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Risperidone and Neurotransmitters: What Does My Experience Indicate?


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#1 dumbdumb

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Posted 31 December 2008 - 01:56 PM


Hi,

I feel like a real schmuck for mucking-up the noots section with a crazyheaddrug question, but I just don't think I'd trust any other public forum to give me a decent response to this question.
ImmInst has the most well-informed and sobre posters - I wouldn't be confident in the feedback I'd get elsewhere.
In any case, there's so much other junk in this section, I don't think it'll derail the board too much. I really, really appreciate the patience you guys will presumably show by allowing this post, and by reading it.

When I was in my mid teens, I was medicated with risperidone/risperdal. I had an overzealous doctor and gullible parents - I did not have schizophrenia, nor do I now.
Yet, while on risperidone, I was in something of a hypomanic if not manic state. My imagination was aflame with incessant exploration, my emotions were brilliantly intense, and I had a wonderful sense of humor.
I've never felt better, actually. It's now nearly ten years later, and I feel devoid of vitality in comparison to those days. Hence my interest in nootropics.
I don't know quite what to make of it all, though. See, I find lots of forum posts on the internet from people who took risperdal and feel that it sapped them of creativity, drive, libido, etc.
I feel sapped NOW - but I certainly didn't at that time. Quite the opposite. So I'm really confused about what that means in regards to how I am to best achieve a healthy brain presently.

My first question is, on the basis of the very simple outline typed above, can any conclusions be drawn about the predominance or lack of any particular neurotransmitters in my noggin, past and present?
Does it indicate that I am now experiencing a deficit in any neurotransmitter? Is that question even relevant?
For what little it might help to mention, I find myself craving dopamine, either in the form of tobacco or in supplements that boost it.

Secondly, and most importantly, is it likely that I felt great despite risperidone - or might it have been, on the contrary, because of it?
If I want to regain some measure of that great emotional wellspring I so enjoyed, ought I to begin on risperidone again? Is there any danger in giving it a try, considering my current dearth of vitality?

Finally, if it is logical to think that risperidone did, in fact, have a positive effect upon me, does it enter into the realm of possibility that other "antipsychotics" might prove even more beneficial?

Thanks again for reading. Have a Happy New Year's Eve.

#2 StrangeAeons

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Posted 31 December 2008 - 02:30 PM

I was overmedicated as a teenager too, and with antipsychotics no less; likewise, I was not actually psychotic. I'm assuming you took the original form of risperdone and not the shiny-new-sustained-release Invega (I got coerced into taking that crap about a year ago by a manipulative and egomaniacal psychiatrist). If so, it might have eliminated from your body fairly rapidly, and your hypomanic state was induced by an upregulation of dopamine receptors, or else some other type of rebound effect. It was probably not the direct action of the drug itself; however your current state might have something to do with the risperdone.

This is just stipulation, but I've found that over the 3 times I've been medicated with antipsychotics in the last ~9 years, things tend to deteriorate for me. Antipsychotics as a whole strike me as a very drastic class of drugs, and I think you should avoid them unless truly necessary. The only one I am even inclined to say is an exception is Abilify (aripiprazole), which has a very high affinity for D2/D3 receptors but exerts an agonist/antagonist effect; as a result it seems to have a somewhat different pharmacological profile. Even so, I would avoid it. Talk to a doctor first before going on any psychiatric meds, most especially antipsychotics.

Tobacco is a very poor choice for dopamine, especially in the frame of life extension. Tobacco supplies nicotine, which is cholinergic; which is functionally a nootropic, but not the best route to dopamine. The popular choice on the threads seems to be low dose selegiline, and in that vein I would recommend asking the doctor about Emsam, which is a transdermal selegiline patch recommended for atypical depression and refractory depression.

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#3 medicineman

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Posted 31 December 2008 - 04:13 PM

resperidone is a great drug in its class. If I was to be forced to be on a anti-psychotic, it would be resperidone. It has shown supreme efficacy and it has a clear side effect profile when compared to most anti-psychotics. I cannot draw a conclusion about your case, it is a bit odd. Too much time has elapsed for such a dopamine desensitization phenomena to persist. Do you have any other symptoms that you can mention?

