Posted by cache-monkey on April 9, 2007, at 15:13:14
In reply to Re: Fellow pharm-geeks: a question about terminology » cache-monkey, posted by Larry Hoover on April 8, 2007, at 10:35:39
Thanks Larry and Saturn for the replies.
Maybe what I'm interested in will be more clear if I give the context. What I'm really wondering about has to do with the dopamine D-2 receptorsYears ago I added Celexa on to Wellbutrin and experienced intense, but transient anxiety which might have been akathisia in retrospect. After I d/c'ed both, I gradually slid into this highly anxious state, both physically and psychically. This worsened when I attempted to quit smoking (previous attempts had only led to anxiety/OCD).
Subsequent treatment with Serzone worsened my anxiety and the addition of BuSpar led to full on chronic akathisia. This relented somewhat when I got off the BuSpar, but now any trial of an anti-psychotic at a low or moderate dose leads to acute akathisia within a week.
The common link seem to be the D-2 receptor. I recently discovered that Celexa (and also SSRIs) increases the expression of the D-2 receptor (http://tinyurl.com/2bs2ub). Further, BuSpar and neuroleptics block it, which can lead to actue and chronic akathisia when a certain percentage of receptors are blocked (e.g. http://tinyurl.com/2v2o7z).
The trouble is, I'm not sure what to make of this. Besides the null that the D-2 system is totally uninvolved, there are two hypothesis that I have:
A) My receptors are down-regulated
* This would be consistent with the acute akathisia from low concentrations of D-2 blockers. I.e. a large percentage of receptors get blocked because there are relatively few of them
* It would also be consistent with my medium term (after start-up, before discontinuation) success with Celexa: I felt better once the D-2 receptors began to proliferateB) My receptors are up-regulated
* This tends to be the effect of mid- to long-term treatment with D-2 blockers
* This is possibly consistent with ongoing akathisia-like issues -- under the assumption that tardive akathisia is like other TDBut I'm not sure that my logic is right here. I'm also really unclear about two other things about the RLS and strong SSRI start-up akathisia? (I also had this during a brief trial with Cymbalta.) Would these be more consistent with up-regulation and low endogenous dopamine?
Anyway, I'm sorry if this is a muddle, but I'm contemplating starting another SSRI in the next few months. My main concern is whether there is reason to believe that going on something like Celexa again could possibly exacerbate some ideopathic or iatrogenic condition in my dopamine system.
If you have a few moments I could really use another brain or two to pick.
Thanks,
cache-monkey
poster:cache-monkey
thread:747867
URL: http://www.dr-bob.org/babble/20070407/msgs/748486.html