abilify to counteract prolactin increase with risperdal

[annoyedpsychiatrist]

Do you guys do this often? Ive done this in the past a while ago, and have used abilify in conjunction with clozapine. Risperdal has been amazing for one of my bipolar patients (shes completely stable on it now) but shes having persistent increased prolactin and galactorrhea. Was considering adding 5mg abilify to try and offset prolactin increase but may have her see endo too.

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[TexasPhysician]

Sometimes it works as low as 1mg. I go up slowly with it.

 

[psychmd03]

I’ve done it a few times all it took was 2mg and it was enough to drop the prolactin and not cause destabilization

 

[Celexa]

Agree low dose abilify definitely worth considering, but also, what dose of risp is she on and how long has she been stable? Lots of patients maintain just fine on 1-2mg. If she's on more than that and has truly been stable you could also start inching down the risp (ie at 0.5mg increments every few months).

 

[annoyedpsychiatrist]

Agree low dose abilify definitely worth considering, but also, what dose of risp is she on and how long has she been stable? Lots of patients maintain just fine on 1-2mg. If she's on more than that and has truly been stable you could also start inching down the risp (ie at 0.5mg increments every few months).

unfortunately shes on a fairly low dose of risperdal already, which thus far has been like the one medication that seemed to really work for her so i hesitate going even lower.

All great advice. Ill throw on a small dose, check after 3 months and consider increasing if need. Maybe ill get an endo consult to get their blessing but i guess we shall see

 

[whopper]

Given that there's several antipsychotics now with much more benign side effect profiles that could work instead of Risperidone, I'd consider just get rid of Risperidone unless this was one of the only meds that worked.

You could try another antipsychotic in the -idone family such as Lurasidone (now generic) or try a differing antipsychotic with low binding D2.

 

[calvinhobbes]

Yes

 

[clausewitz2]

Given that there's several antipsychotics now with much more benign side effect profiles that could work instead of Risperidone, I'd consider just get rid of Risperidone unless this was one of the only meds that worked.

You could try another antipsychotic in the -idone family such as Lurasidone (now generic) or try a differing antipsychotic with low binding D2.

The -idone suffix does not mean they are pharmacologically or indeed chemically similar. It is not a family in any useful sense.

 

[whopper]

The -idone suffix does not mean they are pharmacologically or indeed chemically similar. It is not a family in any useful sense.

Not completely. Meds in a class could have the same suffix due to similar chemical structures. Several meds with similar backbones have been found to have correlations in effect. E.g. Clozapine, Olanzapine and Quetiapine. All cause very similar side effects because their similar structures lend to similar binding profiles hence similar side effects such as sedation, weight gain, agranulocytosis (yes the -apines can all cause it, just that the risk is worse with Clozapine. I've seen agranulocytosis with Olanzapine, and I've seen significantly lowered ANCs on any of the -apines. Anyone on a high dosage of Olanzapine, Quetiapine or Clozapine, I expect to see ANC at least measurably lower after treatment vs before treatment).

The stickler, however, is even a slight change in molecular shape could cause a very different effect. Quetiapine is the least efficacious antipsychotic. Clozapine is the most efficacious. Norquetiapine which is very similar to Quetiapine in structure has SNRI effects not seen in Quetiapine (although it's converted to Norquetiapine in the body so the patient gets it in their body anyway). H20 is safe. H202 is a very different chemical in terms of it's effects on the human body.

So of course just cause it has the same suffix, it can't be considered always very similar, and in fact thinking it's chemically similar could make one think, incorrectly, there will be similar effects in some cases, but I wouldn't say, "it is not a family in any useful sense." If the structure were similar it'd make me think it could possibly work similarly, but know the dynamics of pharmacology, organic chemistry etc makes it too simplistic to make a conclusion out of it. It does, however, add to the thought processes in the hypothetical stages of making a decision.

Palliperidone vs Risperidone, the chemical structures, efficacy, side effect profiles are almost the same. I'm not just talking that they're both antipsychotics. Most patients feel very different effects with different antipsychotics. Most patients I've seen feel these meds are almost the same in all of it's effects.

Broudifacoum is rat poison. It shares several chemical similarities and structure with Coumadin, the main difference is Broudifacoum has a much longer half life, (the slight difference in it's structure causes it to have a longer half-life) but both act as anticoagulants via the same exact mechanism, and the -coum suffix is because of they have the same chemical backbones.

