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JJ17

Zyprexa vs Risperdal for OCD

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1 hour ago, cakepop said:

Have you ever tried Anafranil??

No, I haven’t. Have tried many SSRIS though at high doses, such as:Prozac up to 80mg (2010 or so). Lexapro 30mg. Zoloft 200mg (currently on) and Paxil 40mg. I wonder if the TCA will actually be any more effective then SSRIS since they both have the same goal, in regards to serotonin. But maybe it is... 

Also in response to the other comments sometimes “getting high” can make intrusive thoughts worse for me, but also it had the ability to make me feel artificially happy so that if I had intrusive thoughts they would be stupid/funny things. So normally isn’t an issue. 

But tonight is the worst I have felt in probably over a decade. The only difference is I took 15mg hydrocodone for pain, both physical and emotional pain. It doesn’t seem to blunt my emotions at all. Maybe 

In fact simply thinking about the person I love (which I cannot control, those are the really only intrusive thoughts I ever have) is making me feel like dying to end this misery is a now an option. Why, why can’t I find a medicine to simply help blunt my emotions so I don’t feel suicidal over loving someone who doesn’t love me back? My emotions are normally 1000x more intense than the “average person” so without Benzos and SSRIS I don’t think i’d Still be alive. BUT... Instead of feeling my emotional pain X1000? The Benzos and SSRIS reduces it to maybe only X 200 worse.

Basically even when on multiple drugs that are known to cause emotional blunting which I’m on 3: SSRI, Risperidone, and Benzos - well, my emotions aren’t even blunted!! They are still so intense that I’m back to feeling suicidal. 

I even took an older hydrocodone prescription in hopes it would help numb the intense emotional pain - nope! I still feel so shitty that I could jump off a bridge. I guess my emotional pain is so strong that I still feel intense emotional pain after taking freaking Benzos, SSRI, antipsychotic, AND opioids? 

I really don’t know what else to try or do anymore 

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Before I was diagnosed with anything I was obsessed over someone for about 5 years. Couldn't stop thinking about her no matter what I was doing at the time.

The way I see it, it has more to do with the obsessional part of OCD rather than being intrusive thoughts.

Prozac (80mg) and Zoloft (300mg) didn't seem to be effective enough.

TCAs hit a lot (!) more receptors than SSRIs, Anafranil is considered very effective for OCD for a reason. Besides, it is more of an SNRI than SSRI, if anything.

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13 hours ago, HydroCat said:

Before I was diagnosed with anything I was obsessed over someone for about 5 years. Couldn't stop thinking about her no matter what I was doing at the time.

The way I see it, it has more to do with the obsessional part of OCD rather than being intrusive thoughts.

Prozac (80mg) and Zoloft (300mg) didn't seem to be effective enough.

TCAs hit a lot (!) more receptors than SSRIs, Anafranil is considered very effective for OCD for a reason. Besides, it is more of an SNRI than SSRI, if anything.

Do you think it’s worth a try? I didn’t know it hit more serotonin receptors, that’s good to know. Would it’s added noradrenaline possibly worsen OCD and anxiety though? Or is it’s sertonin action so strong it doesn’t matter? 

My obessive love is so bad that if I don’t get a text message back I assume they no longer care and I can get suicidal. It’s so bad words cannot describe it. I can barely get out of of bed everyday. I haven’t left the house in 3 months! Besides to get food, which is walking distance. 

Haven’t been looking for a job, the pain from the obsessive love thoughts is SO intense I simply cannot function. I cannot even hold down a job. After research I found “obsessive love disorder” and it’s the ONLY disorder that is 99.9% accurate. Problem? It is so rare (affects only 0.1% of population) and not fully understood or known.

I haven’t tried therapy. I also have no insurance so that doesn’t help. Well, I tried talk therapy like 7 or so years ago and it didn’t help. In fact they gave me some stupid advice like “why not fall in love with someone who you don’t find extremely attractive and attached to?” Uhh if I had any control over who I love I wouldn’t even have the problem. 

This sucks. I need something to shut out the obessive love thoughts (and the anxiety it causes) but so far no medication has worked 

Edited by JJ17

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The specific disorder you mentioned may be rare but I believe the same treatment that works for OCD would probably at least help with this one too.

SNRIs are better for me than SSRIs were, the noradrenaline action is more energizing/motivating, it may help you get out of bed and do stuff. Cymbalta was great for me for quite some time.

