Posted by kregpark@yahoo.com on April 21, 2002, at 19:43:15
In reply to Re: Amisulpride + SSRI - WARNING » kregpark@yahoo.com, posted by Ken on April 21, 2002, at 18:46:30
Hi Ken -
My dose was 50, then 25, then 12.5, then 6 then 0 starting from 50 and occurring over 3.5 weeks. That as you know is "low dose". 6mg is specs of a small tablet. Those with schitzophrenia can tolerate perhaps 1200mg or 2000mg for years without any problem. Manic patients could be considered in many ways "opposites" of those with SP behaviorally, and the obvious different biochemically is in DA function (high versus low). These potent DA blockers are not appropriate for anyone even at tiny doses.
Amisulpride was, in fact prosexual without question. There was some mild physical (not mental or "alertness") type sedation. There is mixed dopaminergic effect, it is not "purely" a DA agonist even at the "lowest" doses.
There is some limbic selectivity for pro DA activity, but notice on Medline you will see that an initial pro DA effect in VT gives way to --DA after a couple weeks . There is also significant --DA in striatum and who knows where else. Tardive dyskinesia, for example, is thought to be triggered when excessive DA upregulation (>90%) occurs in striatum. DURATION OF USE OF ANTIPSYCHOTIC WAS FOUND IRRELEVANT TO DEVLOPING TD IN THIS VERY RECENT STUDY. Polypharmacy and individual dynamics are huge factors in whether a acute or chronic reaction or disorder will occur. One time use of a low dose is enough to trigger TD if the user is "primed".
Note than some posters here (I saw one today) mention they get EPS from med changes not involving antipsychotics. That is medication sensitivity. It may be innate or the permanent result of injury or drug toxicity.
In terms of movement disorders antipsychotics are the implicator in the huge majority of drug induced cases, although L-DOPA (Parkinson's) is associated with a fair number of problems also. Of course Parkinson's patients are highly senstivity to *any* dopamine blocker.
Perhaps this is a good example. Would you suggest that low dose amisulpride is safe for all Parkinson's patients?
Social Phobia patients have been shown to have reduced DA receptor density in striatum (one of many studies, observations, etc implicating DA dysfunction in those with SP). SP patients also are 5 times more likely to develop Parkinson's in later life.
What is your evidence that low dose amisulpride is "safe" for affective disorder patients?
A few US atypicals (especially Clozaril which could be considered safe but is not much help for affective disorders) - may be relatively safe (ie; olanzapine). However, also look at info on the substitute benzamides. ie; metaclopramide, sulpride, amisulpride, etc. If you look at the track record for these drugs you will see that in polypharmacy especially, used in affective patients they are far from safe.
Amisulpride is quite potent at blocking DA receptors, much moreso than olanzapine. It is an "atypical" - but certainly a different type of "atypical" than the 5ht-blockers which are the USA "atypicals".
That is why amisulpride, a novel and potentially very useful agent, never made it into the US ... it was being reviewed in recent years but it failed to make it due to safety concerns.
Personally I'm surprised Metaclopramide is still available in the USA (or has it been banned since early 2001 - date of my PDR)... ? ... there is plenty of lawsuit activity from patients taking this drug for nausea developing permanent orofascial dyskinesias and dystonias. I doubt it is would be used much anymore except in cancer patients with poor long term prognosis.
Ray
poster:kregpark@yahoo.com
thread:103469
URL: http://www.dr-bob.org/babble/20020416/msgs/103749.html