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mikl_pls

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About mikl_pls

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  • Birthday 09/11/1987

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  1. I second what has been already said: Prozac has a long half-life and would theoretically create its own taper, but it would be prudent to taper off if you've been on it for a long time, and if it's been only 9 days you shouldn't have any problems coming off of it cold-turkey. The anxiety you're experiencing is very common with SSRIs, especially with Prozac, in the beginning. If you can stick it out, it will get better and you will likely get relief from your symptoms.
  2. Trying to go up to 225 mg makes sense as it is the max approved dose and it is also the dose at which you start to get the benefit of the dual serotonergic + noradrenergic reuptake inhibition. But if after this long you haven't felt anything, you have a few options at hand. 1. You can go beyond 225 mg, usually up to 375-450 mg max, or even up to 600 mg with very close supervision by your doctor. 2. You can switch to something elseโ€”I would recommend giving Cymbalta a try as you have migraines and Cymbalta tends to work well for migraine prevention. 3. You can augment with something like high-dose Remeron (30-45 mg), an atypical antipsychotic like low-dose Abilify (2-5 mg) or Rexulti (0.5-2 mg), or perhaps even Lamictal. Remeron + Effexor is a very common combination; they make a very synergistic pair in boosting both serotonin and norepinephrine. Effexor begins to affect dopamine reuptake inhibition at super-high doses (usually 375 mg and above). Abilify and Rexulti are both approved for the use of adjunctive treatment with an established antidepressant for major depressive disorder. Lamictal is an anticonvulsant mood stabilizer typically used for acute bipolar major depressive episodes, but can be used in treatment-resistant unipolar depressive episodes. There's also always "good old" low-dose lithium, but that's something you generally want to avoid if possible due to the side effects it can cause.
  3. It didn't really start working until I got to 225 mg, and even then it didn't really, really start working until 375 mg which is higher than the typical dose for the XR formulation. I wound up going up to 450 mg before calling it quits for Effexor XR.
  4. Contrary to what one may believe about antipsychotics in general, Latuda and some other antipsychotics have a dose-dependent effect wherein certain dose ranges may be stimulating, some you may not feel anything, and some you may feel a bit sedated. With Latuda, generally low doses are stimulating (20-40 mg), moderate doses tend to be innocuous (40-60 mg), and high doses may be a little on the sedating side (80-160 mg). Try not to be alarmed by the name of the class of medication. There are many mechanisms of action that provide benefits for depressive symptoms. 5-HT1A partial agonism causes downstream dopamine release, 5-HT2A antagonism causes dopamine release in the pyramidal neurons in the prefrontal cortex (I believe), and 5-HT7 antagonism not only helps with serotonin release and subsequently depression, but can help with memory/learning as well as regulating circadian rhythm. 5-HT7 antagonism is Latuda's strongest mechanism of action. The dopamine D2 antagonism occurs on both sides of the neuron: presynaptically it antagonizes the autoreceptors with high affinity, which disinhibits dopamine release, while postsynaptically, it has a more rapid dissociation rate from the D2 neurons and hence doesn't block the effects of dopamine stimulation as much as other antipsychotics might.
  5. Latuda and other antipsychotics are sometimes used as a second-line treatment option for OCD. Latuda has the added benefit of being an atypical antipsychotic wherein it will actually benefit depressive symptoms as well as help with OCD. I hope this answers your question.
  6. Prozac is typically started at 20 mg in adults, but may be started at 10 mg if tolerability is of concern since Prozac can hit you pretty heavily if you have the unfortunate brain chemistry for it. Prozac does take a while to start working since its half-life is so long (it takes weeks to reach steady state in your system). I'd say take it as prescribed until you see your doc next time, then discuss with him/her what you've experienced thus far and ask if you need a dosage increase.
  7. I have had good results with Viibryd off and on throughout the years since it has been out. It will stop working, I'll move on to something else, that will stop working, then I'll eventually come back around to Viibryd and it'll work briefly, then eventually quit working again. It's a nice med, but for whatever reason or another, it just doesn't last long for me. Have you tried something for your headaches like Imitrex, Zomig, or Relpax? FIoricet/Fiorinal? Beta-blockers, Topamax, Depakote?
  8. My pdoc told me some people need supratherapeutic doses of Viibryd, like 60-80 mg, in order to keep them stable. I have also gone off Viibryd 40 mg after it stopped working and revisited it later on (1-3 years later) and I've found that it works again (albeit even more briefly than the first time it worked). I personally have had the most consistent and best results from Cymbalta and Zoloft.
  9. I second this. It sounds like withdrawal symptoms. You need to be on a much higher dose of Effexor XR.
  10. It sounds like withdrawal symptoms from Cymbalta, as it is very prone to causing that. If you can, you might consider talking to your doctor about a Prozac cross-taper and then withdraw from Prozac.
  11. I don't know much at all about EMDR, but I would say it's probably okay to take Xanax before and after. If in doubt, speak with the therapist who is doing the EMDR for you or your pdoc. Yeah, BuSpar, if it works, will take a couple to a few weeks to start working.
  12. My pdoc has me to take half to a whole pill as needed three times a day. In my experience, taking half a dose three times a day regularly, around the clock, instead of as needed is all I need, and I don't even need it all every day. If I take an as needed dose, I do take a whole one, but I'm very benzo resistant, so it takes much more Xanax to make me experience side effects. Sorry, I don't think all this answers your question... lol I think you have a good idea there. If not, you could ask your pdoc if you can take half a tablet around the clock like two or three times a day, which might benefit your anxiety when it reaches steady state levels in your body without side effects. Not trying to tell you how to take your medicine or anything, but just thought I might make a suggestion to consider with your pdoc. ๐Ÿ™‚
  13. I believe so. I think you might do better for depression with 300 mg XR though. 150 mg isn't quite enough to affect depression.
  14. Thank you kindly! I wouldn't say Latuda and Parnate counteract each other in regards to dopamine, but I'm not an expert on this. Also, I had no intentions of telling you how to take your meds when I was talking about your insomnia meds. I was just making an observation and possible suggestions to bring up with your pdoc. ๐Ÿ™‚
  15. Hope it works better for you on the higher dosage! That's a very common side effect of Parnate--when I was on it, I literally couldn't sleep hardly at all, like maybe 1-4 hours at the most. IMO, that combination of meds you take for sleep (Ambien and Klonopin) seem a little redundant because they both work via the same mechanism of action. It might be better to combine one of either Ambien or Klonopin with something like trazodone, low-dose doxepin, or low-dose Seroquel. That way you'd have two pro-sleep mechanisms of action going on simultaneously. But I'm not telling you how to take your medicine by any means! I'm not a professional. Yes, technically it is as dopamine receptor blocker (Latuda and most other atypical antipsychotics), but it also has very potent 5-HT2A antagonism, which disinhibits release of dopamine and norepinephrine (similar to 5-HT2C blockade). It's also a 5-HT1A partial agonist, which causes downstream dopamine release in certain parts of the brain. It also has 5-HT7 antagonism, which is believed to help with depression, circadian rhythm, and cognition (and I think causes disinhibition of serotonin release). So while you are having some dopamine blockade (in the mesolimbin pathway, where there are more D2 receptors), it has serotonin receptor antagonism at 5-HT2A in the mesocortical pathway (where there are more 5-HT2A receptors than D2 receptors). So it releases dopamine where it is needed, and keeps dopamine in control where it's needed too (preventing hypomania, psychosis, etc.) Very glad to hear that! I felt the same way about it myself. That's great! I hope it keeps up for you! Keep us posted on how you're doing! ๐Ÿ™‚
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