So some similarity in structure (and the suffixes in the name are often times based on the structure) does have some weak (or better, but possibly also no) possible meaningful relationship. I wouldn't say it has no benefit "in any useful sense." Patient got agranulocytosis on Clozapine? It would me a bit more hesitant to give any of the -apines. Similarly if a patient had a bad reaction with Penicillin, I'd be wouldn't be surprised if any pencillin-similar meds of similar structure caused an allergy.

 

[clausewitz2]

Not completely. Meds in a class could have the same suffix due to similar chemical structures. Several meds with similar backbones have been found to have correlations in effect. E.g. Clozapine, Olanzapine and Quetiapine. All cause very similar side effects because their similar structures lend to similar binding profiles hence similar side effects such as sedation, weight gain, agranulocytosis (yes the -apines can all cause it, just that the risk is worse with Clozapine. I've seen agranulocytosis with Olanzapine, and I've seen significantly lowered ANCs on any of the -apines. Anyone on a high dosage of Olanzapine, Quetiapine or Clozapine, I expect to see ANC at least measurably lower after treatment vs before treatment).

The stickler, however, is even a slight change in molecular shape could cause a very different effect. Quetiapine is the least efficacious antipsychotic. Clozapine is the most efficacious. Norquetiapine which is very similar to Quetiapine in structure has SNRI effects not seen in Quetiapine (although it's converted to Norquetiapine in the body so the patient gets it in their body anyway). H20 is safe. H202 is a very different chemical in terms of it's effects on the human body.

So of course just cause it has the same suffix, it can't be considered always very similar, and in fact thinking it's chemically similar could make one think, incorrectly, there will be similar effects in some cases, but I wouldn't say, "it is not a family in any useful sense." If the structure were similar it'd make me think it could possibly work similarly, but know the dynamics of pharmacology, organic chemistry etc makes it too simplistic to make a conclusion out of it. It does, however, add to the thought processes in the hypothetical stages of making a decision.

Palliperidone vs Risperidone, the chemical structures, efficacy, side effect profiles are almost the same. I'm not just talking that they're both antipsychotics. Most patients feel very different effects with different antipsychotics. Most patients I've seen feel these meds are almost the same in all of it's effects.

Broudifacoum is rat poison. It shares several chemical similarities and structure with Coumadin, the main difference is Broudifacoum has a much longer half life, (the slight difference in it's structure causes it to have a longer half-life) but both act as anticoagulants via the same exact mechanism, and the -coum suffix is because of they have the same chemical backbones.

So some similarity in structure (and the suffixes in the name are often times based on the structure) does have some weak (or better, but possibly also no) possible meaningful relationship. I wouldn't say it has no benefit "in any useful sense." Patient got agranulocytosis on Clozapine? It would me a bit more hesitant to give any of the -apines. Similarly if a patient had a bad reaction with Penicillin, I'd be wouldn't be surprised if any pencillin-similar meds of similar structure caused an allergy.

Yeah but this is just because paliperidone is literally the main active metabolite of risperidone. It is not a question of "they have similar chemical structures so they have similar effects" but "they are in large part literally the same molecule so they have similar effects." A = A, unsurprisingly.

If you look at the structures for, say, paliperidone and lurasidone, you will rapidly see that they are just not that similar. Lurasidone is, however, very similar to ziprasidone, and indeed this was initially the starting point for developing it. It does end up behaving quite similarly.

 

[whopper]

The main reason why Palliperidone is so similar in structure is cause it's a metabolite.

Also you just supported my argument with the statement," If you look at the structures for, say, paliperidone and lurasidone, you will rapidly see that they are just not that similar. Lurasidone is, however, very similar to ziprasidone, and indeed this was initially the starting point for developing it. It does end up behaving quite similarly."

As I mentioned, similar structure (which doesn't always correlated with similar name and suffixes) does sometimes have correlation, and as I said, it's a weak point of consideration, possibly worth consideration in early hypothetical modes of consideration, but can be useful at times and is not NEVER useful. Sometimes weak, unfortunately, is all you got.

 

[annoyedpsychiatrist]

Given that there's several antipsychotics now with much more benign side effect profiles that could work instead of Risperidone, I'd consider just get rid of Risperidone unless this was one of the only meds that worked.

You could try another antipsychotic in the -idone family such as Lurasidone (now generic) or try a differing antipsychotic with low binding D2.

I could try a newer one but shes failed many other medications and has had some pretty severe episodes in the past so im a bit hesistant

 

[ObsequiousAplomb]

The main reason why Palliperidone is so similar in structure is cause it's a metabolite.

