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Re: Q. for CAM W. re risperdal vs. zyprexa » SLS

Posted by Cam W. on October 16, 2000, at 19:38:50

In reply to Re: Q. for CAM W. re risperdal vs. zyprexa » Cam W., posted by SLS on October 14, 2000, at 9:21:08

> 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.
•I'd probably overreact, too, but you seldom see any EPS problems with Risperdal™ (risperidone) at doses under 3mg daily (except in some elderly people).
> Is there an association between how early in neuroleptic treatment EPS appears and the risk of tardive-dyskinesia?
•I don't think that either can be predicted. It happens when and if it happens. EPS and TD are very patient dependent, you can't guess who will get it, except that seniors are far more vulnerable (classic case of YMMV).
> 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.
•The literature says that Zyprexa works slightly better than Risperdal for mania, but I have seen mixed reviews for both in augmentation of depression. Both do work for many people. Something tells me that Risperdal is better for depressive symptoms. I think I read that somewhere, but I can't be sure of the source.
> I am having a hard time deciding whether I should try Zyprexa next or go back and try risperidone first.
•You and your doc's mutual decision. I'm staying out of that one, as it is outside my area of expertise.
> 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?
•I've heard people say that after 8 months (to a year) that they don't feel as hungry as they use to. But, I have seen about 75% of people gain some noticeable weight with Zyprexa (not everyone, though - Another of life's mysteries). I can't guarantee that after 8 months of eating properly that you won't gain weight, but once aquired, good eating habits become second nature (yeah, right; who am I kidding?).
> 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?
•Perhaps differential cFos induction in the prefrontal cortex and the basal ganglia? See below.
> 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.
•Dr.Phil Seemans (the guy who developed the receptor site theory) gave a talk and basically said that maybe the reason that atypical antipsychotics (AAP) have such low D2 binding affinities, yet exert antipsychotic activity, may be that the AAP may be tweaking the receptor, therefore what you get when you do a binding affinity assay, you are actually only getting snapshot of D2 binding activity. I think that maybe the D2 receptors are somehow preferentially blocked in the prefrontal cortex, but not in the basal ganglia (perhaps due to a modification in the leak of dopamine in the area). These two brain areas seem to both use dopaminergic pathways, but are modulated differently.
> That some modification of the second messenger system by "tweaking" the receptor might produce a therapeutic effect is an exciting idea.
•I don't know if this is true and I can't prove it, but it sounds good (a sure sign that there is some faulty logic in the theory, somewhere).

•Your partner in pondering - Cam




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