![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 20 of 20. This is the beginning of the thread.
Posted by falconman on January 7, 2004, at 6:28:26
Hi,
I've been on amisulpride 100mg for social phobia/depression now for 4 weeks. I don't think its working at all. Still emotionally very flat. Anyone got some advice? Is it worth dropping dose to 50/75mg?
Thanks
Posted by ann72 on January 7, 2004, at 8:12:05
In reply to Amisulpride, posted by falconman on January 7, 2004, at 6:28:26
Falconman, If you have SAD and depression, why did your pdoc put you on a med for schizophrenia? Have you been hearing voices or had any hallucinations?
Posted by btnd on January 7, 2004, at 17:59:21
In reply to Re: Amisulpride » falconman, posted by ann72 on January 7, 2004, at 8:12:05
> Falconman, If you have SAD and depression, why did your pdoc put you on a med for schizophrenia?
Because low doses of Ami (25-100mg) are not used for schizo*. They are used for dysthymia,depression,social-anxiety. MANY studies done on Ami+dysthymia. Works for me at 50mg/day.
Posted by scott-d-o on January 7, 2004, at 23:06:11
In reply to Amisulpride, posted by falconman on January 7, 2004, at 6:28:26
> Hi,
> I've been on amisulpride 100mg for social phobia/depression now for 4 weeks. I don't think its working at all. Still emotionally very flat. Anyone got some advice? Is it worth dropping dose to 50/75mg?
> ThanksI would say it is worth a try, in fact I would probably recommend having started at 50mg/day to being with; this is the dosage most people seem to have success with for depression. It seems people with dysthymic depression respond better with amisulpride as opposed to endogenous/major depression. Does the following sound like you:
Habitually gloomy, pessimistic, humorless, or incapable of fun; passive and lethargic; introverted; skeptical, hypercritical, or complaining; self-critical, self-reproaching, and self-derogatory; and preoccupied with inadequacy, failure, and negative events.
Another option is to try augmenting amisulpride with a medication that blocks dopamine reuptake. Examples are amphetamines, Wellbutrin, Ritalin, etc. I found a combination of sulpiride and Wellbutrin works wonders for my dysthymia/ADD. My current meds are Klonopin, Wellbutrin and sulpiride for social phobia, inattentive ADD, and dysthymia.
If this still doesn't help I would look at meds besides dopaminergic ones. I assume you have already been through some of the SSRI meds? What about tricyclics or Effexor?
scott
Posted by Epiphany on January 8, 2004, at 0:45:44
In reply to Re: Amisulpride » falconman, posted by scott-d-o on January 7, 2004, at 23:06:11
For me, Amisulpride only worked at lower doses. I took it at 25mg. Anything above 50 for me was counterproductive.
Posted by falconman on January 12, 2004, at 14:02:52
In reply to Re: Amisulpride, posted by Epiphany on January 8, 2004, at 0:45:44
> 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
Posted by falconman on January 12, 2004, at 14:08:36
In reply to Re: Amisulpride » falconman, posted by scott-d-o on January 7, 2004, at 23:06:11
> > Hi,
> > I've been on amisulpride 100mg for social phobia/depression now for 4 weeks. I don't think its working at all. Still emotionally very flat. Anyone got some advice? Is it worth dropping dose to 50/75mg?
> > Thanks
>
> I would say it is worth a try, in fact I would probably recommend having started at 50mg/day to being with; this is the dosage most people seem to have success with for depression. It seems people with dysthymic depression respond better with amisulpride as opposed to endogenous/major depression. Does the following sound like you:
>
> Habitually gloomy, pessimistic, humorless, or incapable of fun; passive and lethargic; introverted; skeptical, hypercritical, or complaining; self-critical, self-reproaching, and self-derogatory; and preoccupied with inadequacy, failure, and negative events.
>
> Another option is to try augmenting amisulpride with a medication that blocks dopamine reuptake. Examples are amphetamines, Wellbutrin, Ritalin, etc. I found a combination of sulpiride and Wellbutrin works wonders for my dysthymia/ADD. My current meds are Klonopin, Wellbutrin and sulpiride for social phobia, inattentive ADD, and dysthymia.
>
> If this still doesn't help I would look at meds besides dopaminergic ones. I assume you have already been through some of the SSRI meds? What about tricyclics or Effexor?
>
> scottHi,
thanks Scott. The above descripyion of dysthemia sounds very much like me. I have dropped it down to 50mg. I'll try this for 4 weeks, if there is no progress I'll consider 25mg or a swap to zyprexa. I already take Nardil+clonazepam. I have been through 4 different SSR'is, effexor and clomipramine.
Cheers
Posted by scott-d-o on January 13, 2004, at 16:37:34
In reply to Re: Amisulpride, posted by falconman on January 12, 2004, at 14:02:52
> > 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?
> ThanksI 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
Posted by Michael on January 27, 2004, at 15:58:56
In reply to Clearing confusion about low/high dose amisulpride, posted by scott-d-o on January 13, 2004, at 16:37:34
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
Posted by Ant-Rock on January 29, 2004, at 15:26:39
In reply to Re: Clearing confusion about low/high dose amisulpride, posted by Michael on January 27, 2004, at 15:58:56
Hi Michael,
I was wondering how you got Amisulpride prescribed.
Is it available in the U.S.?
Thank you for any help you can provide me with.
