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Please be patient with me as part of why im asking is from my ocd, not to make any questioning of meds. I just want some positive reassurance.


Just recently i had my risperdal increased to 3 mg to augment citalopram for ocd, depression. Thing is im nervous because i know it starts blocking a lot of dopamine.


I know it cant be as simple as dopamine d2 equals pleasure and motivation? Im hoping the D1 receptors are more important and that the risperdal wont induce any worsening of anhedonic tendencies or amotivation in me. Surely its alpha 2 blockade may increase serotonin and norepinephrine.


I guess im worried about two things. I hope i didnt just max out on the antidepressant properties of risperdal at 2 mg and now 3 is just a heavy dopamine blocker as hopefully its serotonin receptor occupancy will also increase dose dependently


Plus im worried about all these things that implicate dopamine in reward and hope it isnt so clear cut that it will become problematic


Perhaps anyone knowledgable can help elucidate my concerns or knowledge


Thx and sorry about any trouble/ if my post is unclear

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I've been reading a lot on psych meds, neurotransmitters, binding affinity and whatnot.

It was interesting to know what X is supposed to do and what it actually does for my condition.

I noticed that I tend to dive deeper and deeper into the subject when my OCD is out of balance. So that's part of it.

My pdoc does provide “technical” info about the treatment, but he explained to me once that there are so many factors to take into account (metabolism, enzyme interactions, drug-drug interaction, adjustments, receptor up/downregulation and whatnot...) that trying to put things together by reading through the internet is impossible and doesn't improve anything, if not the opposite.

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On 10/17/2020 at 6:11 AM, the maze runner said:

Don't take high doses of risperidone. It will make you anhedonic and robotic.

Any robotic feelings i have are actually before i started risperdal and if its not from an endogenous disorder itself, i simply attribute it to my ssri but i have to take that, been on ssris for over a decade, if not i feel terrible even if i may have directly or indirectly more emotional sensitivity.

Anyway i was hoping for some positivity from people saying their antipsychotic did not make them anhedonic

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The reason that quetiapine and risperidone are oft-used in treatment-resistant OCD is because it is vaguely understood that while dopamine acts as a pleasure chemical and part of the brain's task-reward system, in the hands of someone with OCD, dopamine can also act to chemically reinforce obsessional tendencies. Anything that promotes dopamine can in fact exacerbate obsessional tendencies in individuals who are susceptible. 5HT2A antagonism from AAPs can promote norepinephrine and dopamine release, which can agitate obsessional tendencies in addition to its antidepressant qualities. Amphetamines typically exacerbate obsessive compulsive disorders likely via dopamine efflux. So on and so forth. Think about how addictive cocaine is and how it can reinforce certain behaviors. Now imagine a brain that metaphorically self-administered itself little bits of a similar rewarding substance to reinforce obsessional tendencies, and this is kind of the brain on OCD.

Clomipramine was always regarded as the gold standard for OCD because it had among the highest affinity for the serotonin transporter (next to paroxetine among a few others) and could be dosed to insanely high blood levels that would saturate the transporter to a degree that couldn't be achieve with other serotonin reuptake inhibitors. In addition, chronic inhibition of the serotonin transporter and subsequent chronic stimulation of central serotonin receptors (e.g. 5HT1A) leads to a downstream reduction in the release of dopamine. This may seem strange, but this is an important part of the antidepressant effect. You are less likely to obsess over the things that bother you when dopamine signaling is lower. Inadvertently, however, you cause anhedonia because you intrinsically stop CARING. Hence pairing an antidepressant with an AAP to promote norepinephrine and dopamine release while simultaneously stabilizing dopamine receptors (dopamine antagonism / partial agonism), thereby preventing any of the other problems caused above. In addition, clomipramine is a weak, albeit modest, dopamine antagonist. This may underscore its capability against OCD at high doses.

The same can be said for risperidone. Lower doses preferentially antagonize pre-synaptic dopamine auto-receptors (D2-short) and 5HT2A heteroreceptors, both of which lead to a release in dopamine. With escalating doses, antagonism of post-synaptic dopamine receptors (D2-long) dampens this antidepressant effect. From person to person it varies, but it happens somewhere <2mg. It's important to recognize that this blunting could very well be an important part of your effective treatment, and it shouldn't be written off.

Edited by browri
various terrible spelling and grammatical errors.

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