Also you just supported my argument with the statement," If you look at the structures for, say, paliperidone and lurasidone, you will rapidly see that they are just not that similar. Lurasidone is, however, very similar to ziprasidone, and indeed this was initially the starting point for developing it. It does end up behaving quite similarly."

As I mentioned, similar structure (which doesn't always correlated with similar name and suffixes) does sometimes have correlation, and as I said, it's a weak point of consideration, possibly worth consideration in early hypothetical modes of consideration, but can be useful at times and is not NEVER useful. Sometimes weak, unfortunately, is all you got.

Look at these structures and tell me with a straight face that they're anywhere near "similar enough" that they're just one or two molecules off.

Ziprasidone - Wikipedia

Lurasidone - Wikipedia

en.wikipedia.org

Risperidone - Wikipedia

en.wikipedia.org

These structures share a small portion of a backbone. Other than that, they're so incredibly different that it's hilarious they have the same suffix. A small change makes the most efficacious antipsychotic the least efficacious. The "idones" are incredibly dissimilar.

Also, no idea why you're acting like it's the "apines" that cause agranulocytosis. It's literally every single antipsychotic that causes it.

 

[whopper]

Look at these structures and tell me with a straight face that they're anywhere near "similar enough" that they're just one or two molecules off.

They do have similarities. I can say that with a straight face. I can say that as straight as I can say 1+1=2, but the problem is answering, "

that they're anywhere near "similar enough" that they're just one or two molecules off.

Cause this doesn't make sense unless you're just being way too easy.

A molecule by definition is a collection of bonded atoms, so I could literally just cleave off 2 collections of atoms (hence 2 molecules off) and the same -idone backbones would be there. I could still meet your challenge by erasing everything other than the idone backbone and that'd be 1-2 molecules.

I'm trying to be fair cause I figure maybe you didn't type what you meant-Yes Risperidone and Lurasidone do have similarities, and I never said those specific 2 are "one or two off." 1-2 molecules off, I'm not sure what you mean by that or why that's relevant because 1 molecule could be thousands of atoms or just 2 atoms bonded together. In terms of chemical metrics using "1-2 molecules off" has almost no relevance as far as I can see in terms of discussing pharmacology in the context above as far as I can tell. So I'm a bit confused with your sentence. If I did anything to create this confusion I apologize, but I'm not sure if I did.

Here's an example of just 1 molecule off.

https://www.science.org/doi/10.1126/science.270.5244.1905-a#:~:text=The%20aptly%20named%20titin%20weighs,than%20the%20average%2Dsize%20protein.

"1995 biologists smashed records by cloning the DNA for the largest protein molecule known. The aptly named titin weighs in at a molecular weight of 3 million and consists of a continuous chain of 27,000 amino acids, making it 20 to 50 times larger than the average-size protein."

See what I mean? Your challenge that I say with a "straight face" that it's just 1-2 molecules off is as easy as me cutting a Gordian Knot with a knife. So I think you really didn't mean what you literally wrote.

A small change makes the most efficacious antipsychotic the least efficacious.

As I already stated above. I used the example of H20 vs H202, and Clozapine vs Quetiapine.
(Again Person X: Tell me with a straight face that 1+1=2, Person Y: Sure. 1+1=2).

Quetiapine and Clozapine have chemical similarities in structure, yet their differences make one the most efficicious antipsychotic, the other the least efficacious. I find it odd that you're using a point I already mentioned, acknowledged, and said in the context that this makes my argument one for weak consideration, but still of some consideration. (That's called nuance). Unless you're saying that cause you're supporting my argument? (which I don't get given the tone of the post).

But now getting to the other side of the sword, Quetiapine and Clozapine's similarities are indisputable and not on simpy a superficial level of just having the same suffix, but also chemical structure, similar receptor binding profiles, and several very similar side effects-weight gain, lipid increases, neutropenia, anticholinergic, etc. Clinically, the effects of both meds if given separately to two group of subjects, 20 each, could be difficult to distinguish among even experienced psychiatrists except for the efficacy of the antipsychotic benefit. (Very few side effects would distinguish them, one being hypersalivation). Among the several dozens of possible effects a med could have, one cannot deny that 2 meds, similar structures, simliar binding profiles, having amost the same effects on a person except for the 1 best intended effect (antipsychotic) still is a worthy argument.

