Posted by JohnX2 on October 28, 2001, at 1:15:56
In reply to Re: Post Traumatic Stress Disorder and etc., posted by JGalt on October 27, 2001, at 21:59:18
> I looked up the DSM-IV for PSTD, clearly is not me. I cannot think of a single event that was extremely traumatic at a young age. I had tons of mild to moderate things, but nothing in particular burned into my memory. No flashbacks or nightmares from my childhood that I remember either. I never have had good long term memory. The DSM-IV stated in such a case the cause was likely simple depression. Still might be worth it to look at the crf antagonists just for curiousity's sake.
>
> The second you said jaw and headache problems, dopamine overload popped in my mind. Here's why. GHB greatly slows down (or perhaps stops) the release of dopamine in the brain. However, dopamine continues to be produced in the brain. After the GHB is metabolized, dopamine release resumes, but guess what, you got more dopamine there. No problem, just a pleasant stimulant effect. But never come all the way down from GHB and the dopamine keeps on building up and up to whatever limit there is. I know this because I've done it, twice. Logically what happens is then all that dopamine is released, you have less hunger, and more noticeably, painful headaches and jaw clamping. Too much dopamine. I'm guessing what is happening with you is you're having too much dopamine, then you take an AD such as wellbutrin, dopamine is released to the point that you have practically none left and you are left with the hypodopaminergic state. This would tend to suggest that you have 1. low dopamine storage capacity or 2. are very sensitive to dopamine agonists. Before you used the wellbutrin, the dopamine kept building up and up. Extreme excess of dopamine is hallmark of schizophrenia and mania. The interim period when taking the AD's that you feel relief is when dopamine is at a reasonable level of storage and being released at the same time, as happens in the theoretical normal person. Make sense or did I miss something? You know, now that I write this it occurs to me, why wasn't ghb ever used to treat bipolar syndrom? Since it prevents dopamine from being released, that gets rid of the mania as far as I understand it, and since during mania I don't believe your body stores more dopamine, it simply releases more. Just come down from it every 6 hours and all would be well, then use AD's while in the depressive state.
>Damn you are smart. It took me a long time to figure
this out. I found most of my interesting information
from an article called "buspirone as an antidote
to SSRI induced bruxism". Here it discussed 2 states
which could cause jaw tension, one is hypo-dompaminergic
and the other is hyper-dopaminergic. Since the
pain is gone with the depression and positive
(and or manic) responses, I have to be lead to
believe that the pain is caused by a hypodopaminergic
state. This also correlates so very well with my
thoughts on the concurrent severe emotional numbing,
and my responses to Serzone,Zyprexa,Adderall,Zoloft,
Wellbutrin. The article was specifically dealing
with SSRI induced bruxism and stated cases of Zoloft
causing this. I had this problem with zoloft quite
severly and zoloft seriously obliterated my emotions
to. I think its pinging of the 5ht-2a receptor causes
the problem. The drug buspar is a 5ht-1a partial
agonist and a slight d2 antagonist. The paper
cited cases where buspar cured the zoloft induced
bruxism and theorized that buspar reduced serotonin
levels, and the 5ht-1a agonism does the opposite
of 5ht-2a agonism (they somehow balance each other).
So anti-anxiety meds often try to antagonize
5ht-2a and or agonize 5ht-1a receptors. Most
SSRIS taken chronically will downregulate the
5ht-2a receptors. But they aren't always all that
efficient and this leads to sexual side effects,
emotinal numbing, muscle tension. The pharmaceutical
companies figured this out and scrambled to find
meds that could antagonize the 5ht-2a receptor.
The 1st new-age anti-depressant that did this
was Serzone and it was touted for its lack of
sexual side effects. But it is a dirty med and
screws with too many other receptors making people
like me crash my car. Anyways, the buspar paper
suggested serzone as another alternative to the
bruxism and it did work for me. But now I'm leaning
towards not beating around the bush and testing
one of these nmda antagonists (memantine). Since
Lamictal is working and zyprexa, it seems like
a logical choice. Sorry for the harangue. But
you come back with great insight. If AndrewB
was still posting to this group he would be having
a field day with you!.Ps. there is a cpc viewer for mac. I get patents
downloaded from a service called www.getthepatent.com.
the images are avaliable at the official us patent
site, put this service has a mirror copy of the full
patent images in this very compressed formats. The
web site has links to the CPC viewer.-john
poster:JohnX2
thread:81980
URL: http://www.dr-bob.org/babble/20011025/msgs/82472.html