Posted by Rick on August 23, 2001, at 21:54:54
In reply to Re: SP Cocktail - Your Questions+Surprise Enhancer (?), posted by PaulB on August 23, 2001, at 15:29:35
Paul -
Interesting thoughts.
I think it's worth remembering, though, that an understanding of social phobia in physiological terms is just now beginning. And from the research and expert postulating I've seen, it looks as if the etiology will prove to be extremely heterogeneous. Besides, treatments that shouldn't work in theory often end up working very well (and certainly vice versa, too). This led me back to Thomas Kramer's wonderful “jolt the system” article on “Mechanisms of Action” in Medscape. At the beginning of the essay, he wisely states:
“The question of putative mechanisms of action continues to haunt psychopharmacology. Put simply, we know these drugs work, but we have very little idea how. We make guesses based on the neurochemical effects of these compounds. We have very little proof, and sometimes very little data, about whether the neurochemical effects that we find have anything to do with the therapeutic effect of the medication.”
He then talks about a European serotonin reuptake *enhancer* (!) that defies all logic by working well for depression.
If you’d like to read the whole article – highly recommeded – go to:
http://www.medscape.com/medscape/psychiatry/journal/2001/v06.n01/mh0116.kram/226620.html
(Free but requires simple registation; medical credential NOT required.)But I will include his conclusion here:
“The crucial point in any discussion of mechanisms of action of psychotropic medication is to maintain a healthy respect for our ignorance. Fundamentally, we have no idea how these medications work. It is the nature of high-quality scientific discourse to postulate plausible theories and try to prove or disprove them. When any currently accepted theory no longer explains all of the data, it must be either modified or discarded. Psychopharmacology has had its share of discarded theories. We once thought that schizophrenia was exclusively a disease of dopamine and that depression was exclusively a disease of deficit of either serotonin or norepinephrine. Lately, we have been focused on the idea that "less is more" as far as the mechanisms of action of our medications. It is certainly true that as we have developed medications with less side effects, patients are more likely to take them regularly and stay on them, and, as such, these newer medications have more effectiveness than older ones. We must always remember, however, that until we figure out exactly what psychiatric illness is on a neurochemical level and what medications that seem to make it better actually do, all mechanisms of action for any effective medication may have potential benefit.” (Not surprisingly, Kramer also wrote an insightful defense of polypharmacy: http://www.medscape.com/medscape/psychiatry/journal/2000/v05.n03/mh0509.kram/mh0509.kram.html )
When you say, "I was less enthusiastic about Provigil," are you saying that you used it and was dissatified, or are you saying that its properties don't make sense for anxiety (or both)? Klonopin and Provigil work very nicely together for me, and regarding Serzone's potentiating effect, note that I'm taking about half as much Klonopin as I needed when my only other med was Celexa (and this was before Provigil was added with its stimulating effects). Who knows, concomitant Klonopin and Prvigil may not work for anyone besides Craig and I, but I am ever so grateful I hit on my combo.NG-D 97-1 sounds extremely promising and exciting. AS for the bz anxiety-receptor specific alluded to, it sounds as if benzo originator Roche is in the early stages of working on something with such a proile (press release:
http://www.roche.com/med-corp-detail-2000?id=21).
> Other psycho-babblers suggested Xanax(Judy1) and Provigil(AndrewB). From my experience there is a difference in the level of cognitive impairment and memory problems induced by these two drugs. Xanax causes fewer problems and it is a marked difference.
Are you saying that Provigil causes more memory decline than Xanax?? Or are you indirectly referring back to Klonopin? Regardless, I was surprised to see some recent complaints about memory loss from Provigil, given that it's often viewed as a nootropic memory-enhancer. But I notice that the Provigil monograph does mention some incidence of memory impairment (subjective?) relative to placebo. (Don't know if it's significant.) Now THAT got me thinking...
It's well known that Klonopin can cause episodic amnesia, though not necessarily in everyone. And it's well known that Serzone and other AD's can cause this too, although some of that might be attributable to unresolved depression or inaccurate subjective assessment of memory. Sorry about jumping back and forth here...but since it's unlikely I have more Klonopin in my bloodstream than pre-Serzone (remember, I was taking more K then), wouldn't the amelioration of memory loss upon temporary Serzone discontinuation implicate Serzone as the source of my memory impairment, rather than Klonopin?
Related to that question, here's one thing I've long wondered. Perhaps that sole Klonopin user who has managed to get to this point in my rambling might be able to offer up some thoughts: Specifically, assuming X amount of Klonopin can lead to amnesic effects in someone, can it take a full year or more for this effect to surface? I had minimal memory deficit (it's still not huge, just inconvenient) for the full year that I took 2-3 mg Klonopin minus any AD.
Thanks for the great food for thought.
Rick
poster:Rick
thread:36517
URL: http://www.dr-bob.org/babble/20010822/msgs/76183.html