The "idones" are incredibly dissimilar.

They can be, as they can also have similarites. Palliperidone as mentioned above, is almost identical to Risperidone. I can say that as straight as I can say 1+1=2.

Also, no idea why you're acting like it's the "apines" that cause agranulocytosis. It's literally every single antipsychotic that causes it.

Not all antipsychotics cause it in same degrees. You're arguing without acknowledging the known differences, of which still are poorly understood. This actually is something in our field rarely studied except for Clozapine, but of the data that exists, and just 1 study-THREE OF FOUR BIGGEST OFFENDERS ARE THE APINES.

Antipsychotic drug-induced neutropenia: results from the AMSP drug surveillance program between 1993 and 2016

Neutropenia and agranulocytosis (N&A) are relatively rare, but potentially fatal adverse drug reactions (ADR). This study presents cases of N&A related to one or more antipsychotic drugs (APDs) in psychiatric inpatients. Data on APD utilization ...

www.ncbi.nlm.nih.gov

"A total of 124 cases of APD-induced N&A were documented, 48 of which fulfilled the criteria for agranulocytosis"
"Clozapine had the highest relative risk for inducing N&A and was imputed alone as a probable cause of N&A in 60 cases (1.57‰ of all patients exposed). Perazine showed the second highest relative risk with 8 cases and an incidence 0.52‰, followed by quetiapine (15 cases resp. 0.23‰ of all patients exposed) and olanzapine (7 cases; 0.13‰ of all patients exposed)."

Also, and the data is much older because typical antipsychotics aren't used as much, older data suggested phenothiazines tended to do it more vs the other typical nonphenothiazines. ("But they all cause neutropenia"-I never said they didn't). You're ignoring the nuance and using a black and white perspective, ignoring several dots that if connected together like the study above showing -apines may be, again MAY BE, ONE MORE TIME MAY BE (remember this is science, it's a stepwise progression to understanding) more of a problem with neutropenia vs the others. Remember what I wrote above? This type of stuff is worthy for the hypothetical stage of thought. SCIENCE INCLUDES HYPOTHESIS, NOT JUST CONCLUSIONS.

Mirtazapine has an association with neutropenia.

Neutropenia associated with mirtazapine use: is a drop in the neutrophil count in a symptomatic older adults a cause for concern? - PubMed

Neutropenia associated with mirtazapine use: is a drop in the neutrophil count in a symptomatic older adults a cause for concern?

pubmed.ncbi.nlm.nih.gov

Now one could say, "hey you're wrong Perazine causes neutropenia." I never said it didn't. One could say, "so you're saying Mirtazapnie is an antipsychotic?" I never said it was. One could say other psych meds cause neutropenia. I never said they didn't. One could say idones aren't identical-I never said they were identical. .......etc.

(I will say, however, that Mirtazapine is also having several similarities with apines. Which brings up to me a question-is there something going on with the benzene rings and formation of nitrenium ions? Nitrenium ions have benzene ring backbones as found in the apines, these ions are one of the proposed mechanisms cause oxidant damage to the bone marrow that causes neutropenia).

The -idones and the -apines aren't just suffixes. They correlate to backbone structures in the molecules. That's why quetiapine wasn't named BillyJoeBob. Again I said their similarities are for weak consideration, but (and I'm saying this again) sometimes that's all you got.

 

[clausewitz2]

The -idones and the -apines aren't just suffixes. They correlate to backbone structures in the molecules. That's why quetiapine wasn't named BillyJoeBob. Again I said their similarities are for weak consideration, but (and I'm saying this again) sometimes that's all you got.

I think the point we're trying to make is that if you are to the point where this is what is determining your choice between medications, you might as well choose based on which font on the packaging you prefer. You would not be on shakier empirical ground for forming a belief about the likely efficacy of one versus another than choosine based on "what are the last five letters of the name/does it rhyme?"

 

[ObsequiousAplomb]

Yeah, whopper, You're clearly not reading at all what people are saying in response to you and thinking that you're somehow sounding coherent here. This is sad. Usually, you have good insights. But this coupled with your fanatic devotion to Vraylar+Auvelity...you're sounding like a sophisticated shill.

 

[hamstergang]

You could try another antipsychotic in the -idone family such as Lurasidone (now generic) or try a differing antipsychotic with low binding D2.

Yeah, that's a lot of rambling to try justifying being wrong. Here is the original post that started this line of discussion. We don't have to consider this in the abstract or look to other examples. The question is, is it useful to think of Risperidone and Lurasidone as being in the same family due to their "-idone" ending? The answer is clearly no.