-how is your mood?
-how is your sleep?
-appetite?
-active lifestyle?
-libido? concentration?
-do you interact well with other people?
-your thoughts? racing? faint?
-can you focus on a given assignment? can you read a book for half an hour without something inside you telling you to fuck the book out the window?
-is there any family history of ADHD, depression, schizophrenia, etc.

Resperidone is highly effective in many other areas. It is sedating, it alleviates depression, it increases appetite, it helps in autistic symptoms, can be used for OCD, bipolar disorder, and more.... in psychiatry, misdiagnosis occurs commonly, and a drug used to treat one disease, can alter the course of another. You could have been depressed, and the resperidone helped while it was intended to treat something else.

It seems more logical that you were depressed than any dopamine phenomena you think you might have.. thats just my opinion. have you tried SSRIs or SNRIs?

#4 j03

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Posted 31 December 2008 - 08:22 PM

I have a similar story that you put here. I told a couple doctors and they thought my story sounded absurd

In my teens i was an avid reader and possessed a vivid imagination. After I started on anti-depressants, and resperidone for anxiety I lost both those abilities. I have not read a fiction book in a long time, and do not get any pleasure from it, because my imagination is sapped.

I still feel hollow, and depersonalized most days, and lack motivation for even simple things. Before taking the medication i was different.

I developed dyskinesia (which has stopped), and a horrible case of TMJ(bruxism) that caused me a few years of intense pain (but which was somewhat cured with Rhodiola Rosea - I guess the dopamine boost from that) on those meds.

I was just suffering from a little bit of stress and anxiety at the point where i was prescribed the drugs, and displayed none of these symptoms.

I hope there's other people out there that felt this and found some cure. I would be very interested in hearing their stories. But I suspect as well it has something to do with dopamine. I only twice felt relief from the twitches and bruxism...once on the drug Remeron, and recently on Rhodiola Rosea

Edited by j033, 31 December 2008 - 08:40 PM.


#5 bgwithadd

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Posted 31 December 2008 - 10:20 PM

As medicineman asks for, we need more to go on. Knowing how you normally feel and how you normally felt when younger would be a big help. Did the doctor give any sort of diagnosis?

It could be that you ARE borderline schizo and that it cleared up your thoughts a bit. It could be you're depressed and it worked as a mood stabilizer to lift your depression. It could be that you have atypical bipolar disorder of some kind and that it worked to treat this condition, especially if you tend to be irritable/moody, and don't wake up easily or sleep easily.

If you had ADD and took this, you'd probably have very negative results so you can probably rule that out.

#6 StrangeAeons

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Posted 01 January 2009 - 01:57 AM

Too much time has elapsed for such a dopamine desensitization phenomena to persist.


This is the key problem I have with the "establishment" regarding antipsychotics. The notion that these drugs are transient in nature is, pure and simple, bullshit.
If I recall correctly, 80-90% of the dopamine receptors in the nigrostriatal pathway have to be damaged for tardive dyskinesia to occur; tardive dyskinesia is permanent, this is established medical fact. Now ask yourself, what's happening to the rest of your dopamine receptors before you've hit the point where this type of damage is painfully obvious? Why do so many anecdotal reports indicate that people "do not feel the same" after these drugs? Why does j033 report bruxism and dyskinesia? Why do I have akithisia while I'm awake and myoclonus in my sleep? The truth is, people on antipsychotics have poor prognoses because the drugs are generally tested on schizophrenics; the fact that this does not match the reality of them most commonly (painfully common, in my brief medical career) being used as "mood stabilizers" alters the criteria by which they should be assessed. There is, plain and simple, something slipping through the cracks about these drugs, most especially the esteemed "safe" atypicals.

As per somebody being "borderline" schizophrenic, I think you should study schizophrenia prodrome more. Schizotypy is very poorly understood, and there is very little empirical data to indicate the use of antipsychotics in somebody who is compensating; there are even studies indicating that a dopamine agonist might better aid cognitive impairment in these cases.

