Posted by Cam W. on July 4, 2000, at 21:03:19
In reply to Re: Question for Cam - This is a test. » Cam W., posted by SLS on July 4, 2000, at 7:41:01
Scott
> Cam - You indicated that TD showed up when someone was switched from a combination of a traditional antipsychotic with an anticholinergic to Zyprexa.
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> 1. If the anticholinergic were kept on-board, would TD symptoms have appeared? Was it simply the withdrawal of the anticholinergic drug that was responsible for the emergence of symptoms?•No, I believe that it is the traditional antipsychotic that masks the TD. James has seen papers on this phenomenon.
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> 2. In the absence of an anticholinergic, can the switch from a traditional neuroleptic to Zyprexa (or other atypical neuroleptic) unmask the TD that had been previously masked by the traditional one?•I have seen it once. A person taking 8mg of Orap (pimozide) daily with no anticholinergic was switched to Zyprexa and within 2 weeks he developed the classic tongue movements.
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> 3. Can atypical neuroleptics fail to mask TD in patients for whom a typical neuroleptic had accomplished this?•I believe that iy is the lower level of D2 binding that minimizes the movement disorders when taking the atypicals. This, or 5HT-2 blocade, is possibly why atypicals fail to mask TD.
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> 4.Zyprexa and Clozaril are sometimes used to "treat" TD. Are these drugs added to the offending neuroleptic or substituted for it?•These are substituted for the traditional antipsychotic. I haven't seen Zyprexa used as successfully as Clozaril in treating TD. Clozaril does work for TD, but it takes at least 6 months of high dose Clozaril (700-900mg/day) before you see any significant improvement (usually). I think some people with TD give up on Clozaril treatment too early. This may also be the reason why Zyprexa doesn't seem to work that well for TD (too much weight gain with no noticeable improvement in less than six months may cause people to stop therapy).
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> 5. Do atypical neuroleptics act pharmacologically to reduce TD symptoms in a way dissimilar to typical neuroleptics, or is it that they simply lack an offending mechanism? What would such an offending mechanism be?•Interesting question. I wonder if that is how it works. I can't think of the theories behind why it works, but I think that I did read about it once.
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> 6. Can the acute application of a neuroleptic immediately exacerbate TD symptoms, or does it always reduce them?• I don't know if acute application would exacerbate or mask symptoms. I think that either of these would be typically seen with long term therapy.
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> 7. Does 5-HT2 receptor antagonism act to reduce TD symptoms? If so, have any other drugs with this property been used to treat TD - nefazodone for instance? Has ritanserin ever been played with for this indication?•I really don't think it is the serotonin, but decreased D2 blockade in the limbic system (?).
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> This is a test. You have 7 minutes to complete it and submit your answers. Open book is O.K. Good luck.
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•I don't know if all my answers are totally correct, but hey, it's only a test and there is no need to get 100% to pass. Also, I didn't have any notes at home to use as open book. - Cam
poster:Cam W.
thread:38901
URL: http://www.dr-bob.org/babble/20000630/msgs/39387.html