 

[Celexa]

Question after reading this thread, as some if you are definitely more up on detailed pharmacology than I am. In a circumstance like this, what about switching to paliperidone? The risk of hyperprolactinemia is discussed much more with risp than paliperidone, is that because it's related to other metabolites/medication effect prior to metabolism or just bc paliperidone isn't used as much? And similarly in terms of efficacy, how much can you assume someone can smoothly switch between risperidone and paliperidone in control of symptoms?

Another thought--is the prolactinemia related to peak blood levels mainly, and if so, would switching to an LAI potentially ameliorate it without substantial equivalent dose changes?

 

[annoyedpsychiatrist]

Question after reading this thread, as some if you are definitely more up on detailed pharmacology than I am. In a circumstance like this, what about switching to paliperidone? The risk of hyperprolactinemia is discussed much more with risp than paliperidone, is that because it's related to other metabolites/medication effect prior to metabolism or just bc paliperidone isn't used as much? And similarly in terms of efficacy, how much can you assume someone can smoothly switch between risperidone and paliperidone in control of symptoms?

Another thought--is the prolactinemia related to peak blood levels mainly, and if so, would switching to an LAI potentially ameliorate it without substantial equivalent dose changes?

For the first question, I still get nervous. People are finicky, and no matter how similiar something is, its not the same is how I look at it. Patient was in a phase of her life where she was actively rebuilding: has a job again, repairing finances/relationship with parents, etc. We decided to hold for a bit, monitor and were going to have her see endo. There were questions that she may have had sx before risperdal which makes me wonder what her baseline prolactin was (risperdal was started in the inpatient and I was never able to get a baseline on her).

The LAI is a good thought. I had considered perseris, just because I hate the two week interval of consta

 

[ObsequiousAplomb]

Question after reading this thread, as some if you are definitely more up on detailed pharmacology than I am. In a circumstance like this, what about switching to paliperidone? The risk of hyperprolactinemia is discussed much more with risp than paliperidone, is that because it's related to other metabolites/medication effect prior to metabolism or just bc paliperidone isn't used as much? And similarly in terms of efficacy, how much can you assume someone can smoothly switch between risperidone and paliperidone in control of symptoms?

Another thought--is the prolactinemia related to peak blood levels mainly, and if so, would switching to an LAI potentially ameliorate it without substantial equivalent dose changes?

in my experience paliperidone causes it just as often as risperidone. The majority of the cases of antipsychotic-induced galactorrhea that I have seen are from Invega Sustenna, but that's probably because Invega Sustenna was so widely adopted in community settings while I was in training. Now that Uzedy is so much more convenient to start in the hospital maybe it'll swing back the other way.

 

[milesed]

We have a female patient now on Hafyera with prolactin over 200 and is asymptomatic. She is finally stable and has not done well on any other antipsychotics. We just added 2 mg Abilify and will check prolactin in 1 month- hoping it comes down as we all prefer not to switch, while quite nervous about it being such a long-acting injectable. Of course she waited 6 months before getting labs done, so no baseline.

 

[mistafab]

In my experience doing this, aripiprazole 2-5 mg is all that is needed to reduce the prolactin-related side effects.

I will say though that secondary prolactin elevation is rarely above 100 from antipsychotics in my experience. Usually only primary hyper prolactin is >100.

 

[Stagg737]

Question after reading this thread, as some if you are definitely more up on detailed pharmacology than I am. In a circumstance like this, what about switching to paliperidone? The risk of hyperprolactinemia is discussed much more with risp than paliperidone, is that because it's related to other metabolites/medication effect prior to metabolism or just bc paliperidone isn't used as much? And similarly in terms of efficacy, how much can you assume someone can smoothly switch between risperidone and paliperidone in control of symptoms?

Another thought--is the prolactinemia related to peak blood levels mainly, and if so, would switching to an LAI potentially ameliorate it without substantial equivalent dose changes?

It's more well-documented with risperidone, probably partially in response to the large lawsuit against J&J that's still going on, but paliperidone also has very high rates of prolactin-related side effects. Effects are most likely related to the molecule's greater affinity with a Permeability-glycoprotein in the BBB and permeability through the portal hypophyseal veins leading to increased binding to lactotrophic cells in the anterior pituitary compared with other antipsychotics. How do I know this? The only time I was pimped on the interview trail in residency was when a PD noted I had a graduate degree in molecular biology and asked if I knew why risperidone and paliperidone had such high rates of hyperprolactinemia. Fun times...