The reason that SSRIs are first line treatment instead of TCAs is that the latter, because of hitting more receptors, tend to cause more side effects. That being said, they are not less effective and many times they are even better.

 

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The key to treating OCD seems to be ultra-high occupancy of the serotonin transporter, which is why maximal doses of serotonin reuptake inhibitors are required to achieve therapeutic response in OCD. It just so happens that clomipramine has one of the highest affinities for the serotonin transporter and it's also dosed very high, allowing it to achieve maximal occupancies (>80%). Clomipramine also is a modest dopamine antagonist which may contribute to its positive effect on OCD.

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1 hour ago, browri said:

The key to treating OCD seems to be ultra-high occupancy of the serotonin transporter, which is why maximal doses of serotonin reuptake inhibitors are required to achieve therapeutic response in OCD. It just so happens that clomipramine has one of the highest affinities for the serotonin transporter and it's also dosed very high, allowing it to achieve maximal occupancies (>80%). Clomipramine also is a modest dopamine antagonist which may contribute to its positive effect on OCD.

I tried clomipramine for my OCD, for a good while.......I was on it for about a year......Went all the the way up to 250mg, which is the max recommended dose.

Even at this high dose, it did not improve my obsessions or compulsions at all.

YMMV though, I do think clomipramine is worth a shot if you have OCD....Works well for some folks, but unfortunately, not for me........Nothing I've tried has ever worked for my OCD--still suffering greatly from it.

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15 hours ago, browri said:

The key to treating OCD seems to be ultra-high occupancy of the serotonin transporter, which is why maximal doses of serotonin reuptake inhibitors are required to achieve therapeutic response in OCD. It just so happens that clomipramine has one of the highest affinities for the serotonin transporter and it's also dosed very high, allowing it to achieve maximal occupancies (>80%). Clomipramine also is a modest dopamine antagonist which may contribute to its positive effect on OCD.

Wikipedia claims it can reach 100% occupancy with chronic dosages. Think it’s true? 

It says:

A positron emission tomography study found that a single low dose of 10 mg clomipramine to healthy volunteers resulted in 81.1% occupancy of the SERT, which was comparable to the 84.9% SERT occupancy by 50 mg fluvoxamine.[52] In the study, single doses of 5 to 50 mg clomipramine resulted in 67.2 to 94.0% SERT occupancy while single doses of 12.5 to 50 mg fluvoxamine resulted in 28.4 to 84.9% SERT occupancy.[52] Chronic treatment with higher doses was able to achieve up to 100.0% SERT occupancy with clomipramine and up to 93.6% SERT occupancy with fluvoxamine.[52] O

 

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Which also makes me wonder.... Is fluvoxamine perhaps the “gold standard” for OCD when it comes to SSRIS? That’s pretty high occupancy for it. Possibly higher then even Paxil, but not certain. 

 

Also kinda confused how again does Risperidone potentiate THC? If someone can explain in a simple way lol. I mean being a “dopamine blocker” it seems like it would weaken its dopamine actions, no? I’m wondering if it actually weakens THC, as the one day I missed a dose I felt THC more. 

I mean I understand the whole “by blocking dopamine here it actually will cause in increase in ____ area” I understand that, but doesn’t Risperidone aim more towards serotonin? 5HT2A? Then as the dose increases it starts to block more dopamine..... but it seems like risperidone doesn’t block nearly as much dopamine as some of the “typical” meds. As it just sounds like it’s properties (Risperdal) will always make it more blocking of serotonin over dopamine. Even at increased doses it’s still going to be swayed more toward sertonin, no? 

Confusing med. 

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8 hours ago, JJ17 said:

Wikipedia claims it can reach 100% occupancy with chronic dosages. Think it’s true? 

It says:

A positron emission tomography study found that a single low dose of 10 mg clomipramine to healthy volunteers resulted in 81.1% occupancy of the SERT, which was comparable to the 84.9% SERT occupancy by 50 mg fluvoxamine.[52] In the study, single doses of 5 to 50 mg clomipramine resulted in 67.2 to 94.0% SERT occupancy while single doses of 12.5 to 50 mg fluvoxamine resulted in 28.4 to 84.9% SERT occupancy.[52] Chronic treatment with higher doses was able to achieve up to 100.0% SERT occupancy with clomipramine and up to 93.6% SERT occupancy with fluvoxamine.[52] O

 

Yes it certainly can. Remember, clomipramine is dosed up to like 225mg a day or so despite its high affinity for SERT, which means that at high dose and regular usage, you could obtain maximum SERT occupancy

5 hours ago, JJ17 said:

Which also makes me wonder.... Is fluvoxamine perhaps the “gold standard” for OCD when it comes to SSRIS? That’s pretty high occupancy for it. Possibly higher then even Paxil, but not certain. 

