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JJ17

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  1. I got chills, feels like my skin is crawling sometimes, and feel weird in general. It feels similar to when I had to get off pain meds (high dose and long term) but obviously 50 times milder. Only a few things remind me of it such as the chills. BUT MY MOOD WAS/IS BETTER? Odd. I also noticed that cigarettes (something I have smoked on and off for 10+ years) actually boosted my mood. Never in my life have I felt such an insane buzz from a simple cigarette... What the heck. Also I have taken mirtizapine for so long I lost track. MINIMUM of 5 years nightly if not longer. The withdrawals are worse then SSRI or any antidepressant med I have taken. I took roughly 22.5mg (instead of 30mg) and still feel chills/lack of appetite/horrible sleep/etc. I have quit SSRIS cold turkey before and never had this, mirtizapine must be another monster
  2. So I see the half life is 20-40 hours and was wondering how I experience withdrawal if I miss one dose. Sleep is beyond impossible missing one dose. I have run out a few times recently and EVERY single time I miss a dose I do not sleep AT ALL. My insurance no longer covers it so had some issues filling it... I can feel so tired but my body/brain refuses to shut down. I also take Trazadone and Clonzepam at night so even if I take slightly higher doses of either to try and make up for the missed mirtazapine - nope still get zero sleep. I don’t understand this. Everything I read on the internet people don’t experience insomnia withdrawals unless they miss multiple days/doses, and some don’t even experience it until a week or so in. So how in the world can missing one dose make sleep completely impossible? Taking Clonzepam, melatonin, trazadone - nothing works. I am so tired I feel like I could BLACK OUT from fatigue and overwhelming sleepy feeling - but sleep is IMPOSSIBLE by simply missing 1 dose. How? Why? I’ve slept before when missing my clonzepam dose (3 to 4mg) yet if I miss 1 single dose of 30mg mirtazpine sleep is utterly impossible....How? Why? Anyone else experience this? Can anything even help sleep if you run out? I know mirtizapine has strong antihistamine action but taking OTC antihistamines does absolutely nothing.
  3. So what are the differences from taking 0.5mg to 1.0mg? I thought I read something say that the D2 blocking becomes higher going from 0.5mg to 1.0mg? I also thought I heard that quite a few things change depending on the dose. For example: does Rexulti’s partial agonist actions on 5HT1a become stronger or weaker depending on the dose? What about D2? Or the dopamine system in general does Rexulti become more of an “anti dopamine” med at higher doses and a “partial dopamine booster” at lower dosages? If so what dosages? I know that’s not the proper wording so another way to say it, I am just making it super simple. For example: I know Mirtizapine is one of those meds where it’s method of action(s) vary based on the dose. Very low doses and it’s almost like a super strong anti-histamine and supposedly it takes a certain dosage before it even has any effect on serotonin or NE. Then I believe in higher dosages Mirtazapine is more stimulating since at higher dosages = more potent NE actions. If I remember correctly Rexulti is one of those meds where it’s action(s) can change depending on the dose.
  4. Yeah, I was surprised to hear him say it’s a “night time only med” when I swore I read a lot of people take it in the morning... I’m really not sure why he said that. Anyone else who takes it please let me know when you take it! If majority of people take it in morning I will probably try that first when I start the medicine in a couple days.
  5. My doctor is starting me on 0.5mg Rexulti, and told me it was a night time only medicine. I thought I read many people here take it in the morning? I originally thought I was going to take it in the morning until he said that. So I’m just curious for those who take it: do you take it in the morning or at night?
  6. I have read a lot of good things about Rexulti here and was wondering if anyone could explain if it has “extra” mechanisms of action(s) that other AAP’s don’t have. Like I see on their website it list it as an add on for depression and is FDA approved for that. Most others don’t have approval for that such as Risperidone. I also read people here saying it reduces their flight or fight response and has helped them a lot for anxiety. So now I’m really curious about this med. Is Rexulti more potent then most AAPS adrenergic receptors perhaps to help anxiety? Basically what does Rexulti do different pharmacology wise compared to other meds in its class? I take Risperidone and it doesn’t seem to do anything for depression or anxiety. So if comparing Risperidone to Rexulti what benefits would there be to trying out Rexulti? What difference is there between Risperidone and Rexulti pharmacology Wise that makes them different? I assume Rexulti had to show antidepressant actions or reduction in symptoms better than meds such as Risperidone to get FDA approved for add on treatment for depression.
