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Hi guys, 

ive been on inVega sustenna for three months and my side effects are terrible on this drug. Blanking out, bad memory, lack of creativity, bad focus, slow mind and worse of all, anhedonia. Both sexual and emotional alike. It’s been three months and these things still have not lifted. I know it’s not my illness because my schizophrenia gives me heightened emotions and gets me high, and these side effects all started for the first time since I took the drug. 

Maintena is coming out in my country this December and I was thinking of asking my pdoc to switch to it. I heard that abilify can cause blurred vision and if you’re unlucky td, I’m scared of this. I’ve taken abilify tablet form before for around a week to a month or so at five milligrams, and didn’t get blurred vision or td, would anything change with the injection form? And also what is your experience on this drugs injection form? 

 

Regards.

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1 hour ago, themechanist said:

I Don't think that’s right. Seroquel is the one with the least cases of td, abilify and geodone have the highest rate of td amongst aaps. 

https://psychopharmacologyinstitute.com/antipsychotics/aripiprazole/mechanism-of-action-aripiprazole/

"From a pharmacological perspective, aripiprazole is different to other antipsychotic agents, as it is the only approved antipsychotic that reduces dopaminergic neurotransmission through D2 partial agonism, not D2 antagonism."

It is the antagonists that carry the higher risk for TD. To put it simply antagonists fully block dopamine whereas  partial agonists block partially. This lowers the chance of TD.

 

 

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abilify.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2730062/

"

RISK FACTORS FOR TARDIVE DYSKINESIA

Typical risk factors associated with the development of TD include older age, pre-existing movement or neurodegenerative disorders, female sex, the presence of affective illness, and neuroleptic exposure of more than six months.6 The use of higher-potency, first-generation agents is also more likely to increase the risk of TD and extrapyramidal symptoms (EPS). There is little doubt that conventional antipsychotic agents, compared with SGAs, are more likely to cause TD. However, among the SGAs currently available, those with more transient D2 receptor blockade and lower D2 affinity, such as quetiapine (Seroquel, AstraZeneca), are associated with the smallest risk, at least for EPS and probably TD.

At a therapeutic dose, it is noteworthy that aripiprazole has one of the highest D2 receptor affinities; however, because of its partial agonist properties, it has a lower risk of causing acute EPS and, probably, TD.710 A timely study of exposure to antipsychotic drugs in nongeriatric adults suggests that the incidence of TD with SGAs is 0.8%, compared with 5.4% with haloperidol, a high-potency, first-generation antipsychotic agent.11"

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On 9/3/2018 at 1:19 PM, Dewey said:

What is the lowest rate of TD of any AAP ?  I am currently taking Olanzapine (Zyprexa).

Thank you. 

Clozapine. In fact, it's even used sometimes to treat cases of TD caused by other antipsychotics.

Edited by Russ
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On 9/4/2018 at 1:16 AM, notloki said:

https://psychopharmacologyinstitute.com/antipsychotics/aripiprazole/mechanism-of-action-aripiprazole/

"From a pharmacological perspective, aripiprazole is different to other antipsychotic agents, as it is the only approved antipsychotic that reduces dopaminergic neurotransmission through D2 partial agonism, not D2 antagonism."

It is the antagonists that carry the higher risk for TD. To put it simply antagonists fully block dopamine whereas  partial agonists block partially. This lowers the chance of TD.

 

 

Thanks for your informative reply. What you say makes sense, however if I go by forums and anecdotal evidences then somehow it is an oxymoron. There are many reports online of td on abilify, especially when someone quits it or tapers after taking the drug for a few months. 

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1 hour ago, themechanist said:

Thanks for your informative reply. What you say makes sense, however if I go by forums and anecdotal evidences then somehow it is an oxymoron. There are many reports online of td on abilify, especially when someone quits it or tapers after taking the drug for a few months. 

Most misuse TD and don't know what it really is and how to diagnose it.

There is one constant though. Any drug that fools around with blocking D2 has at least a small chance of TD. 

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The tradeoff though of less risk for TD with Abilify is the higher risk of agitation and akathisia due to the higher intrinsic activity at the dopamine receptors. This can usually be overcome, though, with higher doses of Abilify which would lead to more blockade. When it comes to lowest risk for movement-related disorders, I'm pretty sure classically that clozapine and quetiapine take the cake with olanzapine coming in a close second:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1324958/

Quote

Clozapine fits all of the proposed definitions of atypicality. It has a low propensity for causing EPS after acute administration, does not produce tardive dyskinesia with long-term administration, and does not elevate plasma prolactin levels.

Clinical data indicate that quetiapine is associated with levels of EPS similar to those of placebo across the dosage range and is not associated with elevations in prolactin levels.4,49 It has been suggested that the atypicality of quetiapine may be explained by its ability to transiently occupy D2 receptors.4 This characteristic, unique only to quetiapine and clozapine, permits modest occupancy at the D2 receptors that rapidly declines to minimal levels 12 to 24 hours after the last dose.4,25,50 Like clozapine, quetiapine has a higher relative affinity for 5-HT2A receptors than D2 receptors. In a PET imaging study evaluating the D2and 5-HT2 occupancy of quetiapine at dosages of 150 to 600 mg/day, quetiapine was found to have minimal D2 occupancy (0%–27%) and high 5-HT2 occupancy (19%–94%) 12 hours after the last dose.50Thus, the low D2 occupancy of quetiapine combined with its ability to transiently occupy these receptors may explain the very low risk of EPS with this agent.4 Antipsychotic effects are achieved with rapid but transient binding (58%–64% D2 occupancy at 2–3 hours after a dose, declining to minimal occupancy by the end of a 12-hour dosing interval).50 This transient binding appears to be sufficient for clinical efficacy of quetiapine,50 while never approaching the 78% threshold of D2 occupancy necessary for EPS.

Clinical data suggest that the occurrence of EPS with aripiprazole is similar to that with placebo, and it does not appear to elevate prolactin levels.10,60 However, EPS and akathisia have been reported to occur during ari-piprazole therapy.10,64,65 In a PET study evaluating aripiprazole 0.5 to 30 mg/day in 15 healthy subjects, a dose response in D2- and D3-receptor occupancy was found. Receptor occupancy increased from below 40% at 0.5 mg to over 90% at 30 mg/day.66 These results suggest that administration of high doses of aripiprazole would lead to an increased risk of EPS; however, no EPS were observed in patients receiving high doses (30 mg/day) of aripiprazole in this study. The authors suggest that the lack of EPS may have to do with the partial agonistic activity of aripiprazole.66 However, in clinical trials evaluating aripiprazole for the treatment of schizophrenia and bipolar mania, akathisia has been reported.10,62 At this time, the data are too limited to draw definitive conclusions regarding the EPS profile of aripiprazole.

So basically, clozapine and quetiapine carry the lowest risk on paper because of the rapid dissociation from the dopamine receptors. Olanzapine has a similar dissociation interval which may underlie its low propensity for akathisia similar to that of quetiapine or clozapine. However, risperidone and ziprasidone seem to be more likely to cause EPS based solely on their receptor occupancy at therapeutic doses and higher propensity for elevated prolactin where quetiapine, clozapine, and olanzapine were less likely to cause this. And while aripiprazole did carry a paradoxically low rate of EPS relative to its dopamine receptor occupancy, as @notloki indicated, the partial agonist effect allows for some dopamine signaling, thus reducing the risk for EPS. This did not however, reduce akathisia, which is still fairly prevalent with aripiprazole treatment and could be explained by the higher intrinsic activity at dopamine receptors of that agent.

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