Clomipramine was the gold standard for the long time and still kind of is. But I would say of the SSRIs, fluvoxamine has become the gold standard. Because it's an SSRI, it's theoretically more tolerable than TCAs, and therefore, they would try you on that first then move to clomipramine if it didn't work out.

A doctor who was feeling heroic can also prescribe these together as well. The body breaks down clomipramine into desmethylclomipramine (DMC) which is less of a serotonin reuptake inhibitor and more of a norepinephrine reuptake inhibitor. It just so happens that fluvoxamine inhibits the metabolism of clomipramine into DMC allowing you to "give preference" to the parent drug and reduce exposure to the metabolite. This method is usually down in slow escalating doses.

5 hours ago, JJ17 said:

Also kinda confused how again does Risperidone potentiate THC? If someone can explain in a simple way lol. I mean being a “dopamine blocker” it seems like it would weaken its dopamine actions, no? I’m wondering if it actually weakens THC, as the one day I missed a dose I felt THC more. 

I mean I understand the whole “by blocking dopamine here it actually will cause in increase in ____ area” I understand that, but doesn’t Risperidone aim more towards serotonin? 5HT2A? Then as the dose increases it starts to block more dopamine..... but it seems like risperidone doesn’t block nearly as much dopamine as some of the “typical” meds. As it just sounds like it’s properties (Risperdal) will always make it more blocking of serotonin over dopamine. Even at increased doses it’s still going to be swayed more toward sertonin, no? 

Confusing med. 

In some ways risperidone can potentiate THC and in others it blocks it. THC activates CB1 receptors which triggers downstream dopamine release. Risperidone does this as well via 5HT2A antagonism (potentiation). However, risperidone also blocks dopamine receptors, which can modulate some of THC's activity.

Keep in mind that for a medication, it has an affinity for that receptor and in escalating doses it has different occupancies which are partially based on the dose and the compound's affinity for a given receptor or transporter. Occupancy is measured in a percent and describes how many of the dopamine receptors are occupied by risperidone at a given dose.

Typically, dopamine receptor occupancies of 80% or so are required for sufficient antipsychotic effect. However, at lower doses of risperidone, you wouldn't be achieving occupancies of the dopamine receptors this high. I'm not sure what risperidone's occupancies are at given doses, but we'll say for example that 1mg might render 50% occupancy of dopamine receptors. Then you still have 50% of the receptors that THC could activate with its downstream dopamine release.

But wait, it gets weirder. Dopamine blockade ENCOURAGES more dopamine release. It's part of the feedback loop. When receptors sense activation, they slow down the release of the neurotransmitter that activates them to basically "control the flow". So by blocking SOME of the dopamine receptors, you induce dopamine release with the potential to activate unoccupied or less-occupied receptors.

Also remember that some AAPs are preferential to certain pathways in the brain as you mentioned. For example, aripiprazole (Abilify) is more preferential to the mesocortical/mesolimbic pathways (which is preferred as this is where the antipsychotic effect comes in) and tends to not disrupt dopamine signaling in the striatum which can lead to motor side effects, prolactin elevations, etc.

Finally, keep in mind that all AAPs have a generally higher affinity for serotonin receptors than for dopamine receptors. This means that at lower doses, most of these drugs are in fact more serotonergic. With a higher affinity for serotonin receptors, meaningful occupancy can occur at lower doses with less occupancy of dopamine receptors due to their lower affinity for them. The net result is an antidepressant and anxiolytic effect that works perfectly as a booster to antidepressants.

Drugs like SSRIs indiscriminately increase serotonin signaling which inherently suppresses dopamine neurotransmission, leading to things like anhedonia. Symptoms of depression like this that oftentimes don't respond to an antidepressant, typically respond to a compound that will have a net increase in dopamine signaling. This is why bupropion (Wellbutrin) is so often used as a booster to pure SSRIs like escitalopram (Lexapro). However, as I indicated, low dose AAPs can have a similar dopaminergic effect by blocking serotonin receptors and restoring some of the dopaminergic function.

