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cache-monkey

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  1. Dreamer- Thanks for the input. So ADD could definitely be in the mix. The worry with meds is that the physical restessness gets worse in the long run with meds. I'm wondering what your son's experience has been. I.e. did it seem that when the meds wore off (or when/if he tapered them) that his tics/restlessness were worse than before starting? ~cache-monkey
  2. Thanks for the suggestion. I actually did try that briefly, but only at a very low dose per my pdoc's directions (lowest dose in the starter pack). I don't remember what else I was on along with it, but I do remember getting "augmentation". I.e. as the Requip wore off, I felt physically worse than worse. Blargh ... more weight on the "my dopamine system is royally fucked" hypothesis. I wish there was a real dopamine system stabilizer. ~cache-monkey
  3. Hi all, I tried searching the boards, but I haven't found a whole lot of people (other than VE) discussing Strattera. I'm wondering, in particular how it might be expected to affect someone who's anxiety prone (mental and physical), dysthymic, has seasonal affective disorder, and probably Bipolar 2.75 ... Ok, maybe that's too specific. Let's focus on the (increase in focus/mood) vs. (increase in anxiety) ratio, as compared to, say, Wellbutrin. Any info would be greatly appreciated. ~cache-monkey
  4. Although I've been historically an over-share sort of fellow, I can understand the difficulty of discussing something that must be incredible painful for you. But in addition to the quality of your relationship with your doctors your decision to reveal this information probably hinges on what, exactly it is. In particular, you might want to consider asking whether the nature of this information would fundamentally change your treatment in any way. I.e. is it something that might be diagnostically important and/or long-term treatment? Is it something that is psychodynamically adding to any underlying stress or trauma? I think the latter one is particularly relevant because holding something traumatic in can subvert it into the somatic system and/or lead to an overburdened HPA due to the increased allostatic pressure. This could potentially get in the way of long-term healing. BTW, I'm in no way attempting to fish for details here. But as hard as it might be, moving forward sometimes can mean really addressing the past. If you have a good trust relationship built up with your tdoc/pdoc (or anyone else) that might be a good place to do that. Just a couple of thoughts. Good luck with your decision. cache-monkey
  5. Hmm. I agree that Cymbalta's binding profile makes it about 10 times more potent blocker of serotonin transport than norepinephrine transport. But I happened to run across this study a number of years ago. It indicates that in the prefrontal cortex, Cymbalta just juices the NE relative to 5-HT and DA (600% vs. 110% and 60% increase in extracellular levels). The study also indicates that BuSpar (on which my anxiety, especially the physical component, skyrocketed) boosts NE and DA, but lowers 5-HT (160%, 100%, -50% resp.). I think this is what I was basing my assessment on, as well as an increase in anxiety on Remeron . But then the study in question was a rat study, and the common NE mechanism between BuSpar and Remeron is alpha-2 blockade, which might be an entirely different animal than direct autoreceptor inhibition. So maybe I bring up a pure NE reuptake blocker like Strattera. Well here's the thing that I realized later in the day. It was amazingly calming while I was on it, but after it wore off I felt worse; especially the restless body business. Makes me wonder if maybe there really might be some sort of tardive akathisia. Again, maybe an argument for Strattera (+low-dose SSRI?) In any case, I do apreciate your input. Thanks, cache-monkey
  6. Yeah, that's pretty much me. Serves me well professionally, but definitely bordering on OCD/hypochondria in the health domain. Had not heard any of this. Looked up the metabolism again and remembered that I'm genetically an intermediate CYP-2D6 metabolizer and probably phenotypically a poor metobolizer because I'm on Prozac. This means that the NE-favoring metabolite (hydroxybupropion) accumulates much more than in normal metabolizers. (Plus hydroxybup inhibits 2D6 itself, adding the the wacky phamacodynamics.) Maybe that's why I felt wound up on Wellbutrin mono-therapy. I've been on benzos for about 2 1/2 years. At this point I've pretty much habituated, as has become apparent as I've tried to titrate. I also smoke tobacco. (The effects aren't always immediate. Sometimes it's about keeping my blood level above a certain point.) Here there's an issue of dependence, as well. So I'm a little leery of getting involved with a third habit-forming substance. Anyway, thanks for your input. I'll make sure to talk explicitly with my pdoc about this at our next meeting. We'd left off last time talking about Lyrica last time, so he might want to try that route first. (It might be good for the anxiety and restless body issues...?) Best, cache-monkey
  7. Actually, my pdoc hasn't, largely because I hadn't really thought of this as ADD because I can get hyperfocused when I'm on a deadline. I'll bring it up with him next time I see him. Thanks for the suggestion. I guess I'd been thinking of it more in relation to my physical jitteriness, which I didn't bring out enough in my windy post. The concern here is something like "tardive akathisia", which I don't understand so wellbut has something to do with the dopamine system. Also, one thing that I forgot to mention is that I was on low-dose selegeline (also pro-dopamine) for a while and that made my mental and physical jitteriness worse, which makes my reaction to Ritalin all the more puzzling. ~cache-monkey