Anyway, here's an article talking about it more in depth if you're interested:

Prolactin Elevations and Permeability Glycoprotein

Article AbstractObjective: To examine the role of permeability glycoprotein (P-gp) and its substrates in the mechanism of hyperprolactinemia.Data Sources: PubMed and Google Scholar were queried with the search term permeability glycoprotein crossed with antipsychotic, neuroleptic, prolactin...

www.psychiatrist.com

 

[ObsequiousAplomb]

We have a female patient now on Hafyera with prolactin over 200 and is asymptomatic. She is finally stable and has not done well on any other antipsychotics. We just added 2 mg Abilify and will check prolactin in 1 month- hoping it comes down as we all prefer not to switch, while quite nervous about it being such a long-acting injectable. Of course she waited 6 months before getting labs done, so no baseline.

If she's asymptomatic, why did you check the prolactin?

 

[vanfanal]

Somewhat related...I saw someone today on bupropion xl 300daily + aripiprazole 5mg. I'm assuming the bupropion is not for smoking cessation. I left it for now, but in my head I'm thinking does this make any sense since these have opposing MOAs...

 

[Celexa]

Somewhat related...I saw someone today on bupropion xl 300daily + aripiprazole 5mg. I'm assuming the bupropion is not for smoking cessation. I left it for now, but in my head I'm thinking does this make any sense since these have opposing MOAs...

It's illogical on its face but not particularly severely compared to a lot of nonsense we see... the type of thing if the patient isn't doing well I'd definitely change but if they were objectively doing well I'd probably shrug and leave be.

 

[aim-agm]

Somewhat related...I saw someone today on bupropion xl 300daily + aripiprazole 5mg. I'm assuming the bupropion is not for smoking cessation. I left it for now, but in my head I'm thinking does this make any sense since these have opposing MOAs...

Aripirazole is only avid for D2, so bupropion can still result in increased dopamine activity at other dopamine receptors.
Aripiprazole would also be more on the agonist side of the partial agonist activity at low dose, so might have compound rather than opposing effect with bupropion in the case.
In select cases, you can treat someone with comorbid schizophrenia and ADHD with antipsychotic+stimulant (including amphetamines) with benefits for both conditions.

 

[clausewitz2]

Somewhat related...I saw someone today on bupropion xl 300daily + aripiprazole 5mg. I'm assuming the bupropion is not for smoking cessation. I left it for now, but in my head I'm thinking does this make any sense since these have opposing MOAs...

Wellbutrin's major active metabolite has more affinity for NET than DAT and its AUC is like 20x greater than bupropion itself so it's really more a norepi transport inhibitor anyway.

 

[calvnandhobbs68]

Somewhat related...I saw someone today on bupropion xl 300daily + aripiprazole 5mg. I'm assuming the bupropion is not for smoking cessation. I left it for now, but in my head I'm thinking does this make any sense since these have opposing MOAs...

It's illogical on its face but not particularly severely compared to a lot of nonsense we see... the type of thing if the patient isn't doing well I'd definitely change but if they were objectively doing well I'd probably shrug and leave be.

Guys you can't take MOA totally literally all the time either though (even though @clausewitz2 is totally right about the actual MOA of bupropion anyway). I wouldn't call it "illogical on it's face" at all.

I have absolutely had kids where I've had to go stimulant + abilify/risperidone and have had a response. There's been actual trials on stepped treatment with stimulant + antipsychotic too:

https://www.jaacap.org/article/S0890-8567(20)30064-2/fulltext

 

[Celexa]

Guys you can't take MOA totally literally all the time either though (even though @clausewitz2 is totally right about the actual MOA of bupropion anyway). I wouldn't call it "illogical on it's face" at all.

I have absolutely had kids where I've had to go stimulant + abilify/risperidone and have had a response. There's been actual trials on stepped treatment with stimulant + antipsychotic too:

https://www.jaacap.org/article/S0890-8567(20)30064-2/fulltext

My initial quick response is somewhat biased by the subpopulations I work the most with which include a lot of somatic symptoms/somatic delusions and hallucinating delirious inpatients. So I spend a lot more time thinking about the dopaminergic properties than the NE and easing patients away from it and other dopamine agonists. You're both absolutely right of course that it's an oversimplification of the mechanism of wellbutrin in the broader sense.