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About browri

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  1. do you usually take the immediate release or controlled release tablets? Yes I figured there would be, but like I said, they have long half-lives and accumulate quite a bit. I could adjust the doses accordingly. I'm still on a fairly low dose of Rexulti and I could still bump the Trintellix to 20mg in the winters. That is a major part of it. However, one difference is that I felt like oxcarbazepine was actually soothing. Like when I took the immediate release tablets, I remember feeling very calm and "feel-good-y" after I took it. It helped with my anxiety better than Depakote does I think, and where Depakote has pretty much no positive impact on my depression, oxcarbazepine was actually more helpful as an anxiolytic (and antidepressant when combined with an actual AD). Well that may be because it induces its own metabolism, requiring constantly higher doses to maintain plasma levels.
  2. Yeah when I took generic immediate release oxcarbazepine, my dose was 300mg tid (900mg daily). When we converted to the Oxtellar XR (extended release oxcarbazepine) I went to 1200mg because the bioavailability of oxcarbazepine in the extended release form is lower. Based on that, I would say my target dose would be somewhere between 600mg and 800mg like many, although I understand you can go as high as 1600mg on it, which is not something I'm interested in. I did consider the enzyme induction, but my other two medications, Trintellix and Rexulti, both have very long half-lives, and I'm hoping that dose increases would be sufficient to compensate for the enzyme induction assuming I don't go too high on carbamazepine. @centaurus aside from the fact that you felt oxcarbazepine was weaker, how would you say oxcarbazepine and carbamazepine compared from a tolerability perspective? I do have some concerns that carbamazepine may not be able to control mixed states as well as valproate as I do have a tendency to rapidly cycle and experience minor mixed states, which valproate of course is the king of. However, oxcarbazepine actually worked pretty well for me and we really only needed just a little bit more, so I'm wondering if carbamazepine may have worked.
  3. Oh yes! I forgot all about that! Very similar to low-dose amisulpride.
  4. I suppose another good question to add to this is whether anyone has taken both carbamazepine and oxcarbazepine at some point in time and can describe to me their experience with each and their differences if any.
  5. I'm sure many here take carbamazepine, but I'm more specifically interested in the Equetro brand. Has anyone here tried Equetro before and had any luck? Anyone here who has taken both generic carbamazepine and Equetro and felt there may have been any differences? Before taking Depakote ER, I was taking Oxtellar XR, which is the extended release brand of oxcarbazepine. I needed something more calming than that because we needed the anti-convulsant to pull the mood-stabilizing weight. Reason being is that appropriate mood-stabilizing doses of AAPs pretty much invariably cause akathisia for me. So the AAPs need to take a back seat and act as a booster. We decided to switch to Depakote, but I have gained quite a bit of weight. I'm not totally convinced that I even want to switch, but oxcarbazepine did do a good job, and I understand that carbamazepine can be even more calming. As always, thanks in advance!
  6. No problem! I kind of want to try mirtazapine too, but if I were to change anything out right now, I would probably change the Depakote out for Equetro (fancy brand of carbamazepine). Oxcarbazepine worked really well for me when I went to the Oxtellar XR tablets, but I just wish it could have been more calming. My pdoc has said in retrospect that carbamazepine probably could have worked better for me if I was looking for something a bit more settling than oxcarbazepine, but we ended up on Depakote, which has worked really well. Only thing with the Depakote is some weight gain, which I'm not too thrilled about.
  7. Oh of course, but a timid pdoc who is strict about following guidelines would at least have to admit that a combo of an atypical+typical has empirical evidence to back up its use.
