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About mikrw33

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  • Birthday 09/11/87

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  1. I think with riluzole you can go up to 200 mg, but that may have just been for trial sake. It could be that the max dose is 100 mg/day.
  2. So at my last pdoc appointment (1/5/17), she finally switched me to Parnate, and she even let me keep my Adderall (although she lowered the dose)! She said to stop the Adderall at first and try to not take it if I can, but today, I added 2.5 mg twice a day (5 mg/day) and it was wonderful! (Get to that in a second...) My current regimen: CHANGE NEW Amphetamine Salts (Adderall) 10 mg po bid PRN (changed from Adderall XR 40 mg to amphetamine salts 20 mg prn) Titrating off Emsam (selegiline transdermal system) 6 mg/24 h as per titration schedule (changing antidepressants) Lamotrigine (Lamictal) 25 mg po bid (50 mg) (Adding again, taken before) Pramipexole (Mirapex) 0.25 mg po qid (1 mg) (Added) Titrating onto Tranylcypromine (Parnate) 10 mg 1 po q AM-bid (currently taking bid) (20 mg) (changing antidepressants) Zonisamide (Zonegran) 100 mg 1 po q AM + 2 po qhs (300 mg) Vraylar (cariprazine ) 1.5 mg 1 po q AM (discontinued from regimen...) Alprazolam (Xanax) 2 mg 1 po qd prn (changed from alprazolam ODT (Niravam) for insurance purposes) Benztropine (Cogentin) 2 mg ½-1 po bid prn (incr. from 1 mg) So my titration schedule for coming off of Emsam is as follows: 1/6/17 Emsam 6 mg 1/8/17 Emsam 6 mg 1/9/17 Start Parnate 10 mg 1/11/17 Emsam 6 mg 1/15/17 Emsam 6 mg; incr. Parnate to 10 mg 2x/day 1/20/17 Emsam 6 mg 1/26/17 Emsam 6 mg 2/2/17 Emsam 6 mg; also next pdoc appointment (may increase Parnate!) 2/9/17 Emsam 6 mg 2/17/17 Emsam 6 mg—LAST EMSAM DOSE Anyway, so the first week or so when I was on 10 mg of Parnate and reducing the Emsam 6 mg use, things were very rocky. I wasn't feeling myself, wasn't feeling like doing anything, just felt like laying around and doing nothing. The amphetamine withdrawal was pretty bad too. Things came to a culmination of feeling the worst on Sunday 1/15/17, when I was to increase the Parnate dose to 20 mg/day. But I think that was because for the two days preceding I only took my Mirapex once a day, which I'm sure screwed with my mood pretty badly. I've heard you have to watch out for that with dopamine agonists. Anyway, so the next day wasn't so bad, but yesterday (1/17/17) was the first day I felt "good!" I felt lighter, colors were brighter and there was an increased/wider color gamut, which I actually felt the light and colors as a tingly feeling in my chest which made me feel almost euphoric. I was more conversational, more outgoing, and felt like doing more. Today (1/18/17), I decided to add 2.5 mg Adderall BID (5 mg) to my Parnate (starting small but will build up to a bigger Adderall dose), and WOW! What an improvement! I felt everything I felt yesterday but way more intense! It was amazing! Today I felt the best I've felt in a long, long, loooong time!!! I hope this effect never fades away! Anyway, I just felt like sharing my experience thus far with Parnate, which just at 20 mg, is proving to be quite amazing! The dietary limitations aren't so bad at all. This drug truly is amazing.
  3. Haha! Thanks @kaflyboy. That means a lot. All I really did is quote from a book this time though.
  4. Gotcha. I was just saying perhaps one of those others might work better is all. But if you're satisfied with amisulpride then there's no reason to change.
