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Re: Dysthymia/Treatment Resistant Depressions

Posted by JohnB. on April 10, 1999, at 3:02:23

In reply to Re: Dysthymia/Treatment Resistant Depressions, posted by Elaine on April 9, 1999, at 23:16:52

Thanks for the interest in Dysthymia/Treatment Resistant Depression. I'm 37 and have had excruiting, chronic depression since age 15; needless to say, it's a subject near and dear to me. I've been trying different meds/cocktails for a dozen years with minor success. I've been involved in psychotherapy as well, which has been helpful. But, as many of you know, meds can help some but often never touch the core feelings of emptiness, hopelessness, and total inability to experience emotional satisfaction or pleasure. Joy and contentment are completely unknowable (unfeelable?) to me. So, I really latch on to any new medical stuff aimed at treating these "inner peace" symptoms.

Nick: Thanks for the info. I must say that I would agree that the classic neuroleptics aren't good choices for treating depression for the reasons you stated. However, the important point about the AYTYPICAL neuroleptic Amisulpride is its ability to enhance dopaminergic action at LOW doses and block dopaminergic action at HIGH doses, unlike the traditional anti-psychotics which block dopamine receptors generally. Dysphoric states would be expected from any dopamine blocker. Because Amisulpride doesn't block dopamine receptors at low doses and because it targets its dopamine enhancing action in specific emotion centers only, its action as a pharm at this dose is more targeted for mood disorders than for psychotic illness. Of course, chlorpromazine would be superior to placebo for depression; almost any drug would. But Amisulpride would clearly be superior to Chlorpromazine for treating depression because low dose Amis. enhances dop. where it counts and CHLORP. blocks dop. generally. I suppose you could say that Amisulpride (at low doses) wouldn't qualify being called a neuroleptic. We'll have to wait and see for further studies.

Elaine: I haven't read anything about Amulsipride and mania. My guess is that targeting dopamine receptors in the Limbic brain only might bypass any mania-triggering which seems to be more of an attentional/organizational/flow problem in moment-to-moment consciousness controlled at other sites in the brain. Just a guess, though. Most of this is just guesswork anyway, isn't it?

Anne: Nick wasn't lumping Effexor and Pazil into the neuroleptic class of drugs; he was merely listing AD drugs that had some indirect dopamine enhancing properties. The best way I know how to explain the seemingly contradictory dopamine enhancing abiltity of an otherwise dopamine blocking drug is that Amisulpride acts on dopamine differently at neuro-receptor sites. Some drugs stimulate the production of dopamine, some drugs block actions by agents that would otherwise remove available dopamine (re-uptake inhibitors), some drugs block dopamine receptors to prevent/reduce neurotransmission, and others act in other ways to facilitate the dopamine system. Amulsipride, like several new AD's, seems to target it's action even more specifically, in this case to dopamine receptors of the pre-synaptic neuron (as opposed to the neuron receiving the impulse, ie post--synaptic) The idea to remember here is that the drug is not doing its thing broadly/everywhere, so to speak. So, apparently when Amisulpride is taken a lower does, it's blockade of dopamine is limited to one neuron (pre-synapse only) which actually stimulates an increase in dopamine to compensate. At higher doses, this phenomenon doesn't occur and dopamine blockade is the result. HOW and EXACTLY WHERE a med acts at nerve receptor sites seems to be crucial, not so much for what the meds do but for how the nerons compensate for what the meds are doing.(which might make things worse) I hope I've helped some. It's all too complicated for me and there's so much science doesn't know!

Anyway, thanks again. Any more new information from anyone out there would be greatly appreciated.




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