#7 OneScrewLoose

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Posted 01 January 2009 - 02:23 AM

I thought I'd add to this discussion by saying that I am on 300mg of Seroquel (antipsychotic) for anxiety and insomnia. It's works great, but it kinda craps on my memory. :( I hope to get off it eventually, as much of my anxiety and insomnia has come from stomach problems I didn't know about and that are only now being treated.

#8 medicineman

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Posted 02 January 2009 - 05:09 PM

Too much time has elapsed for such a dopamine desensitization phenomena to persist.


This is the key problem I have with the "establishment" regarding antipsychotics. The notion that these drugs are transient in nature is, pure and simple, bullshit.
If I recall correctly, 80-90% of the dopamine receptors in the nigrostriatal pathway have to be damaged for tardive dyskinesia to occur; tardive dyskinesia is permanent, this is established medical fact. Now ask yourself, what's happening to the rest of your dopamine receptors before you've hit the point where this type of damage is painfully obvious? Why do so many anecdotal reports indicate that people "do not feel the same" after these drugs? Why does j033 report bruxism and dyskinesia? Why do I have akithisia while I'm awake and myoclonus in my sleep? The truth is, people on antipsychotics have poor prognoses because the drugs are generally tested on schizophrenics; the fact that this does not match the reality of them most commonly (painfully common, in my brief medical career) being used as "mood stabilizers" alters the criteria by which they should be assessed. There is, plain and simple, something slipping through the cracks about these drugs, most especially the esteemed "safe" atypicals.

As per somebody being "borderline" schizophrenic, I think you should study schizophrenia prodrome more. Schizotypy is very poorly understood, and there is very little empirical data to indicate the use of antipsychotics in somebody who is compensating; there are even studies indicating that a dopamine agonist might better aid cognitive impairment in these cases.


60-70% destruction of nigrostriatal dopamine manifests as parkinsons. according to your numbers, everyone on anti-psychotics is a walking to be-parkinsonian.

but i wont disagree with your main point. some doctors are trigger happy with their prescription pads, and research on anti-psychotics are still underway. anti-psychotics such as resperidone and quetiapine are much more easier to tolerate, and they don't manifest the extrapyramidal symptoms as bad as their cousins do. of course they are not side effect free like anything else..

#9 StrangeAeons

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Posted 03 January 2009 - 06:20 PM

60-70% destruction of nigrostriatal dopamine manifests as parkinsons. according to your numbers, everyone on anti-psychotics is a walking to be-parkinsonian.

but i wont disagree with your main point. some doctors are trigger happy with their prescription pads, and research on anti-psychotics are still underway. anti-psychotics such as resperidone and quetiapine are much more easier to tolerate, and they don't manifest the extrapyramidal symptoms as bad as their cousins do. of course they are not side effect free like anything else..


OK, so my numbers were off a tad; it's still by and large acknowledged that the longer you take antipsychotics, the higher your risk of TD/EPS; so in a way I agree with your inference. There are other dopamine systems to worry about, too. My point was to merely use one pathway as an example; the gist is that you can extrapolate there may well be similar damage to other pathways that flies under the radar. When I was on Geodon back in my teens the stuff made me damned near narcoleptic; but I couldn't sleep if I didn't take it. My sleep patterns are more messed up than ever now. Likewise, it's been nearly a year since I've taken Invega and for some reason my prolactin levels came back elevated twice in the past few months.

As per the atypicals as a whole, I'd say metabolic syndrome is pretty nasty too. The data on weight gain I saw with risperidone and olanzipine was downright depressing. Insulin resistance is a bitch, too. I think docs should prescribe atypicals with metformin at the very least for people who are already obese, and get routine bloodwork done.

Getting back to the OP's point, I'm sticking to my "rebound effect" theory. If you ask for risperidone in a shrink's office, you will likely get Invega (paliperidone) which is risperidone in a shiny new time-release capsule that comes out as a hollow shell in your poop. Hooray!

I'd advise against trying antipsychotics again, but should you try the Invega and notice it's effects different than Risperdal, I'd venture to say my rebound theory was correct.