At higher doses though, you lose some of the antidepressant effect of risperidone by occupying a higher level of dopamine receptors. Like my example with the SSRI that after weeks of treatment suppresses dopamine signaling, once you get to higher doses of AAPs, the positive effect that you get of dopamine activation via serotonin blockade is washed out by the fact that you're also blocking most of the dopamine receptors and thus you would again feel anhedonic. Some might call it "AP-induced depression".

Let me know if any of this doesn't make sense or if you have other questions.

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Thanks, and yes that makes sense. I believe Risperidone occupancy for 5HT2A is around 80% and around 50-60% for D2. That is, at 1mg, which is my current dose. 

But.... I need dopamine and also need it reduced. Like I cannot win here lol. Increased dopamine gives me motivation, energy, and makes social interactions not as bad. I actually feel somewhat “normal” after smoking pot. It used to make me paranoid as hell 10 years ago. Only difference is my brain was a teenagers back then - now I’m grown and also been on max dose SSRIS for like a year straight. So maybe the SSRIS somehow cancel out the marijuana induced paranoia, for me. As I just feel content. 

Same thing with other dopamine releasers/reuptake inhibitors such as Ritalin and Dexedrine - they make me feel more confident, content, talkative, motivated, etc. Which sometimes that helps distract me from my obession over someone - but sometimes it can make the anxiety feeling worse. Generally though boosting dopamine in me seems to have drastic positive effects. Just anxiety can get worse, and my love obessions if I’m not in a good mood or what not. Which my love obsessions control my life’s emotions.... 

I’m fact the only reason I take Risperidone is in hopes it will reduce my obession over someone I love. I don’t know what part of the dopamine reward system part of the brain that is thought to occur in - but if you happen to know: is there a better option then Risperidone if my ENTIRE goal is to suppress obessive love thoughts/feelings/etc? 

I mean if I do NOT take pot, Ritalin, adderall, or something like that I feel not only depressed and blah for the day, but my love obessions are still around in full force. So it seems even when “low on dopamine” I might get apathy towards life in general, but my love obessions doesn’t go away. If I boost dopamine (via the meds I mentioned above like Ritalin) I feel way better overall, but my love obessions are somewhat intensified - yet at the same time I feel better overall so I can distract myself much easier to get my mind off it, to something positive....So yeah, I dunno. 

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On 1/13/2019 at 4:15 AM, JJ17 said:

Thanks, and yes that makes sense. I believe Risperidone occupancy for 5HT2A is around 80% and around 50-60% for D2. That is, at 1mg, which is my current dose. 

Right so the net result there would be dopamine modulation but not necessarily blockade. Because you block 5HT2A more potently and you're also blocking D2 at about 50%, at that dose it leans more towards dopamine enhancement, because both activities result in dopamine release with the dopamine blockade making sure it doesn't get "out of control".

On 1/13/2019 at 4:15 AM, JJ17 said:

But.... I need dopamine and also need it reduced. Like I cannot win here lol. Increased dopamine gives me motivation, energy, and makes social interactions not as bad. I actually feel somewhat “normal” after smoking pot. It used to make me paranoid as hell 10 years ago. Only difference is my brain was a teenagers back then - now I’m grown and also been on max dose SSRIS for like a year straight. So maybe the SSRIS somehow cancel out the marijuana induced paranoia, for me. As I just feel content. 

Well serotonergic enhancing agents generally increase serotonin activity which will reduce dopamine release, thus staving off some of THC's psychotomimetic effects. Just the same, THC should temporarily restore dopamine signaling and thus reduce SSRI-induced side effects like anhedonia, agitation, and insomnia.

On 1/13/2019 at 4:15 AM, JJ17 said:

Same thing with other dopamine releasers/reuptake inhibitors such as Ritalin and Dexedrine - they make me feel more confident, content, talkative, motivated, etc. Which sometimes that helps distract me from my obession over someone - but sometimes it can make the anxiety feeling worse. Generally though boosting dopamine in me seems to have drastic positive effects. Just anxiety can get worse, and my love obessions if I’m not in a good mood or what not. Which my love obsessions control my life’s emotions.... 