It's probably better to e-mail me privately, due to the rules here.
Anthony
(e-mail: xxx.)
Posted by scott-d-o on January 29, 2004, at 16:23:27
In reply to Re: Clearing confusion about low/high dose amisulpride » Michael, posted by Ant-Rock on January 29, 2004, at 15:26:39
> Hi Michael,
> I was wondering how you got Amisulpride prescribed.
> Is it available in the U.S.?
> Thank you for any help you can provide me with.
> It's probably better to e-mail me privately, due to the rules here.
> Anthony
> (e-mail: xxx.)pdocs in the U.S.A. can still prescribe it like any other med.. it isn't against the rules for a doctor to prescribe a non-FDA approved med, unless its like heroin or some other sched I substance.. once u get the script u usually have to fax it to a pharmacy overseas or depending on the law in that country u may not need one.. if you can get it prescribed than you can e-mail xxx, you can order it from them; they will definitely ask for a script thou, so don't bother otherwise.
btw, i think it is against the rules to even exchange e-mail addresses for the purposes of obtaining meds without a script.. dr. bob? ;-)
Posted by Dr. Bob on January 29, 2004, at 16:56:10
In reply to Re: Clearing confusion about low/high dose amisulp » Ant-Rock, posted by scott-d-o on January 29, 2004, at 16:23:27
> if you can get it prescribed than you can e-mail xxx, you can order it from them; they will definitely ask for a script thou, so don't bother otherwise.
They may ask for a script, but their web site doesn't say that...
> i think it is against the rules to even exchange e-mail addresses for the purposes of obtaining meds without a script.. dr. bob? ;-)
Yes:
http://www.dr-bob.org/babble/faq.html#illegal
Bob
PS: Follow-ups regarding posting policies should be redirected to Psycho-Babble Administration, thanks.
Posted by Michael on January 29, 2004, at 18:46:18
In reply to Re: Clearing confusion about low/high dose amisulpride » Michael, posted by Ant-Rock on January 29, 2004, at 15:26:39
Hi Anthony,
I didn't get it prescribed - I just got it from overseas... And that was a couple of years ago, I just have some left from then. I don't think it has been approved by FDA, and therefore it's not available in the US.
As Scott said, any doctor in the US can prescribe it, if you can get them to do it. As for where to get it now - I'm not really sure... I've looked a little, but don't have anything as of yet.
michael
> Hi Michael,
> I was wondering how you got Amisulpride prescribed.
> Is it available in the U.S.?
> Thank you for any help you can provide me with.
> It's probably better to e-mail me privately, due to the rules here.
> Anthony
> (e-mail: xxx.)
Posted by scott-d-o on January 29, 2004, at 23:36:56
In reply to Re: obtaining meds without a script » Ant-Rock » scott-d-o, posted by Dr. Bob on January 29, 2004, at 16:56:10
> They may ask for a script, but their web site doesn't say that...
>I don't think their web site says anything at all? I could forward the e-mail to you of them asking me for a script and refusing to sell w/o one..
Posted by michael on March 1, 2004, at 18:50:42
In reply to Re: Clearing confusion about low/high dose amisulpride, posted by Michael on January 27, 2004, at 15:58:56
Hello all,
Just wondering: if you have tried it...
1 - what kinds of results (pos/neg, or helpful or not).
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]3 - what other meds do you take with it?
Thanks for any feedback. Mostly curious if some have found dosages less than 50mg/day to be effective.
michael
> 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
>
>
Posted by scott-d-o on March 2, 2004, at 8:20:07
In reply to low dose amisulpride, posted by michael on March 1, 2004, at 18:50:42
> 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
> >
> >
>
>
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
> > >
> > >
> >
> >
>
>
Posted by jparsell82 on March 2, 2004, at 17:33:39
In reply to Re: low dose amisulpride, posted by scott-d-o on March 2, 2004, at 8:20:07
Hey, what's the half-life on these meds? I'm soon to be getting my Amisulpride. They are the 200mg tabs though, so I hope I don't need a dose smaller than 50mg or it may be a little tricky trying to cut them up.
Posted by scott-d-o on March 2, 2004, at 19:16:17
In reply to Re: low dose amisulpride, posted by jparsell82 on March 2, 2004, at 17:33:39
> Hey, what's the half-life on these meds? I'm soon to be getting my Amisulpride. They are the 200mg tabs though, so I hope I don't need a dose smaller than 50mg or it may be a little tricky trying to cut them up.
sulpiride is 8hrs, amisulpride is 12hrs. you should be able to find 50mg capsules.
Posted by michael on March 2, 2004, at 20:05:24
In reply to Re: low dose amisulpride, posted by scott-d-o on March 2, 2004, at 19:16:17
> > Hey, what's the half-life on these meds? I'm soon to be getting my Amisulpride. They are the 200mg tabs though, so I hope I don't need a dose smaller than 50mg or it may be a little tricky trying to cut them up.
>
> sulpiride is 8hrs, amisulpride is 12hrs. you should be able to find 50mg capsules.
>
>This is a good site on amisulpride: http://www.priory.com/focus13.htm#Pharmacology
It says in part, "There are two absorption peaks - one hour post-dose and a second 3-4 hours after taking the tablet. The elimination half-life is 12 hours."
I used to have a good one on sulpiride too, but it's gone now...
This is the end of the thread.
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