Posted by SLS on October 14, 2000, at 9:21:08
In reply to Re: Q. for CAM W. re risperdal vs. zyprexa » anita, posted by Cam W. on October 13, 2000, at 23:39:26
Hi Cam.
Regarding my side effects with risperidone:What I experienced was sort of like a combination of weakness and stiffness. I can't say that I was slowed-down at all. I didn't experience any tremulousness except in the legs when I would climb stairs. I guess I overreacted, but it was upsetting to have to walk so deliberately just to make sure that I didn't trip over my own feet. I couldn't help but to think that this was EPS, especially since it was my impression that risperidone was the most likely of the atypicals to produce them.
Is there an association between how early in neuroleptic treatment EPS appears and the risk of tardive-dyskinesia?
It is hard to tell, but risperidone may have been helping a bit. Except for the weight-gain thing, I have a better gut feeling about the efficacy of Zyprexa for treating depression. Of course, gut feelings leave quite a large statistical margin of error and everyone is different. What is your impression regarding these two drugs for treating depression? Interestingly, Zyprexa has been known to occasionally cause mania in schizoaffective disorder.
I am having a hard time deciding whether I should try Zyprexa next or go back and try risperidone first.
Regarding Zyprexa and weight gain: You often cite 8 months or so as being the time period within which most of the weight gain occurs. After this, the rate of gain plateaus. My question is, if I were to starve myself during these first 8 months and manage to maintain my current weight, would I then be able to eat normally after this 8 month period without experiencing some sort of rebound weight gain?
Thank you, Cam.
> I think that the 5HT-2A/D2 ratio of Zyprexa is greater than Risperdal, but as to in vivo binding affinities, I'm not sure. Anyways, I am starting to think that tweaking the receptor, rather than irreverisibly binding to it causes different second messenger responses. In other words, the atypical antipsychotics may not need to bind tightly to the receptor to result in a medicinal effect. So, looking at binding affinities of atypical antipsychotics may be misleading (then again, I can't prove this).Are you saying that this receptor "tweaking" is how these drugs exert their therapeutic effects, or that the benefit of this type of dynamic is that it yields fewer side effects or a diminished risk of TD?
Regarding TD, it would be my guess that to allow each receptor to be stimulated regularly, although with decreased frequency, would still allow for the continuation of second messenger events, and thus prevent an increase in gene transcription to upregulate the membrane. The percentage of occupancy at any one moment might be similar to the older drugs, but it would be like a game of receptor keep-away. How frustrating and demoralizing this must be for the D2s. Just babbling.
That some modification of the second messenger system by "tweaking" the receptor might produce a therapeutic effect is an exciting idea.
- Scott
poster:SLS
thread:46302
URL: http://www.dr-bob.org/babble/20001012/msgs/46339.html