I’m fact the only reason I take Risperidone is in hopes it will reduce my obession over someone I love. I don’t know what part of the dopamine reward system part of the brain that is thought to occur in - but if you happen to know: is there a better option then Risperidone if my ENTIRE goal is to suppress obessive love thoughts/feelings/etc? 

I mean if I do NOT take pot, Ritalin, adderall, or something like that I feel not only depressed and blah for the day, but my love obessions are still around in full force. So it seems even when “low on dopamine” I might get apathy towards life in general, but my love obessions doesn’t go away. If I boost dopamine (via the meds I mentioned above like Ritalin) I feel way better overall, but my love obessions are somewhat intensified - yet at the same time I feel better overall so I can distract myself much easier to get my mind off it, to something positive....So yeah, I dunno. 

So in that case a combination of an antidepressant+risperidone+stimulant should modulate most steps in that path. The antidepressant+risperidone increases serotonin signaling overall while preventing certain serotonin receptors from being activated thus modulating the serotonin system and increasing dopamine release. Then the stimulant+risperidone works to increase dopamine release but also modulate at the "receiving end" (post-synaptically on D2). 

I agree that dopamine in particular is frustrating because you need it but you also need to control it. This is why I love my current combo. On its own, Trintellix not only increases serotonin signaling (via serotonin reuptake inhibition) but increases signaling of several other neurotransmitters as well by blocking certain serotonin receptors (5HT1A agonism increases dopamine output, 5HT3 antagonism increases dopamine, histamine, acetylcholine, and norepinephrine output, blockade of 5HT7 and 5HT1D and partial agonism of 5HT1B increases serotonin output). Enhance that with Rexulti (further 5HT1A agonism, 5HT2C partial agonism, 5HT2A antagonism, 5HT7 antagonism, all leading to increased norepinephrine and dopamine output as well as serotonin for 5HT7) and you've got a solid antidepressant effect. Then Vyvanse+Rexulti (dopamine releasing agent combined with dopamine receptor partial agonism) modulates the dopamine pathway for me. Depakote controls serotonin turnover (metabolism) and synthesis of new catecholamines like dopamine, norepinephrine, and epinephrine and increases my brain's GABA supply thus reducing my need for moderate dose benzos for anxiety. Mix the increased GABA supply with Rexulti's potent alpha adrenergic antagonism and you've got a pretty strong anxiolytic effect as well even with the Vyvanse on-board, and the adrenergic blockade actually leads to more serotonin release making Rexulti both a direct full agonist of the 5HT1A receptor and an indirect agonist via adrenergic blockade. It's a very dynamic cocktail which has suited me very well, and I do have obsessive rumination problems similarly to you.

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I’m not sure how long I’ve been on Risperidone now for.... 2 months? Or so. I also started on clomipramine recently. Last 10 or so days I feel very “BLAH” like I could find out I’m dying tomorrow and would be okay with it. 

For risperidone I went up to 2mg a couple of times but went back down to 1mg, and have been on 1mg for roughly 2 months or so.  

But... for the past 10 or so days I have been taking 25mg of clomipramine per night. In addition to my max dose SSRI + Risperidone + other meds. Doctor was fine with it. 

But Now? Now I feel kind of “blah”. No, rather EXTREMELY “blah”. I don’t even want to drive 30 seconds across the street to the grocery store. I have no motivation, or energy really. I feel like all those people who complained “SSRIS made me feel little emotions or like a zombie” - that’s probably me right now, yet my OCD is still around. I will say that my love attachment doesn’t cause me instant anxiety and urge to jump off a bridge ASAP (as it did before) instead now? Now I still feel depressed/unmotivated, PLUS I still feel my OCD issues, just to a lesser extent. So it helps somewhat but damn it’s making me feel BLAHHHHHHH. 

My sertonin must be sky high from 200mg Zoloft + 25mg clomipramine + 5HTP + L-Tryptophan and melatonin combo I take at night. While all these medications somewhat reduces my OCD/love issues, I can still unfortunately feel it. Which sucks. 

I literally cannot do ANYTHING until I take my prescribed Ritalin (gives me some energy and motivation) OR I have to smoke pot. Otherwise I have zero motivation/energy. My guess is the dopamine boost from either pot or Ritalin is what “helps my mood temporarily”. Which I don’t want to have to do either of those things to have enough motivation to even go outside... 

