Posted by KaraS on November 8, 2004, at 0:14:16
In reply to Re: resuming the thread » KaraS, posted by zeugma on November 7, 2004, at 13:07:13
>>...about the dangers of Seroquel. Still, I think it's bad practice to prescribe an AP for an AD side effect. You should by all means tell your friend about your concerns.
I think I'm going to post something here to see what kind of feedback I get on the issue of using Seroquel or Amisulpride for anxiety/depression respectively. Risk vs benefit.
> > > > > That's a commendable aim. I thought I was killing two birds with one with the nortriptyline/methylphenidate combination. As my pdoc said, though, I seem to have killed one bird- the narcolepsy, not the ADD.
> >
> > I thought it was the other way around.
> >
> Well, so did I. Strattera helped my ADD, but at the cost of intolerable s/e. Provigil also helped my ADD, to a much greater extent than Strattera, but again at an intolerable cost. Ritalin does increase my responsiveness. I mean this in the sense that sleep specialists do: it is easier to get a reaction from me on Ritalin than when not medicatated, just as it's easier to rouse someone from stage 1 sleep than from stage 4.
>
> It is interesting that on the website Stanford University's center for sleep research, Strattera has been added to the list of narcolepsy meds. This is in keeping with my observations, that Strattera reduced cataplectic attacks to zero, until I added Klonopin. Of course it is not a stimulant, and worsens EDS, but it is a very powerful REM suppressor, in keeping with its affinity for the NE transporter.Yet the Strattera did end up making you tired eventually...
> I had an episode of hypnagogic hallucinations last night, during the 'trough' period for nortriptyline to take effect. I think the Ritalin helped, because I was awake enough to not look at the hallucinatory content (i.e., I 'closed my eyes' during the dream). So I think that Ritalin makes me more wakeful, although I'm still fatigued and the heightened 'responsiveness' may actually aggravate my ADD, by speeding my reaction time, in contrast to Provigil, which slowed it. It's a complicated situation I have here.If I understand this correctly, the "fix" for one problem may have a detrimental effect on the other so you're trying to find some kind of balance that you can function on - and your next test is to see if Ritalin LA 60 mg. will be the answer?
> > I can only imagine since I haven't experienced anything like it. It doesn't sound like you are able to be upfront about any of this with the people you work with or for. That must make it all the more difficult.
> >
> > Well, people last year saw me crash on caffeine and Strattera, but those crashes made me virtually speechless, and so I said nothing. Crashing on ritalin causes the anger I mentioned before, and I have been so alarmed about the feelings of those around me, as well as for my job itself, that I have explained my condition to several colleagues. I am hoping that the 30 mg Ritalin LA am, plus 30 mg LA pm, will keep my methylphenidate levels high enough for a long enough time that this effect doesn't happen.Telling some of your colleagues must have been a relief. I hope that they were understanding and supportive.
> > > > > Abilify MIGHT not be an agent that causes TD. It is still a new med so it is still uncertain, but I recall reading an article that compared its structure to clozapine, an agent known not to cause TD.
> >
> > Yes, it's always to soon to say for sure until a med has been around for a long time and tested out in the real world.
>
> Well, I think Abilify can cause marked akathasia, but it is only a partial agonist of the D2 receptor, and while partial agonists by their nature have ambiguous effects (compare with buspirone), I do think that it is safer from a TD pov than anything other than clozapine. Clozapine, by the way, is an option, although (get this) it requires weekly blood monitoring. I would think that it would be an option for anyone with severe, treatment-resistant depression. But not a pleasant one. Maybe less pleasant than ECT. But its efficacy is striking.>An AP and once a week labs - definitely last resort. Good to know there are other options I guess.
>I think that statement is an index of your level of depression :( I hope you can find something soon that helps. I've probably asked this before, but are you experiencing complete anhedonia?
I have had a rough couple of days. Definitely anhedonic now but overall I have not been. Hope this doesn't last because I really feel terrible now. I think it's related to some recent events and that it will change once some things calm down.
> [about Parnate]
> >
> > Yes, very seriously. I just left my doctor a message to that effect. It's one of the most powerful ADs there is and it might have the potential to reduce the density of the DA autoreceptors. All indicators seem to be pointing in that direction now. I'm terrified to try it though for many reasons - the biggest of which is that it seems like it's one of the strongest, most comprehensive ADs. If this doesn't work, what hope would I have left?
> >
>
> Well, I understand your reluctance. One thing that may (or may not) console you is that MAOI's are NOT considered the most broadly effective AD's by everyone, although this is highly disputed. Most meta-analyses suggest that amitriptyline and clomipramine are the most effective of all AD's.Really? Good old Elavil? You're the second one recently to bring up Anafranil. Why do the best ADs have to cause weight gain? I still have it in my mind that Parnate is the next thing to try for me. I like the idea that the serotonergic activity isn't unopposed. Do you believe I'm thinking about this correctly given my condition?
ECT is supposed to be the most effective of all treatments. One study I read suggested that nortriptyline, if kept in a plasma level range of 90-130 ng/mL, is as effective as ECT.
I would love to try nort again if I could do something about the tachycardia. I loved the energy I had on it. What about Pindolol with it?
> All of these drugs have idiosyncracies that makes response a highly individual matter, although some effects, such as Strattera's anticataleptic effect, would probably qualify as universal given the close association between NE reuptake inhibition and REM suppression.Didn't know that. With REM suppression, can the sleep be adequate or restorative?
(Dreaming, by the way, can occur in the absence of REM, although cataplexy can't. There is a particular anatomical reason for this that would take this parenthesis beyond the bounds of relevance.) There is also the matter of the therapeutic relationship between pdoc and patient. If this is suboptimal, it may interfere with your response.
>
> > What did you and your doctor decide your next move should be?
>
> I am doing the dosing change. He also told me that my response to meds was more typical of a narcolepsy than a pure ADD patient. This helps me in that it clarifies aspects of my diagnosis.You've suspected this for quite some time now, no?
My next move is to meet with my ADD coach this week. These, I understand, are not drastic moves. But there are no obvious, drastic moves that i can see right now.
>Maybe tweaking is what you need to try now while you work on the nonmed therapy.
Kara
poster:KaraS
thread:406397
URL: http://www.dr-bob.org/babble/20041103/msgs/413098.html