#10 Ben

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Posted 04 January 2009 - 01:17 AM

I too was prescribed risperidone as a teenager by an overzealous psychiatrist who incorrectly thought I was schizophrenic (Am detecting a pattern here?) Since, I've felt different, I used to be very mentally sharp and focussed and feel as if I've lost a lot of that, hence my interest nootropics.

Edited by Ben - Aus, 04 January 2009 - 01:19 AM.


#11 bgwithadd

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Posted 04 January 2009 - 11:32 PM

As per somebody being "borderline" schizophrenic, I think you should study schizophrenia prodrome more. Schizotypy is very poorly understood, and there is very little empirical data to indicate the use of antipsychotics in somebody who is compensating; there are even studies indicating that a dopamine agonist might better aid cognitive impairment in these cases.


Yet you are saying that it's due to the reaction to the med, which makes no sense at all. A reaction is not going to be stronger than the first action. These drugs have a strong effect on blotting out anxiety and that can help tremendously with schizophrenia (or a variety of other problems). That's almost certainly why it helped the original poster, but the real question is what is the original problem?

#12 StrangeAeons

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Posted 05 January 2009 - 03:21 AM

Yet you are saying that it's due to the reaction to the med, which makes no sense at all. A reaction is not going to be stronger than the first action.


This is a massive fallacy. Look up the serotonin theory of depression, and why it turned out to be a myth. The true antidepressant properties of SSRI's were not a result of an increase in serotonin, but rather of a complex biological response to the initial MOA. Likewise more directly, the theory behind low dose naltrexone is upregulation through antagonism, which is identical to the hypothesis I have put forth regarding the OP.

#13 bgwithadd

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Posted 05 January 2009 - 08:22 AM

Yet you are saying that it's due to the reaction to the med, which makes no sense at all. A reaction is not going to be stronger than the first action.


This is a massive fallacy. Look up the serotonin theory of depression, and why it turned out to be a myth. The true antidepressant properties of SSRI's were not a result of an increase in serotonin, but rather of a complex biological response to the initial MOA. Likewise more directly, the theory behind low dose naltrexone is upregulation through antagonism, which is identical to the hypothesis I have put forth regarding the OP.


Sorry, but it's not disputable that antipsychotics can improve schizophrenia symptoms (which is not to say it's the best possible treatment).

I wasn't referring to naltroxene at all anyway, which is a red herring to this thread in the first place.

Edited by bgwithadd, 05 January 2009 - 08:23 AM.


#14 StrangeAeons

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Posted 05 January 2009 - 05:51 PM

Sorry, but it's not disputable that antipsychotics can improve schizophrenia symptoms (which is not to say it's the best possible treatment).

I wasn't referring to naltroxene at all anyway, which is a red herring to this thread in the first place.


Did I ever contend that antipsychotics can't improve symptoms? This is beside the point, we have no conclusive reason to believe the OP is schizophrenic. To assume because they responded to antipsychotics that they were schizophrenic would be quite a revelation in psychiatric diagnosis, don't you think?
The effects described in response to the risperidone in this post seem somewhat paradoxical to the typical effects of dopamine antagonism. I indicated LDN as a counterargument to your allegation that a "secondary" action could not be more prominent than the initial MOA, and LDN is in fact directly analogous to my assertion that it was possible there was an increase in dopaminergic activity from the risperidone; notably the advent of Invega indicates that a controlled-release form was advantageous, and this could easily be because a paradoxical response in a patient that was schizophrenic would worsen their symptoms. This may not have been the universal response, but there are undoubtedly idiosyncratic responses likely due to individual hepatic metabolism and other forms of elimination.
Entirely aside from that hypothesis, there is the matter of 5HT2A antagonism to consider in the instance of atypicals; this would likewise explain the more anti-depressive effect of risperidone on the poster, in which case they would fare far better on Trazodone or possibly even Tianeptine.

#15 dumbdumb

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Posted 05 January 2009 - 08:01 PM

Hello again, everybody.