Im trying to figure out what’s more likely to be the cause of zero motivation/energy: Risperidone OR clomipramine? Maybe the Risperidone took a couple months to kick in for the apathy.... Or maybe it’s the clomipramine. I don’t know. 

Edited by JJ17

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From what you describe it seems to me like one of these:

(in my opinion the first ones are more likely)

1. Serotonin reuptake options are maxed out. If so, Buspar may be helpful because for the 5HT1A receptor it mimics the effect of serotonin, leading to downstream dopamine release.

2. Serotonergic meds took you so far but you actually need a noradrenaline/dopamine boost. Have you tried Wellbutrin somewhere along your  way?

3. You may be taking too much of serotonergic drugs in a way that your serotonin receptors are desensitized (the SSRI “flat affect”)

I'm leaving the MAO option out at this time.

P.S. not a doctor, just an OC guy with too much interest in psychopharmacology.

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5 hours ago, HydroCat said:

From what you describe it seems to me like one of these:

(in my opinion the first ones are more likely)

1. Serotonin reuptake options are maxed out. If so, Buspar may be helpful because for the 5HT1A receptor it mimics the effect of serotonin, leading to downstream dopamine release.

2. Serotonergic meds took you so far but you actually need a noradrenaline/dopamine boost. Have you tried Wellbutrin somewhere along your  way?

3. You may be taking too much of serotonergic drugs in a way that your serotonin receptors are desensitized (the SSRI “flat affect”)

I'm leaving the MAO option out at this time.

P.S. not a doctor, just an OC guy with too much interest in psychopharmacology.

I agree with HydroCat's assessments here.

1. There's nothing in your cocktail doing 5HT1A agonism. Some people have described buspirone (Buspar) as being good for anxiety but activating as well in some ways due to the downstream dopamine release. If you talk to your pdoc about buspirone, the recommendation would be to keep the dose lower to avoid the dopamine receptor blockade that buspirone can have in higher doses. Alternatively, you could replace the sertraline (Zoloft) with vilazodone (Viibryd) or vortioxetine (Trintellix) to get the 5HT1A agonism. I personally found vilazodone to be quite activating, and I find vortioxetine to be similarly activating, but vortioxetine has actually improved my sleep, whereas if I didn't take vilazodone before 9AM, there was no sleeping that night.

If you do add on buspirone to your current sertraline+clomipramine cocktail, you could talk to your pdoc about coming down on the sertraline to the average dose of 50mg. The 5HT1A agonism from buspirone will make lower doses of antidepressants "go further".

2. Sertraline in higher doses actually has a modest affinity for dopamine transporter (DAT) inhibition similarly to bupropion (Wellbutrin). However, bupropion will likely give you more bang for your buck. You could work with your pdoc to reduce the sertraline to 50mg and add 150mg of bupropion to balance out the cocktail a bit more. Alternatively, you could go for California Rocket Fuel (venlafaxine(Effexor)+mirtazapine(Remeron)) although theoretically, you could achieve a similar effect with any norepinephrine reuptake inhibitor combined with alpha adrenergic receptor type 2 antagonism. If you didn't want to overhaul the entire cocktail, you could talk with your pdoc about a combo of sertraline+bupropion+mirtazapine. Mirtazapine will block alpha-2 adrenergic receptors which will cause downstream serotonin release and thus indirect agonism of 5HT1A. It will also block 5HT2C which will increase norepinephrine and dopamine release. Then bupropion will inhibit the norepinephrine and dopamine transporters (and sertraline will inhibit SERT, and even DAT as well at higher doses) to make those three neurotransmitters persist in the synapse. The net result should be dramatically increased signaling of serotonin, norepinephrine, and dopamine. 

3. A very good point...200mg of sertraline is a very high dose and it doesn't surprise me that you feel kind of flat and unmotivated at this point, even with the DAT inhibition at that dose. And you might be moving into risperidone doses that won't help you any further for SSRI-induced anhedonia (e.g. 2mg). Remember that with increasing serotonin, the brain will try to push down dopamine signaling as a balancing act. So you want to work with your pdoc to find a cocktail that strikes a balance among serotonin, norepinephrine, and dopamine. Right now your cocktail is really serotonin heavy, thus inhibiting dopamine neurotransmission and that is compounded by the dopamine antagonism from risperidone.

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Not much of a contribution, but I find this topic really interesting. 