  8. So this kind of lends to some of what I was mentioning earlier with mirtazapine. Buspirone is an agonist of the 5HT1A receptor, but in higher doses, it starts to hit the dopamine receptors in a way similar to antipsychotics, and this limits its use in depression as monotherapy, but it explains why low dose as an augment to an antidepressant works quite well. There's a new drug coming out in the next year called gepirone (Travivo) which has a similarly potent agonist effect at the 5HT1A receptors but doesn't have the dopamine dampening effects of buspirone in higher doses. It will be the first drug in that particular class to be approved as monotherapy for depression in the U.S. and the labeling will likely include data indicating its low to non-existent propensity for sexual dysfunction relative to other available antidepressant agents. This will make it the second antidepressant after Trintellix to get FDA-approved data added to the labeling to indicate that the drug has a reduced incidence of treatment-emergent sexual dysfunction relative to comparable available agents. Trazodone is distinctly different in that most of its effects are mediated through antagonism of 5HT2A and H1. It's not as well-rounded of an effect because it misses out on the 5HT2C antagonism as well as most of the alpha adrenergic antagonism of mirtazapine, which is why trazodone has kind of gone to the wayside as antidepressant monotherapy and is just used as a sleep aid.
  9. This is true. It is generally agreed that an SSRI's inhibiting effect on the transporter is not what translates into antidepressant effect, but rather the subsequent downstream activation of the 5HT1 family of receptors that actually generates the effect via interactions with the various other systems (e.g. activating 5HT1A increases dopamine release). However, this has an indiscriminate activating effect on ALL of the serotonin receptors, which we know is a bad thing. You definitely want to antagonize a significant amount of the other receptors. This is where things like insomnia and agitation come from for many people when starting antidepressants. Most people don't realize that ~80% of the body's serotonin supply is located in the gastrointestinal tract. Widespread activation of the serotonin syndrome can cause nausea, diarrhea, etc. One of the mirtazapine's prime effects is its antagonism of 5HT3 like ondansetron (Zofran), which is likely how it reduces nausea. Trintellix has this same effect at a similar or greater potency, yet nausea is one of its common side effects. Well, Trintellix inhibits the serotonin transporter and directly agonizes (fully) the 5HT1A receptor, and is a 50% partial agonist at 5HT1B, which likely causes more nausea than the 5HT3 antagonism is actually worth, although worth noting that statistically the Trintellix nausea does go away over time. This is mirtazapine's advantage. It has the antidepressant mechanism of action of all the available atypical antipsychotics without significant dopamine antagonism and no transporter inhibition to really speak of. In this way, mirtazapine works to modulate systems rather than pulling out a biological "brake line" or "dampener" (i.e. the transporter) in the brain. It's also why it's so often used as an augmenting strategy alongside low-dose AAPs as AD augments for MDD.
  10. Most interesting is that the following were listed as both the most efficacious AND the most tolerable: Valdoxan (agomelatine) Lexapro (escitalopram) Trintellix (vortioxetine) With this in mind it confuses me that agomelatine still isn't approved in the U.S. So supposedly mirtazapine is so good at what it does because of blocking alpha 2 adrenergic receptors which, when blocked, increase both norepinephrine and serotonin output. The increased serotonin signaling leads to activation of 5HT1A receptors making mirtazapine an indirect agonist there. If you do that without serotonin reuptake inhibition, it should make for a more calming effect similar to buspirone (BuSpar).
  11. This is true, but I believe APA guidelines allow for the use of moderate to high dose atypical antipsychotics in combination with a low-dose typical antipsychotic as a booster. American psychiatrists are very serious usually about following the guidelines and pretty much everywhere else in the world they're more adventurous. It would be the combination of multiple moderately dosed atypicals or a combination of multiple atypicals and typicals that would be contraindicated and labeled as "no benefit".