Sorry to have taken a while to respond. First of all, thanks a million to everyone who's taken the time to read and reply; I appreciate all the feedback.
Let me begin by answering the specific, numbered questions asked of me:
1. My mood is terribly inconsistent. Some days pass by in a gray blur of lethargy and sulleness, while on others I awaken by leaping out of bed with a song in my heart, pledging to make the most of the day. I am, in any case, never content with myself.
2. My sleep is better than most peoples'. Approximately 8 hours a night, beginning from 7 PM to 9 PM and waking usually before sunrise.
3. My appetite is also inconsistent. Sometimes I am disgusted by the thought of eating, but on some days I am positively voracious for the entire day. On such days, I have an unusual craving for meat and sweets.
Skipping a few now, since they're answered further on.
My libido has also decreased since I was younger, but I still feel that I could engage in sexual activity at least four days a week.
My concentration is awful; I'm all over the place. Can't stay put in a book or behind a paper. I'm always trying to find a distraction to bring some quicker form of gratification; typically, videos or stories that are humorous, or simple games.
I interact very well with other people; I regret afterwards not having acted differently, but nevertheless I always seem to particularly good impressions upon people, even when I fear I've done the opposite.
There's all kinds of crazies in my family. Couldn't begin to list the various problems. But they all seem rather different from me; I'm not remotely like any of those people, don't act or think or speak as they do.


I'm not asserting that risperidone killed my creativity, as some others have - quite the opposite, I was at my most creative while I was on it. It is precisely because this condition seems contrary to the experiences of so many other people that I posted this question. I just can't understand why it would be so. PetaKiaRose's theory of receptor sensitivity makes sense, though I'm not sure how to use that knowledge to improve my present dearth of certain cognitive/emotional qualities that I believe I used to enjoy a greater wealth of.

I had been particularly imaginative, emotional and energetic for the whole of my life; taking risperidone did not bring this condition about, nor did ceasing to take risperidone end it. It only so happened that the time in my life at which I had the greatest intensity of emotion and curiosity coincided with my taking risperidone. There may be no relation whatever, but I thought it a very interesting question as to why any sort of hypomania (or symptoms of it) should be able to occur in a person taking risperidone, as, according to everything I've read, the medication should effectively snuff that sort of thing out.

Allow me to clarify: I am not asking this forum how to treat schizophrenia. I do not have schizophrenia. I am just trying to get some clearer picture of the particulars of my neurochemistry, to aid me in plotting the most effective course of exploration into the realm of nootropics. Presently, I'm inclined towards selegiline, though I am finding the combo of bacopa, ashwagandha and rhodiola rosea to be pretty envigorating presently - along with the standard stack of ALCAR, Piracetam, Aniracetam, DL Phenylalinine, AlphaGPC, Multi-Vitamins, Sulbutaiamine, Chocamine, Idebenone, yadda yadda yadda. I might as well mention that, again contrary to the experiences of others, when I boost my dopamine with these various supplements or with tobacco, I have far less of a temper than I do when unsupplemented; an increase of dopamine seems to have the opposite effect on me in that regard.

Before I was on risperidone, I was on prozac, during which time I was still very energetic and inquisitive, but not to the same extent as I was while on risperidone.
After the risperidone, I took one called "geodon," which quelled my excitibility markedly, as well as my pruning the outgrowing branches of my personality; I became contemplative and introverted on it.
I ceased taking it, and my personality reverted to a state not altogether dissimilar from my situation while on risperidone, however all of my perceived qualities were, as I've indicated before, less intense.

Since that time, they have continued to fade; I am 24 now, and the past four years a blur, really, as if out of a dream, during which I felt no great impulses that I could retain with any consistency; I've lost enthusiasm for my plans and discoveries, very much unlike myself as I was before turning 20.

I've been taking far better care of myself in all respects during the past four years than I had at any time previously. I weighed over 200 lbs when I was 16, and reached a peak of 250 at the age of 20. By 22, I had come down to 170, and though I've gained some of that back, I remain in much improved physical condition and consume far healthier foods, while exercising regularly.

I don't claim to be saying anything of any value with my thread here; I'm not trying to posit and conclusions on anything. The whole point is that I'd just like to understand my brain's peculiarities better, since I'm clueless as to why it should be functioning in the manner it has.

Thanks again, take care.

Edited by dumbdumb, 05 January 2009 - 08:38 PM.