  7. I had a similar experience on my first dose of Paxil - felt more talkative, happy, etc. It lasted only for a few hours though. Also happened on very first dose of Wellbutrin which lasted only a couple of hours. SSRIS actually start to work (not therapeutic wise) within 30 minutes or so. I remember reading a study or article that showed they started to reuptake serotonin as soon as the medication was absorbed - so about 30 to 60 minutes. So some of us might feel the medicine immediately, even if it’s only reuptaking (for example) say 5% of serotonin after one dose (vs the average of 80%) while others won’t feel the small change. Yes, I know SSRI’s don’t work that way occupancy wise, it was just the best example I could think of.
  8. Also found this on drugbank website that explains how Risperidone works: The primary action of risperidone is to decrease dopaminergic and serotonergic pathway activity in the brain, therefore decreasing symptoms of schizophrenia and mood disorders [3, 4, 11]. Risperidone has high affinity binding to serotonergic 5-HT2A receptors versus dopaminergic D2 receptors in the brain [2, 3]. Risperidone binds the D2 receptors with lower affinity than the traditional, first generation antipsychotic drugs, which bind with very high affinity. A reduction in extrapyramidal symptoms in Risperidone use is attributed to its moderate affinity for dopaminergic D2 receptors [7, 11, 5]. Mechanism of action Though its mechanism of action is not fully understood at this time, current focus is on the ability of risperidone to inhibit the D2 dopaminergic receptors and 5-HT2A serotonergic receptors in the brain. Schizophrenia is thought to be caused by an excess of dopaminergic D2 and serotonergic 5-HT2A activity, resulting in overactivity of central mesolimbic pathways and mesocortical pathways, respectively [3, 4, 5]. D2 dopaminergic receptors are transiently inhibited by risperidone, reducing dopaminergic neurotransmission, therefore decreasing positive symptoms of schizophrenia, such as delusions and hallucinations. Risperidone binds transiently and with loose affinity to the dopaminergic D2 receptor, with an ideal receptor occupancy of 60-70% for optimal effect [7, 10]. Rapid dissociation of risperidone from the D2 receptors contributes to decreased risk of extrapyramidal symptoms (EPS), which occur with permanent and high occupancy blockade of D2 dopaminergic receptors [6, 7]. Low affinity binding and rapid dissociation from the D2 receptor distinguish risperidone from the traditional antipsychotic drugs. A higher occupancy rate of D2 receptors is said to increase the risk of extrapyramidal symptoms and is therefore to be avoided [6, 7, 8]. Increased serotonergic mesocortical activity in schizophrenia results in negative symptoms, such as depression and decreased motivation [11, 12]. The high affinity binding of risperidone to 5-HT2A receptors leads to a decrease in serotonergic activity. In addition, 5-HT2A receptor blockade results in decreased risk of extrapyramidal symptoms, likely by increasing dopamine release from the frontal cortex, and not the nigrostriatal tract. Dopamine level is therefore not completely inhibited [5, 7]. Through the above mechanisms, both serotonergic and D2 blockade by risperidone are thought to synergistically work to decrease the risk of extrapyramidal symptoms. Risperidone has also been said to be an antagonist of alpha-1 (α1) alpha-2 (α2) receptors, and histamine (H1) receptors [11]. Blockade of these receptors is thought to improve symptoms of schizophrenia, however the exact mechanism of action on these receptors is not fully understood at this time [11, 12]. https://www.drugbank.ca/drugs/DB00734 Good read and matches what many of you have said, such as while it does generally decrease dopamine activity it increases dopamine release in some areas.
