude any 5HT effects - and potentiate the NA effects.