#16 bgwithadd

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Posted 05 January 2009 - 09:27 PM

Did I ever contend that antipsychotics can't improve symptoms? This is beside the point, we have no conclusive reason to believe the OP is schizophrenic. To assume because they responded to antipsychotics that they were schizophrenic would be quite a revelation in psychiatric diagnosis, don't you think?

I didn't assume that at all. That's just one of half a dozen possibilities I brought up.

The effects described in response to the risperidone in this post seem somewhat paradoxical to the typical effects of dopamine antagonism.

Not really. Much like most antidepressants they can have a blunting affect, it's typical for someone who actually has a serious problem to improve when medicated with mood stabilizers because the negatives are far outweighed by the positives. It will likely help dramatically with someone who has bipolar, anxiety, schizophrenia, and possibly with other problems as well.

Also, plenty of people don't get the negative effects of the atypical antipsychotics at all.

I indicated LDN as a counterargument to your allegation that a "secondary" action could not be more prominent than the initial MOA, and LDN is in fact directly analogous to my assertion that it was possible there was an increase in dopaminergic activity from the risperidone; notably the advent of Invega indicates that a controlled-release form was advantageous, and this could easily be because a paradoxical response in a patient that was schizophrenic would worsen their symptoms. This may not have been the universal response, but there are undoubtedly idiosyncratic responses likely due to individual hepatic metabolism and other forms of elimination.

It's possible, but it seems like a very remote possibility that depends on a freak mutation that doesn't seem to be documented anywhere before now.

Entirely aside from that hypothesis, there is the matter of 5HT2A antagonism to consider in the instance of atypicals; this would likewise explain the more anti-depressive effect of risperidone on the poster, in which case they would fare far better on Trazodone or possibly even Tianeptine.

That's possible, too, but it's another out there possibility because it's such a weak mechanism.

Edited by bgwithadd, 05 January 2009 - 09:29 PM.


#17 bgwithadd

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Posted 05 January 2009 - 09:43 PM

Hello again, everybody.

Sorry to have taken a while to respond. First of all, thanks a million to everyone who's taken the time to read and reply; I appreciate all the feedback.
Let me begin by answering the specific, numbered questions asked of me:
1. My mood is terribly inconsistent. Some days pass by in a gray blur of lethargy and sulleness, while on others I awaken by leaping out of bed with a song in my heart, pledging to make the most of the day. I am, in any case, never content with myself.
2. My sleep is better than most peoples'. Approximately 8 hours a night, beginning from 7 PM to 9 PM and waking usually before sunrise.
3. My appetite is also inconsistent. Sometimes I am disgusted by the thought of eating, but on some days I am positively voracious for the entire day. On such days, I have an unusual craving for meat and sweets.
Skipping a few now, since they're answered further on.
My libido has also decreased since I was younger, but I still feel that I could engage in sexual activity at least four days a week.
My concentration is awful; I'm all over the place. Can't stay put in a book or behind a paper. I'm always trying to find a distraction to bring some quicker form of gratification; typically, videos or stories that are humorous, or simple games.
I interact very well with other people; I regret afterwards not having acted differently, but nevertheless I always seem to particularly good impressions upon people, even when I fear I've done the opposite.
There's all kinds of crazies in my family. Couldn't begin to list the various problems. But they all seem rather different from me; I'm not remotely like any of those people, don't act or think or speak as they do.


I'm not asserting that risperidone killed my creativity, as some others have - quite the opposite, I was at my most creative while I was on it. It is precisely because this condition seems contrary to the experiences of so many other people that I posted this question. I just can't understand why it would be so. PetaKiaRose's theory of receptor sensitivity makes sense, though I'm not sure how to use that knowledge to improve my present dearth of certain cognitive/emotional qualities that I believe I used to enjoy a greater wealth of.

I had been particularly imaginative, emotional and energetic for the whole of my life; taking risperidone did not bring this condition about, nor did ceasing to take risperidone end it. It only so happened that the time in my life at which I had the greatest intensity of emotion and curiosity coincided with my taking risperidone. There may be no relation whatever, but I thought it a very interesting question as to why any sort of hypomania (or symptoms of it) should be able to occur in a person taking risperidone, as, according to everything I've read, the medication should effectively snuff that sort of thing out.