  8. Here's a link to a health bulletin that summarizes the results from a study that explictly looks at this issue. The key is that in this study they prospectively tracked people and explicitly asked them about sexual function, as opposed to relying on spontaneous reports. The rate of sexual side effects in that sudy is as follows (listed from worst to best): • citalopram, 72.7%; • paroxetine, 70.7%; • venlafaxine, 67.3%; • sertraline, 62.9%; • fluvoxamine, 62.3%; • fluoxetine, 57.7%; • mirtazapine, 24.4%; • nefazodone, 8%; • amineptine (now only available in developing nations), 6.9%; and • meclobemide (not available in US), 3.9% Looking at just the SSRIs, the worst for sexual side effects are (in my opinion) the best for anxiety, and vice-versa. In terms of the other two that you can get in the US: a lot of people can't stand the weight gain and sedation from Remeron/mirtazipine, while nefazadone has the whole (incredibly rare) black box liver thing and is a bit hit-or-miss for anxiety. Good luck, cache-monkey
  9. My current therapist does hypnosis. It isn't the whole "wave the watch, snap the fingers, go to sleep, wake up and you're cured thing". Right now it's basically like guided meditation to deal with my anxiety issues through getting into a trance-like state of relaxation. This is actually working to some extent. My therapist tells me that after a point we could use this to take on some of the core issues that I've been semi-consciously repressing. I.e. I allow myself to lower my guard enough to actually deal with them but not so much that I'm overwhelmed. (Not being able to find the balance is implicitly what's been leading me to repress in the first place.) So maybe hypnotherapy might help if you are aware of something that you're repressing. I suppose that, in principle, the guided meditation could be used as a discovery tool, but (in my opinion) conventional therapy is a lot more likely to help you find out what that is. So I'd stick with with that, or DBT for behavior/ideational change. Best, cache-monkey
  10. Hi all, It's been a while since I've posted here. I had a very interesting experience with Ritalin today that's prompted me to question a few things. But before I get to that, I'll lay out my history. This is kind of long, so you can skip down to my explicit questions, which I've marked with triple asterisks (***). Current DX: Anxiety and Bipolar, NOS. For most of my life I've been highly anxious; in recent years there has been a more pronounced physical component (restless legs, general tension). I also have borderline-like traits (scared of feeling trapped) due to some bad stuff that happened when I was young. Finally, there are seasonal fluctuations in mood that have been getting more noticable over the last 5 years or so: winter lows and summertime increases in energy and agitation. Oh, and I generally feel very removed from my underlying emotions. The Bipolar DX was largely arrived at empirically due to increased anxiety/agitation in response to a number of antidepressants (see below). My current therapist doesn't see any evidence of it and my only hypomanic-like episodes have been due to benzo tapering. (I did have a summer of partying in my early 20s that could have been hypomania or could have been about breaking free from some emotionally repressive relationships from childhood.) An annotated med history is at the end if you want to read it, but currently, I'm on 15 mg of Valium and 800 mg of magnesium daily. I also take 2.5 mg of Prozac every other day. Prozac has been very helpful in terms of my mood, but I've also found myself feeling wound up both physically (heart palps and restless legs). This has been particularly strong as I tapered from 17.5 to 15 on the valium over the last couple of weeks -- I had to reduce the Prozac to compensate. Dopamine: Today, I tried some Ritalin (~5mg) that a friend had given me as an experiment. I was expecting to get hyped up, especially since I hadn't taken any valium yet. Instead the _opposite_ happened. I felt amazingly calm and collected. I also felt like my physical jitteriness subsided quite a bit. I didn't feel like I needed the benzo at all until this feeling wore off about 4 hours later. *** My bipolar DX is questionable, but if it were true, would dopaminergics have the potential to be calming in the short-term but destabilizing over the long term? Or is it what you see up-front what you get? *** Is my reaction to Ritalin indicative of anything? Possibly dopamine hypoactivity? This would explain my extreme akathisia from very small doses of zyprexa and seroquel. It could also explain the initial akathisia from SSRI start-up and my difficulty with benzo tapering (high serotonin => transitorily low dopamine). Finally, increased dopamine is one of the common links between the smoking and the two treatments that have worked: Celexa+Wellbutrin and Tegretol+Klonopin. (The other common mechanisms are l-type calcium channel blockade and increases in GABA sensitivity due to allopregnanolone.) *** What does this mean for treatment? I would be worried about Ritalin due to its potential for habit-formation. The other option would be Wellbutrin agumentation. Here I'm the problem is that I really don't react well to norepinephrine, which WB seems to have relatively more action on. Are there any other non-stim dopaminergics that I'm forgetting about? *** Could Ritalin or Wellbutrin worsen dopamine dysfunction in the long run? Anyway, if you've read this far: thanks and I'd apreciate any ideas you might have. My pdoc is good, but I'm a really weird case. Best, cache-monkey Meds and combos that have NOT worked: > Wellbutrin alone - lift in mood, but increased agitation/anxiety (ag/anx) to the point of OCD-like behavior > Serzone, Sezrone+BuSpar, Serzone+BuSpar+Xanax - no mood lift, increased ag/anx > Cymbalta+Xanax - frank akathisia > Lamictal+Xanax - increased anxiety and first/only panic attack > Lithium+Klonopin - some lift in modd, but increased anxiety from Li+; had to d/c because of nephrogenic diabetes insipidus > Depakote+Klonopin/Valium - horrible sleep, low mood and mental function, no real reduction in ag/anx and maybe it got worse > Atypical neuroleptics+Klonopin - All gave akathisia at low doses (e.g. Zyprexa at 2.5 mg and Seroquel at anything above 25 mg) > Lexapro+Klonopin - felt more tense > Have also tried Trileptal, Keppra and Campral, all of which left me feeling down and had pain and/or itching as a side effect. Also, trying Lamictal again led to SJS-ish symptoms. What's worked? > Celexa+Wellbutrin - felt very good ... limited anxiety, but I did have impulsivity in terms of binge-drinking and procrastinating (but no more than the "normals" I was going to school with); I was was actually in touch with my emotions and could act on them. D/c'ed because I felt like my depression was gone > Benzos - help calm me, but leave me feeling blue and flat > Tegretol+Klonopin - reacted similarly to Celexa+Wellbutrin, but with greater gains in anxiety both psychic and physical. Had to d/c due to SJS-like reaction > Magnesium - a little calming > Smoking - rarely fails to calm and lift mood [edited for grammar]
  11. Are you in the clinical trial for it? I have very similar symptoms, and did pretty well on Tegretol (a relative of licarb). Unfortunately, I went allergic. Did the doc who gave it to you mention anything about allergic cross-sensitivity between the two, or ask whether you'd had an allergic reaction to Tegretol? Please let me know, cache-monkey
  12. What you're going through definitely sounds like it could be akathisia, at least from my experience of it. I know how horrible this feeling must be, and am sorry that you have to be going through it. Try to hang in there as best you can. If you have any Inderal (propanolol), Cogentin (benztropine), or Symmytrel (amantadine) on hand these might help reduce the symptoms. Upping your dose of Xanax could also be a good short-term fix. I'm inclined to agree with this advice. I'd at least back down the Risperdal dose to 0.5 mg and see if things seem better. And talk to your pdoc ASAP. While the meds listed above can help the symptoms of akathasia, I think there's a real concern that these just mask the symptoms. Since it's possible for any kind of EPS to go tardive, switching meds is probably the ideal strategy. Maybe to a less EPS-prone AAP like Seroquel, although this might not work so well for someone who's akathisia primed. I'm not sure what your med history is, but an anticonvulsant might be a better way to go... Good luck, cache-monkey
  13. I'm actually trialling this next for my BP-NOS/WTF. First I need to switch off of Klonopin, since I really feel like it has precipitated my allergic reactions to other meds. I have a sample pack that I'll probably start sometime in May. I'll post my response (although I'm probably not representative in any regard). ~cache-monkey
  14. Apparently Philip Seeman, one of the pioneers in this area, has found a method that potentially reverses dopamine supersensitivity. This recent study seems to indicate that one hour of local anaesthesia reduces the density of high-affinity D-2 receptors in rats undergoing ethanol withdrawal, which is equivalent to dopamine hypersensitivity. Seeman has even even patented this idea for potential human use. ~cache-monkey
  15. The study did differentiate between BP I and BP II. The full text is available at: http://content.nejm.org/cgi/content/full/NEJMoa064135 . Apparently, the BP II folks did slightly, but not quite significantly worse on AD+mood-stabilizer than placebo+mood-stabilizer, while the outcomes for BP I people were completely statistically indistinguishable. I agree with you in terms of pure experimental validity. But I think the point of the study was to look at a non-experimental population. Out here, most of us do have co-morbid conditions, on a variety of mood stabilizers, and still depressed. So it seems incredibly relevant to be trying to identify the average true-population treatment effect of AD therapy. That being said, I think that the sample size might have been too small given the tremendous heterogeneity. This would lead to under-powered results, i.e. a failure to find significant differences in outcomes by treatment, and so could be driving the non-results. I think that the results of the study are actually quite likely true. If we take a BPer and give them just one randomly-chosen antidepressant some might get better, while others clearly do worse. On average there will be no positive effect, as found by Sachs et al. I think what the study misses is the process of search for the "right" antidepressant. E.g., doing horribly on Prozac, but improving on Celexa. With repeated reassignment after failures or deterioration (like in the STAR*D trial) the results might be quite different. It's the second feature of the study that I think is even more interesting. Specifically, while the raw numbers might hint at it, there doesn't seem to be a statistically significant deterioriation in mood stability in the AD group. This could be again an issue of the sample being underpowered. But if we take it on its face, this implies that there is no reason for doctors to be pulling their patients off of their antidepressants. If anything, it should encourage the doctrinal "ADs make you worse" docs to be willing to let their patients undergo AD trials. The problem is that I feel like this is getting a little less play from the media, and has a strong possibility of being overlooked by the AD-wary docs. Just my random thoughts, cache-monkey
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