  12. Glad we can help That's going to be to your favor. I'm at a point where I may go read about a medication to find out how it works but I don't go and read side effects until I'm well a ways into the medication. It'll ease up. When it comes to the physical symptoms of discontinuation in my experience, It's the first week I'd say that's the hardest and it gets better from there. Patience is needed and I know it's hard to come by. Not crazy at all. I know quite a few people with ADHD that calm down quite a bit on stimulants and get better sleep because of them. Geodon does have serotonergic enhancing properties as you get into higher doses, and this may be why the higher doses didn't work for you. Geodon is both a norepinephrine reuptake inhibitor and serotonin reuptake inhibitor but it's stronger at norepinephrine and hits serotonin at higher doses. However, Geodon blocks serotonin receptors at lower doses. Good idea. I think they make individual dose bottles as well that are like seven days of a specific dose, and you pdoc might have those as well of the 0.5mg for you to work with. Well now that I think about it because of Geodon's serotonin reuptake inhibition I'm surprised your pdoc didn't want you to come off that as well to try the Nardil due to potential serotonin syndrome. It should be just fine with Rexulti because Rexulti doesn't have the inhibiting effects on the norepinephrine and serotonin transporters. I still think you should try it. Oooooo good that you posted that. So what's interesting about these genetic tests is that they aren't really good at telling you what will work. They're better at telling you what WON'T work. In this case, it says you have two of the major short alleles on the serotonin transporter, which means you have low amounts of the serotonin transporter and higher amounts of serotonin. I am similar, I have 3 short allele repeats. This sometimes means that the patient will not be able to tolerate medications that inhibit serotonin reuptake (inhibit SERT, the serotonin transporter). I also see your 5HT2C SNPs which would indicate more chance of weight gain. In the second page, it's best to pay close attention to the ones with the green check marks because those are the ones that are least likely to have metabolic interactions. It doesn't mean those ones will work, it only means that your body metabolizes them normally. Of not is loxapine, which I'll talk about later in this post. Also mentioned is trifluoperazine (Stelazine) which has been getting some buzz on the boards here as of late. It's apparently very calming. According to her Genomind test, amoxapine would be contraindicated, but..... ....loxapine is the parent drug, which makes it a tad weird that Genomind would say that loxapine is safe but amoxapine is not. Britton777, loxapine is part of the typical antipsychotic class like Haldol, Thorazine, Stelazine, etc. However, it was dosed at 50-100mg two to three times a day. Pdocs realized after some time that low dose loxapine behaves more like an atypical antipsychotic, meaning at doses of <50mg daily, it actually more potently blocks serotonin receptors than dopamine receptors. Greater affinity for serotonin receptors over dopamine receptors is what sets atypical antipsychotics like Zyprexa, Seroquel, and Risperdal apart from the older typical antipsychotics. I personally found loxapine to be helpful for agitation during the day, but it's easy to not realize that the body is breaking loxapine down into amoxapine, which is a norepinephrine reuptake inhibitor as well similarly to ziprasidone (Geodon). Therefore, during the day if I took 5mg for anxiety/agitation, I would sometimes feel the adrenergic effects of it, which I didn't like. It was better for me at 10mg before bedtime. My pdoc is using it this way on a few of his patients. That pretty much sums it up. With Rexulti, you won't get the serotonin reuptake inhibition that could potentially be causing your insomnia, and you won't get the norepinephrine reuptake inhibition that can cause physical symptoms of anxiety and panic. Also of note Britton777, I think you mentioned somewhere that in addition to the Geodon and Ativan, you also take prazosin. You should talk to your pdoc about potentially coming off of that as you titrate from Geodon to Rexulti. Prazosin is a potent blocker of alpha adrenergic receptors and that's how it mediates its effects in PTSD and other mood disorders. Rexulti also happens to be a potent blocker of these receptors, and that is believed to be one of the reasons why Rexulti is so good in PTSD. Taking Rexulti and prazosin together would be redundant and would likely just contribute to side effects like low blood pressure on standing (orthostatic hypotension).