  9. Are you still taking Risperidone? If so any update if it’s working? I’m debating trying it twice daily (once in morning and once at night) as I wonder if by the time I wake up a lot of it’s effects maybe have worn off. I felt like 2mg was blocking “too much dopamine” as it seemed to weaken my ADHD med Ritalin quite significantly. Ritalin helps with energy/focus/motivation/attention/etc for me, but if I increased the Risperidone dosage it would weaken those Ritalin effects. So I went back down to 1mg only. Does anyone think it would be a good idea to take Risperidone twice daily? I have read some people take it twice daily, once in morning and once at night. Although I’m not sure if those people are doing it for its antipsychotic effect or for off-label use like OCD. But I still wonder if maybe taking it during the day might “calm the mind” so to speak, which in turn maybe would help OCD? I know day time sedation could be an issue but should go away with time. I might try this, just wondering if anyone else had experience with once daily dosing vs twice daily.
  10. My doctor had me on 16mg and up to 20mg at one point. I had such a high tolerance and he kept upping my dose. Then he switched me from 18mg Clonzepam daily to 30mg of Dizepam daily. He also decided to go on vacation right after for a month or so. Which 18mg clonzepam (PER DAY) is equal to 270mg Dizepam (PER DAY) according to one conversion chart. So yeah, I had terrible withdrawals and ended up in the hospital, which they wrote me a script for 5mg Dizepam every 8 hours, so I was back to hospital in a couple days..... It was a mess. But the OP only takes 2mg daily and plans to eventually tamper down someday which is a good thing. But ever since that happened I always tell people to take the smallest dose of Benzos possible (That’s just my personal opinion though) that they can.
  11. Yup, you’re right my experience is very rare and everyone’s situation is different. I used a horrible choice of words. Benzos (like clonzepam) do work wonders for anxiety. So for the OP my only advice (personally not a doctor) is to try to take the lowest dose possible of Benzos. So instead of the doctor being worried about 50mg being too high a dose of Seroquel I personally think the doctor should be more concerned about the lowest possible dose of Benzos. But it seems the OP isn’t on high dose Benzos which is good. Sorry OP, I for some reason thought you were taking a much higher dose (I probably mixed up what you said Ned wise) as 2mg a day isn’t high dose. So you don’t need to worry about anything. I was up to 20mg a day. So my experience was horrible, but 99.99% of people won’t ever experience that.
  12. Edit: bad way to say it. I’m a rare case just try to keep Benzo dose as low as possible. But like others said maybe just stick to 50mg Seroquel . That’s still a VERY VERY low dose.
  13. So I changed my meds again... Added 150mg Wellbutrin and it’s only been roughly a week and already noticed more talkative/motivated/etc. But I also have increased anxiety (nothing too bad) and sometimes upset stomach. This is the ONLY antidepressant that I felt side effects from at a standard dose (even if mild) but at the same time it seems like mild side effects means the medicine is working, at least for me. NOW... As for Risperidone I have been on 1mg for 4-5 months now, and tried 2mg for 3-5 days, didn’t notice a difference so went back down to 1mg. I’m pretty sure 5 days or so isn’t enough time to work, though. But I also didn’t notice any side effects from Risperidone, it almost feels like “I take nothing”. Maybe I need a higher dose? Maybe my brain only responds to higher doses? As I have the same “issue” with SSRIS. I had no side effects from: Paxil, lexapro, Prozac, or Zoloft at normal doses - and no positive changes either - so it felt like I was “taking nothing”. It wasn’t until I went to the max or higher dosage (40mg-60mg Paxil, 200mg Zoloft) that I felt minor side effects, but also at the same time felt some benefit from the medicine. Maybe some minor side effects are a sign they are working (at least for me) ? I think my brain is so used to so many medicines that it takes high doses to even affect me, both side effect wise and benefit wise. As far as Risperidone and OCD, what method of action is believed to help OCD? At 0.5 mg to 1mg it’s “weak” in terms of D2 dopamine blocking. It isn’t until 2mg that it supposedly reaches the D2 occupancy needed for antipsychotic effects. BUT I don’t know if that matters when using it to try and treat OCD. Is higher D2 occupancy from Risperidone a good or bad thing for Obessive thoughts? Since I don’t feel anything from taking 1mg maybe I need to up the dose?
