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Re: My Disappointment here + My early years SLS

Posted by undopaminergic on August 24, 2021, at 12:36:42

In reply to Re: My Disappointment here + My early years undopaminergic, posted by SLS on August 24, 2021, at 10:36:02

> Hi, UD.

Hi SLS.

> > I've also had temporary remissions with some drugs, such as pramipexole which transiently resolved even my stubborn anhedonia.
>
>
> Maybe you should try combining Nardil with pramipexole? Between Nardil and Parnate, I found Nardil to be a much better anti-anhedonic drug.
>

Interesting. The difference between them is essentially the GABAergic metabolite of Nardil, and Parnate's "amphetaminergic" action.

Yes, I would definitely want to try a classic MAOI, but I don't have a "MAOI doctor".

I also want to re-try pramipexole at higher doses, but given that they think I have schizophrenia, I don't think I would be able to get it.

A combination? Yes, why not?

My initial move was to try a higher dose of Surmontil (I'm on 150 mg), but the doctor didn't like that, so we agreed to try Latuda, and next, I'm going to suggest a switch to asenapine (Sycrest, Saphris). That will be the last antipsychotic for this round. Next after that? Substitute another TCA for Surmontil? Try vortioxetine? But I've lost most of my interest in that one after the failure of Latuda to elicit any effect; I was hopeful about its serotonin 5-HT7 antagonism. I'm also thinking of combining a SSRI with an antipsychotic that blocks serotonin 5-HT2A and -2C, so maybe I'll suggest sertraline to be added to the asenapine. What do you think?

> It is also pro-social. However, mania can occur with Nardil, especially in bipolar disorder. I would be prepared and have on hand Zyprexa (olanzapine) as an antidote. It should work quickly, and you might be able to continue with Nardil and discontinue the Zyprexa once you get through the critical period early in treatment. Euphoria is a common experience for people in the very beginning of treatment, even people who are not bipolar. However, even without intervention, it usually resolves in unipolars. People often go chasing the eurphoria afterwards with dosage escalation.
>

Well, at least I don't think I would have a problem getting Zyprexa. In fact, I was only able to get them to stop it in connection with starting clozapine.

> > > It was an amazing coincidence that I saw his name on one of the doors while sitting in the waiting room for my very first visit to a psychiatrist. I was accepted into the research program at Columbia Presbyterian / New York Psychiatric Institute in 1982.
>

I would like to get involved in research, but I don't know how.

> > > All they had to work with were MAOIs, tricyclics, and lithium.
>
> > Really only those? What about antipsychotics like chlorpromazine, stimulants like methylphenidate and amphetamine, barbiturates and benzodiazepines?
>
>
> Good point. I was referring to depression, but I should have been more specific. Stimulants were definitely used as prior to the serendipitous discovery of MAO inhibitors in the late 1950s. They were then used primarily as augmenters. At the time I entered the program in 1982, Xanax (alprazolam) was being looked at for depression, with good reason. It is the most euphoric of the benzodiazepines.
>

It's my understanding that it has been revisited more recently?

As for recreational benzodiazepine use, not all users prefer alprazolam. Why's that, if it's the most euphoric?

> In addition, another benzodiazepine, adinazolam, was also being looked at for depression. I tried in 1984, I believe. My doctor, Baron Shopsin, was surprised to see it work so well for some of his patients. I experienced *no* sedative or anxiolytic effect. It was amazingly clean, but it didn't produse an improvement in my depression. I think adinazolam is approved in Japan.
>

There are interesting drugs available for prescription in some countries. In Japan and many other Asian countries, there is, for example, a drug called nimetazepam which is particularly sought after by recreational users.

> So is rolipram, a phosphodiesterase inhibitor. I imagine it works intracelullarly along the second-messenger cascade.
>

I remember reading about that many years ago.

>
> One other thing. While I was a research patient at the NIH in 1992, I was one of the first people to have his brain imaged by a PET scan. Not fun. My head was completely immobilized in a cast of my face and head. The image on the left is almost exactly like mine.
>
> https://www.mayoclinic.org/-/media/kcms/gbs/patient-consumer/images/2017/05/15/20/19/c7_pet_depression-8col.jpg
>

Interesting!

-undopaminergic


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