Allow me to clarify: I am not asking this forum how to treat schizophrenia. I do not have schizophrenia. I am just trying to get some clearer picture of the particulars of my neurochemistry, to aid me in plotting the most effective course of exploration into the realm of nootropics. Presently, I'm inclined towards selegiline, though I am finding the combo of bacopa, ashwagandha and rhodiola rosea to be pretty envigorating presently - along with the standard stack of ALCAR, Piracetam, Aniracetam, DL Phenylalinine, AlphaGPC, Multi-Vitamins, Sulbutaiamine, Chocamine, Idebenone, yadda yadda yadda. I might as well mention that, again contrary to the experiences of others, when I boost my dopamine with these various supplements or with tobacco, I have far less of a temper than I do when unsupplemented; an increase of dopamine seems to have the opposite effect on me in that regard.

Before I was on risperidone, I was on prozac, during which time I was still very energetic and inquisitive, but not to the same extent as I was while on risperidone.
After the risperidone, I took one called "geodon," which quelled my excitibility markedly, as well as my pruning the outgrowing branches of my personality; I became contemplative and introverted on it.
I ceased taking it, and my personality reverted to a state not altogether dissimilar from my situation while on risperidone, however all of my perceived qualities were, as I've indicated before, less intense.

Since that time, they have continued to fade; I am 24 now, and the past four years a blur, really, as if out of a dream, during which I felt no great impulses that I could retain with any consistency; I've lost enthusiasm for my plans and discoveries, very much unlike myself as I was before turning 20.

I've been taking far better care of myself in all respects during the past four years than I had at any time previously. I weighed over 200 lbs when I was 16, and reached a peak of 250 at the age of 20. By 22, I had come down to 170, and though I've gained some of that back, I remain in much improved physical condition and consume far healthier foods, while exercising regularly.

I don't claim to be saying anything of any value with my thread here; I'm not trying to posit and conclusions on anything. The whole point is that I'd just like to understand my brain's peculiarities better, since I'm clueless as to why it should be functioning in the manner it has.

Thanks again, take care.

It sounds like you have ADHD to me.

The obvious reason is the lack of concentration and the inability to control what you say but there's lots of others in there. "I had been particularly imaginative, emotional and energetic for the whole of my lifeow self esteem", lack of self awareness, weight up and down, craving for sweets.

Drugs like this can be used to treat ADHD, especially for people who are hyper. It's hardly the best treatment because antipsychotics have side effects that suck, but it can actually help with the focus when your mind is racing all over the place.

Because of your sleep patterns, I really doubt it's bipolar of any kind.

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#18 medicineman

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Posted 05 January 2009 - 10:09 PM

Informative post I must say. But back to the OP.

Have you had your thyroid levels checked? I wouldn't say you are depressed as defined by the DSM criteria. You do have atypical symptoms. But thats the thing, no one is a text book or a syndrome fact sheet. Do you have panic disorder?

I know this sounds out of bounds, but what do you think about yourself? Are you happy with the way you look? Are you sensitive to rejection? Do you sometimes take comments a bit seriously?

You said on days you eat like crazy, especially sweets and such. This is more or less a sign of comfort eating. Do you go through phases of weight gain and loss frequently? And one last question. Your mood, does it change during the progression from day to night? Do you feel better or worse as the day goes by?

I think resperidone might have been overkill. My uncle had a slight constant lowering of mood. He engaged in such activities as comfort eating, doing other things he normally wouldn't do just to try to lift his mood up (funny he didn't attribute his actions to his mood). At first I thought he was bipolar. But after speaking to him, I realized that his mood was at a constant mild low. He didn't even seem to know it too well. He spoke to a psychiatrist, who prescribed him a low dose of amisulpride, and lo and behold, he is much better.

Let me just tell you a bit about amisulpride. What is different about this anti-psychotic is the fact that at low doses, it actually improves dopaminergic transmission. It is also safer than conventional neuroleptics. In high doses, it starts to exert its ability to black dopamine. Before hopping on another neuroleptic, do explore your options regardind SSRI's, or MAOI's.




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