  14. I’m not sure how long I’ve been on Risperidone now for.... 2 months? Or so. I also started on clomipramine recently. Last 10 or so days I feel very “BLAH” like I could find out I’m dying tomorrow and would be okay with it. For risperidone I went up to 2mg a couple of times but went back down to 1mg, and have been on 1mg for roughly 2 months or so. But... for the past 10 or so days I have been taking 25mg of clomipramine per night. In addition to my max dose SSRI + Risperidone + other meds. Doctor was fine with it. But Now? Now I feel kind of “blah”. No, rather EXTREMELY “blah”. I don’t even want to drive 30 seconds across the street to the grocery store. I have no motivation, or energy really. I feel like all those people who complained “SSRIS made me feel little emotions or like a zombie” - that’s probably me right now, yet my OCD is still around. I will say that my love attachment doesn’t cause me instant anxiety and urge to jump off a bridge ASAP (as it did before) instead now? Now I still feel depressed/unmotivated, PLUS I still feel my OCD issues, just to a lesser extent. So it helps somewhat but damn it’s making me feel BLAHHHHHHH. My sertonin must be sky high from 200mg Zoloft + 25mg clomipramine + 5HTP + L-Tryptophan and melatonin combo I take at night. While all these medications somewhat reduces my OCD/love issues, I can still unfortunately feel it. Which sucks. I literally cannot do ANYTHING until I take my prescribed Ritalin (gives me some energy and motivation) OR I have to smoke pot. Otherwise I have zero motivation/energy. My guess is the dopamine boost from either pot or Ritalin is what “helps my mood temporarily”. Which I don’t want to have to do either of those things to have enough motivation to even go outside... Im trying to figure out what’s more likely to be the cause of zero motivation/energy: Risperidone OR clomipramine? Maybe the Risperidone took a couple months to kick in for the apathy.... Or maybe it’s the clomipramine. I don’t know.
  15. Thanks, and yes that makes sense. I believe Risperidone occupancy for 5HT2A is around 80% and around 50-60% for D2. That is, at 1mg, which is my current dose. But.... I need dopamine and also need it reduced. Like I cannot win here lol. Increased dopamine gives me motivation, energy, and makes social interactions not as bad. I actually feel somewhat “normal” after smoking pot. It used to make me paranoid as hell 10 years ago. Only difference is my brain was a teenagers back then - now I’m grown and also been on max dose SSRIS for like a year straight. So maybe the SSRIS somehow cancel out the marijuana induced paranoia, for me. As I just feel content. Same thing with other dopamine releasers/reuptake inhibitors such as Ritalin and Dexedrine - they make me feel more confident, content, talkative, motivated, etc. Which sometimes that helps distract me from my obession over someone - but sometimes it can make the anxiety feeling worse. Generally though boosting dopamine in me seems to have drastic positive effects. Just anxiety can get worse, and my love obessions if I’m not in a good mood or what not. Which my love obsessions control my life’s emotions.... I’m fact the only reason I take Risperidone is in hopes it will reduce my obession over someone I love. I don’t know what part of the dopamine reward system part of the brain that is thought to occur in - but if you happen to know: is there a better option then Risperidone if my ENTIRE goal is to suppress obessive love thoughts/feelings/etc? I mean if I do NOT take pot, Ritalin, adderall, or something like that I feel not only depressed and blah for the day, but my love obessions are still around in full force. So it seems even when “low on dopamine” I might get apathy towards life in general, but my love obessions doesn’t go away. If I boost dopamine (via the meds I mentioned above like Ritalin) I feel way better overall, but my love obessions are somewhat intensified - yet at the same time I feel better overall so I can distract myself much easier to get my mind off it, to something positive....So yeah, I dunno.
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