I take 125 mg of clomipramine and although it seemed like it was working (my intrusive thought was a lot less frequent in the last few months) I still relapsed about two weeks ago. Initially 125 mg was helping, but now I'm having the same continuous intrusive thought again. Very frustrating. 

I think my brain keeps adjusting to serotonergic medication, it just doesn't do anything special anymore.
And side effects are tolerable, but I have a lot of different side effects right now (all mild, but still annoying) and I wonder if I shouldn't go back to an SSRI since clompramine and SSRI's essentially work the same.

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So I changed my meds again... 

Added 150mg Wellbutrin and it’s only been roughly a week and already noticed more talkative/motivated/etc. But I also have increased anxiety (nothing too bad) and sometimes upset stomach. This is the ONLY antidepressant that I felt side effects from at a standard dose (even if mild) but at the same time it seems like mild side effects means the medicine is working, at least for me. 

NOW... As for Risperidone I have been on 1mg for 4-5 months now, and tried 2mg for 3-5 days, didn’t notice a difference so went back down to 1mg. I’m pretty sure 5 days or so isn’t enough time to work, though. But I also didn’t notice any side effects from Risperidone, it almost feels like “I take nothing”. Maybe I need a higher dose? Maybe my brain only responds to higher doses? 

As I have the same “issue” with SSRIS. I had no side effects from: Paxil, lexapro, Prozac, or Zoloft at normal doses - and no positive changes either - so it felt like I was “taking nothing”. It wasn’t until I went to the max or higher dosage (40mg-60mg  Paxil, 200mg Zoloft) that I felt minor side effects, but also at the same time felt some benefit from the medicine. Maybe some minor side effects are a sign they are working (at least for me) ? I think my brain is so used to so many medicines that it takes high doses to even affect me, both side effect wise and benefit wise. 

As far as Risperidone and OCD, what method of action is believed to help OCD? At 0.5 mg to 1mg it’s “weak” in terms of D2 dopamine blocking. It isn’t until 2mg that it supposedly reaches the D2 occupancy needed for antipsychotic effects. BUT I don’t know if that matters when using it to try and treat OCD. Is higher D2 occupancy from Risperidone a good or bad thing for Obessive thoughts? Since I don’t feel anything from taking 1mg maybe I need to up the dose? 

 

Edited by JJ17

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AFAIK it is unclear which mechanism actually causes intrusive thoughts.

Again, only from my personal experience, Amisulpride (a pure D2/D3 antagonist) was useless for my intrusive thoughts, while both Risperidone and Abilify (D2/D3+5HT2A antagonists) were pretty good.

So a higher dose may do the trick, not only because of D2 occupancy.

Besides that, a low dose will have more antagonist action on presynaptic D2 receptors and as the dose goes up it gradually occupies postsynaptic D2 too. I am not sure if that is a good or a bad thing though, never went past the 1mg.

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1 hour ago, JJ17 said:

NOW... As for Risperidone I have been on 1mg for 4-5 months now, and tried 2mg for 3-5 days, didn’t notice a difference so went back down to 1mg. I’m pretty sure 5 days or so isn’t enough time to work, though. But I also didn’t notice any side effects from Risperidone, it almost feels like “I take nothing”. Maybe I need a higher dose? Maybe my brain only responds to higher doses? 

As I have the same “issue” with SSRIS. I had no side effects from: Paxil, lexapro, Prozac, or Zoloft at normal doses - and no positive changes either - so it felt like I was “taking nothing”. It wasn’t until I went to the max or higher dosage (40mg-60mg  Paxil, 200mg Zoloft) that I felt minor side effects, but also at the same time felt some benefit from the medicine. Maybe some minor side effects are a sign they are working (at least for me) ? I think my brain is so used to so many medicines that it takes high doses to even affect me, both side effect wise and benefit wise. 

This sounds familiar to me. Although from SSRI's I did have a lot of effect in the first 5 years, but side effect wise I just had restless legs and vivid dreams (with higher dosages). It didn't really feel like I was on medication and I could even miss a few pills without getting into trouble. 
Some people get side effects from 5-10 mg's of Lexapro but I needed 20 mg in order for it to work.

With risperidone it also feels like "I take nothing", only the first day it made me sleepy because I took it in the morning instead of before bed. 
But I haven't been on it that long (just over a week), so I can't tell if I will have any benefit. If it does kick in it would be the ideal med for me: better sleep, a clearer mind during the day and no troubling side effects. 

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