Posted by michael on March 2, 2004, at 17:33:16
In reply to Re: low dose amisulpride, posted by scott-d-o on March 2, 2004, at 8:20:07
Scott,
Thanks for sharing your experience - I appreciate all of the detailed info & feedback.
Just wanted to note that as Scott perceived, I'd be equally as interested in the same type of info/experiences with 50mg-150mg/day of SULPIRIDE (as opposed to amisulpride).
> > Hello all,
> >
> > Just wondering: if you have tried it...
> >
> > 1 - what kinds of results (pos/neg, or helpful or not).
>
> mostly positive, reduction in anxiety, increased energy, antidepressant effects. the only thing that bothers me is that when I stop taking it I tend to get worse which makes me wonder if it is a good solution for long-term treatment. I wonder how it effects DA receptor sensitivity in the long term. it obviously increases dopamine release thru DA autoreceptors antagonism without affecting the postsynaptic receptors too much. I am very sensitive to dopamine meds and absolutely cannot tolerate any other antipsychotic out there due to their antidopaminergic effects. they turn me into a total zombie even at low dose.
>
> > 2 - what dose have you found to be effective?
> > [do some use less than 50mg/day? 25mg? or? I find 50 to be too much, am trying 25]
>
> I've only taken sulpiride. 50-100mg/d is effective for more of an activating effect, while 150mg/d causes a more pronounced anti-anxiety effect. I think this correspondes to 25-50mg/d, and 75mg amisulpride, respectively.
>
> > 3 - what other meds do you take with it?
>
> klonopin[1.5mg/d] + sulpiride[100mg/d]:
>
> this was a great combination
>
> klonopin + lexapro[5mg/d] + sulpiride:
>
> even better
>
> klonopin + adderall[20mg/d] + sulpiride:
>
> a little bit too activating. I speculate the low-dose sulpiride potentiates the adderall's DA release.
>
> klonopin + lexapro + adderall + sulpiride:
>
> the jury is still out on this one. I'm considering dropping the adderall and just going back to the klonopin + sulpiride w/ maybe a low-dose of lexapro. however, I have a script for adderall and sulpiride is a pain to get so that is what's stopping me. I definitely need at least one dopaminergic med to be functional.
>
> > Thanks for any feedback. Mostly curious if some have found dosages less than 50mg/day to be effective.
> >
> > michael
> >
>
> yes, dosages that low are effective for dysthymia but less so for anxiety.
>
> hope this helps,
> scott
>
>
>
>
> > > Scott-
> > >
> > > Good description. I am only writing to add that for dysthymia/etc., even 50mg MAY be too much. It was too much for me - made me sleepy (very), etc.
> > >
> > > My point being that if one has those type of side effects (sedation/cognitive dulling), one may want to try even less than 50mg/day - despite the fact that that seems to be the lowest dose that is used most often in the studies.
> > >
> > > I tried it at 50mg a couple of times (a few years ago) and had the sedative/cognitive issues both times. So much so that I Had to stop. I think I only made it a couple weeks before I could barely get up for, much less function at, work.
> > >
> > > It only recently occured to me that those side effects were what was expected at higher doses - as you noted - so perhaps a lower dose would actually be helpful for me.
> > >
> > > I just decided to try it again at 25mg. It's only been a week or so, but I think it may be helping this time, and at least not giving me the bad side effects - at least not yet. We'll see if that changes... Of course, this is just my experience - ymmv.
> > >
> > > michael
> > >
> > >
> > > > > > For me, Amisulpride only worked at lower doses. I took it at 25mg. Anything above 50 for me was counterproductive.
> > > > >
> > > > > What specifically do you mean by counterproductive- What effects did you get off 100mg?
> > > > > Thanks
> > > >
> > > > I can't speak for the above poster, however, the reason amisulpride may only be effective at very low doses is due to the type of receptors it binds to. The two different types we are concerned with are presynaptic (also called autoreceptors) and postsynaptic. When dopamine binds to a postsynaptic receptor, it transmits the nerve impulse to the receiving cell. However, autoreceptors are located on the dopamine-producing cells themselves and help the cell gauge how much dopamine to release into the synaptic space (so when dopamine attaches to these receptors it causes a *reduction* in dopamine release.)
> > > >
> > > > Any dose of amisulpride is going to cause more dopamine to be released from these cells by blocking these autoreceptors and "tricking" the cell into releasing more dopamine. However, as the dose of amisulpride gets higher, it begins to bind to both the autoreceptors *and* postsynaptic receptors. Thus, more dopamine is still getting released, but amisulpride is also binding to those postsynaptic receptors and blocking dopamine transmission, so the released dopamine cannot really do much since it can't knock the amisulpride off the postsynaptic receptors. Thus the overall effect here would be a *decrease* in dopamine transmission, even though more is still being released. Generally, this is going to lead to sedation/cognitive and sexual side effects and the positives will be that it will help with schizophrenia and reduce anxiety. These effects are what led antipsychotics to first be labeled as "major tranquilizers", while benzodiazepines were later deemed "minor tranquilizers."
> > > >
> > > > The reason for the efficacy of low-dose amisulpride in dysthymia is that the amisulpride binds to mostly just the autoreceptors and leaves the postsynaptic receptors alone, allowing the increased dopamine that has been released to naturally bind to the postsynaptic receptors and having the overall result of an increase in both dopamine release and transmission. I suppose the key in getting this medication to work for dysthymia is finding the "window" that has this overall effect, thus I believe the dosage should start out really low and be moved up slowly until an effective dose is reached. However, dose should *never* exceed 200mg/d for the treatment of dysthymia.
> > > >
> > > > I'm sure this was way more information than you wanted to know. ;-)
> > > >
> > > > My intent in posting this was just to clear up any confusion regarding the drug's action because when I look on this board most people seem to be perplexed by it; now hopefully they can just be redirected to this post.. Unfortunetly, many pdocs (esp. in the USA) have never even heard of this medication and can provide little help so I realize this board is the only resource for many patients.
> > > >
> > > > scott
> > >
> > >
> >
> >
>
>
poster:michael
thread:297519
URL: http://www.dr-bob.org/babble/20040228/msgs/319456.html