Posted by franco neuro on April 9, 2005, at 11:35:19
In reply to Re: Read this before answering my previous post » franco neuro, posted by KaraS on April 9, 2005, at 0:13:37
> Sorry to hear that the Wellbutrin is still tiring you out. How long do you plan to trial it? (I wonder if rEEG could have predicted that response. I'm so sick of trying things that don't work out as I'm sure you are too.)
Thanks. Actually, I didn't take it this morning. I wanted to give it another week or so but it was too fatiquing. Not sure if the fEEG or Brain Mapping would predict something like that.
>Yes, I have been taking thryoid medication for a few years now. How about you?
I had been taking Braverman's "Pathroid", which is his T3/T4 formula, for about a month but I stopped the last few days on Wellbutrin. Will start again tomorrow morning.
> I didn't know that either. So you think that amisulpride is probably not any worse in this respect than any other antipsychotic?
I think it may be somewhat better. But that's only my humble opinion.
> Nope. I was thinking of hydergine. I just knew it was a "smart drug" so I associated it with Ach. (but thanks for trying to save me :-))
Sure you weren't thinking of arganine? :-)
> This may seem like a dumb question, but if you suppress glutamate do you run the risk of increasing anxiety (because glutamate eventually becomes GABA)?
I don't know. But according to Dr. Braverman's Brain Mapping I'm high in GABA. (Which should also suggest I'm high in glutamate.) You would think being high in GABA would suppress anxiety but it hasn't. It may be because a hyperglutamatergic state trumps GABA's calming effects by it's overstimulation of the NMDA receptor. Too much glutamate initially may cause too much dopamine release in stressfull situations which converts too quickly to NE than epinephrine. This is what over time causes the DA deficit. Glutamate actually does cause DA secretion, but I think it's being chronically elevated is what overstimulates the DA auoreceptors ultimately causing a decrease in dopamine release.
> Also, if you keep glutamate from stimulating dopamine autoreceptors, does that then lead to downregulation or a decrease in the number of those DA autoreceptors?
I think Dr. Goldstein is implying that without glutamate overstimulating the autoreceptors, the synapse will return to a more normal state of affairs. I.e. you would be able to secrete a "proper" amount of DA without the overexcited autoreceptor prematurely shutting down it's release from the presynaptic neuron.
> Guaifenesin is the stuff in cough syrups that is supposed to loosen mucous, right? You can get that in pills? Is it over the counter? I'm very curious as to how that will work for you. Have you thought about acamprosate at all?
Yep. It's been used by that Dr. St. Amand for a while but he didn't know how it worked. Dr. Goldstein explains that it antagonizes the NMDA glycine receptor which is why it's helping some CFS FMS patients. It is over the counter. I bought it last year online after reading St. Amands book. I bought it but never bought his theory so I didn't take it. I will try it now.
> Have you thought about acamprosate at all?
No. But it's funny you mentioned it. My friend on the Lamictal is looking for the final ten or twenty percent improvement. So Dr. Braverman suggested Campral.
"Campral (acamprosate) has in vitro affinity for GABA type A and GABA type B receptors, so it's been assumed that the therapeutic effects of acamprosate are due to actions on GABA receptors. However, acamprosate does not share most of the other effects of GABA receptor modifying drugs, such as antianxiety, hypnotic, or muscle relaxant activity. It is therefore possible, perhaps likely, that the effects are mediated some other way. Acamprosate is structurally related to l-glutamic acid (l-gutamate), which is an excitatory neurotransmitter. It's been proposed that acamprosate decreases the effects of the naturally-occurring excitatory neurotransmitter glutamate in the body. Since chronic alcohol consumption disrupts this system, and the changes last many months after alcohol ingestion is stopped, it's possible that acamprosate somehow restores the glutamate system towards normal. It's thought, no matter how it acts, that Campral decreases the pleasant "high" associated with alcohol consumption, and thus decrease the frequency of relapse during abstinence."
Sounds like an interesting med. I don't get that nice relaxed feeling after a couple of beers that I used to get. I just feel irritated. However, on the rare occasion when I have 7 or 8 drinks. Like my cousin's wedding a few months ago. I notice that while I have a hard time sleeping and wake up a little woozey, my body also feels better the next day and I'm very horny! I'm still trying to figure out what this means. The alcohol is obviously relieving something in my brain. I found some absracts that say at higher amounts alocohol is indeed a glutamate/NMDA antagonist. And the withdrawal effects that alcoholics have may be due to the increased glutamate/NMDA activity when the alcohol is stopped. Interesting huh?
> Yikes! 400 mg. is a lot of Lamictal, isn't it?
Not really. It is the top of the range, but if you tolerate it well enough at that dose you can cautiously go higher. Even to 600mg or more. My fiend and Dr. Braverman are considering this right now.
> Have you been diagnosed as bipolar? My doctor thinks I might have a soft bipoloar condition because I haven't responded fully to antidepressants and I have periods of more anxiety/agitation.
I was wondering about this, but was almost certain I'm not bipolar. As a matter of fact I wish I were. I haven't had anything approaching hypomania in 20 years. Dr. Barverman gives Millon psychological tests as part of his initial battery of tests. It measures all kinds of psychological problems. I scored over 100 on anxiety and dysthymia (my 2 highest scores) and 0, i repeat, 0, for bipolar. Also zero or near zero for two other bipolar markers. I also came up high for somataform disorder (reflecting physical issues) and compulsiveness. Basically, I think it was spot on. If you do turn up being somewhat bipolar it's all the more reason to try Lamictal.
> Wow. That's quite a cocktail. Has he been on Mirapex for long or is this a new addition? It seems like all of the people on this board who have tried it, developed a great deal of fatigue on it after a while (though not initially).
I need to get more info. as to what order he added them, but I'm pretty sure he took the entire cocktail for about 2 years before he started tapering. He actually gave me his phone number and said I could call him to discuss it if I wanted. As far as I know he's not selling anything and seems quite sincere. I think he's so happy he got well that he wants to help out if he can. I will call him at some point soon, but I don't want to start hounding him and scare him away. :-)
It's hard to get moving. Believe me I've spent so much money on this wild goose chase I don't even want to think about it. I'm not even woking right now. The company that I worked for for 10 years was bought by a competitor and put out of business last year. I'm living off of my savings. I really need to start working again but I'm worried that if I end up trapped in a stressful situation again it'll surely kill me. I'm so stress averse right now. I think that definitely reflect a state of low chatecholamines. I'm not sure if Dr. Goldstein's theory is my problem, but his description of the typical neurosomatic patient fits me perfectly. The genetic predisposition, the childhood stress, the broken right arm at 6 and 14 causing chronic pain (irritating the brain), etc. And how neurosomatic patients are almost incapable of becoming addicted to drugs. Which was backed up on my Millon test. How the SSRI's haven't helped.
But the fact that I did have a couple of almost "normal" days after stopping the Zoloft proved to me that I can feel good agian. And that it is all related to brain chemistry. I'm sure I'll never feel 20 again, but I'll take a healthy 39. We really have no choice but to keep on trying.