  13. Well truthfully when you've tried as much as you have, it's easy to see why any new pdoc would want to throw the newer stuff at it to see what sticks. I would say not to read into that too much. I'm pretty sure the pharma reps are pitching this as a calming AAP with similar antidepressant and mood stabilizing effects to Abilify but less incidence of agitation or akathisia, and more of a chance of improving sleep quality overall. When it comes down to a chemical compound structure, Abilify would be the most similar. In my experience with a few different AAPs, I've found it to have calming and antidepressant effects similar to Zyprexa, but it wouldn't make sense to use your experience with Zyprexa to guess what your experience would be like with Rexulti because from a chemical structure perspective and when it comes to their pharmacology/pharmacodynamics, they are not very similar. I actually ready your case in your previous post, so I'm pretty familiar with it. Well my experience has been pretty different then. It's been really good for my sleep and while it hasn't had much of an anti-manic effect on its own, combined with Depakote it has been a pretty good mood stabilizer for me. And while it isn't good on its own for me as an anti-manic, it is very good at calming down intrusive thoughts or ruminations. Has your sleep continued to be better since coming off Zoloft? That may be key. You may fall into a group of people who just gets really bad insomnia from serotonergic-enhancing agents. This could potentially include MAOIs. So I would say to keep track of how your sleep has been overall since coming off Zoloft and if it comes back when you start Nardil, then perhaps you back down from that and focus on the Geodon and Rexulti and determine what you want to do there. Oh no worries. This is what we do. We support each other. 😊 Continue to trudge ahead with the Zoloft/Remeron wash-out, keep using your Ativan as-needed, continue the Geodon and try the Rexulti for a few days at half a 0.5mg tablet or even smaller pieces if you can make it happen. Rexulti has a long half-life so don't worry too much if the pieces aren't evenly sized. You're trying to ease your body into it anyway. Do you have just seven 0.5mg tablets and seven 1mg tablets, or did your pdoc provide supplemental bottles on top of that. And when do you see your pdoc again?
  14. One of the key differences between Rexulti and Geodon is that Geodon is a norepinephrine reuptake inhibitor. This increases the amount of norepinephrine in the synapse and can ramp up the "fight or flight" response. Geodon does also have some noradrenergic blocking effects that balance this out. Nevertheless, Geodon still manages to cause panic or anxiety for some people. It's the same reason that Seroquel can cause physical symptoms of anxiety, norepinephrine reuptake inhibition combined with noradrenergic antagonism. Rexulti on the other hand just blocks alpha adrenergic/noradrenergic receptors which has a calming effect on anxiety. This effect is currently being studies for its use in PTSD when combined with Zoloft. I believe they may already be in Phase 3 trials for Rexulti in PTSD to add to its indications as an antidepressant add-on and schizophrenia. It's also in Phase 3 for bipolar disorder and there have been some mixed results on its use for agitation in Alzheimer's dementia. If your pdoc said you COULD take both but left it up to you, if it were me, I would titrate across from the Geodon. You're on a low dose of Geodon as it is, so the withdrawal shouldn't be TOO terrible. But also keep in mind that you'll be starting Rexulti. So perhaps I agree with argh that you continue washing out from the Zoloft and Remeron and slowly come off of the Geodon. I would say to keep the Ativan for the time being. What doses of Rexulti do you have on hand in the starter back? Do you have the 14-day starter pack with one week at 0.5mg and one week at 1mg, or do you have the 7-day starter pack with four 1mg tablets and three 2mg tablets? Hopefully it's the 14-day. I know the pills are tiny, but I would recommend splitting the 0.5mg tablets to start for a few days. Have you confirmed that your insurance will cover Rexulti?
  15. Lucid dreaming can happen when coming off of antidepressants. Song looping in the head makes me think rumination, and that's where Rexulti will probably help. Rexulti could also help with the physical anxiety symptoms. The electric "shrill" sensation though sounds like Zoloft withdrawal. I find that if it seems to be connected to your eye movement, then it's SSRI withdrawal. You'll be looking in one direction and then you move your eyes to look in another direction and it makes an electric shock sensation through your whole body. It's very uncomfortable. Just ride it out though. Zoloft will cause withdrawal but it isn't as bad as Paxil or Effexor. Shakiness and dizziness could also be SSRI withdrawal. I remember coming off of Zoloft feeling kind of "flu-ey" and shaky. The Geodon has some norepinephrine enhancing effects that could be contributing to the physical anxiety symptoms. Additionally, you'll probably want to come off of the Geodon if you're going on Rexulti, but you should definitely talk to your pdoc about it first.