  5. Riluzole (Rilutek) is a drug used to treat amyotrophic lateral sclerosis. Riluzole preferentially blocks TTX-sensitive sodium channels, which are associated with damaged neurons. Riluzole has also been reported to directly inhibit the kainate and NMDA receptors. However, the action of riluzole on glutamate receptors has been controversial, as no binding of the drug to any known sites has been shown for them. In addition, as its antiglutamatergic action is still detectable in the presence of sodium channel blockers, it is also uncertain whether or not it acts via this way. Rather, its ability to stimulate glutamate uptake seems to mediate many of its effects. In addition to its role in accelerating glutamate release from presynaptic terminals. These effect combined could significantly reduce glutamate signaling and cause indirect antagonism without acting at glutamate receptors themselves. Memantine Pharmacology Glutamatergic (NMDA recepetor) A dysfunction of glutamatergic neurotransmission, manifested as neuronal excitotoxicity, is hypothesized to be involved in the etiology of Alzheimer's disease. Targeting the glutamatergic system, specifically NMDA receptors, offers a novel approach to treatment in view of the limited efficacy of existing drugs targeting the cholinergic system. Memantine is a low-affinity voltage-dependent uncompetative antagonist at glutamatergic NMDA receptors. By binding to the NMDA receptor with a higher affinity than Mg2+ ions, memantine is able to inhbit the prolonged influx of Ca2+ ions, particularly from extrasynaptic receptors, which forms the basis of neuronal excitotoxicity. The low affinity, uncompetitive nature, and rapid off-rate kinetics of memantine at the level of the NMDA receptor-channel, however, preserves the function of the receptor at synapses, as it can still be activated by physiological release of glutamate following depolarization of the presynaptic neuron. The interaction of memantine with NMDA receptors plays a major role in the symptomatic improvement that the drug produces in Alzheimer's disease. However there is no evidence as yet that the ability of memantine to protect against NMDA receptor-mediated excitotoxicity has a disease-modifying effect in Alzheimer's, although this has been suggested in animal models. Serotonergic (5-HT3 receptor) Memantine acts as a non-competitive antagonist at the 5-HT3 receptor, with a potency similar to that for the NMDA receptor. Cholinergic (nicotinic acetylcholine receptor) Memantine acts as a non-competitive antagonist at different nicotinic acetylcholine receptors (nAChRs) at potencies possibly similar to the NMDA and 5-HT3 receptors, but this is difficult to ascertain with accuracy because of the rapid desensitization of nAChR responses in these experiments. In can be noted that memantine is an antagonist at α7 nAChR, which may contribute to initial worsening of cognitive function during early memantine treatment. α7 nAChR upregulates quickly in response to antagonism, which could explain the cognitive-enhancing effects of chronic memantine treatment. It has been shown that the number of nicotinic receptors in the brain are reduced in Alzheimer's disease, even in the absence of a general decrease in the number of neurons, and nicotinic receptor antagonists are viewed as interesting targets for anti-Alzheimer drugs. Dopaminergic (D2) Memantine acts as an agonist at the Dopaminergic D2 receptor with equal or slightly higher affinity than to the NMDA receptors. Sigmaergic (σ1 receptor) It acts as an agonist at the σ1 receptor with a low Ki of 2.6 µm (2600 nM). The consequences of this activity are unclear (as the role of sigma receptors, in general, is not yet that well understood) and memantine is probably too weak at the sigma binding site to exhibit significant agonist effects, only exhibiting partial agonism or antagonism. Some of memantine's adverse effects arise through this route. —Wikipedia Memantine Memantine, a derivative of amantadine, is already FDA approved for the treatment of moderate to severe Alzheimer's disease and is considered a low-affinity, non-competitive, open-channel NMDA receptor antagonist. Memantine has essentially no psychotomimetic effects at therapeutic doses (5-20 mg/day), a key distinction from ketamine. In addition, memantine has been utilized clinically for over 15 years showing good tolerability in large patient populations. Unfortunately, most controlled clinical trials have not demonstrated memantine to have robust antidepressant effects. In an eight-week double blind placebo-controlled trial (n = 32), memantine (5-20 mg/day) failed to improve symptoms of depression in patients with MDD (Zarate et al., 2006). More recently, a proof of concept study (n = 29) also failed to show any benefit of memantinee augmentation (5-20 mg/day) of lamotrigine (stable dose of at least 100 mg/day for four weeks prior to randomization) for patients with bipolar depression over an eigh-week trial (primary outcome time point). However, memantine was observed to have a significant antidepressant effect early on in the treatment (up to four weeks) during its titration (Anand et al., 2012). Lastly, a 12-week, double-blind placebo controlled pilot study (n = 35) evaluated memantine (10 mg twice daily) for treatment in late-life depression and apathy after a disabling medical event, but not affective or function improvement was observed when compared with placebo (Lenze et al., 2001). With regard to tpositive outcome trials, a larger study (n = 80) alcohol-dependent patients with MDD were randomized to memantine 20 mg/day or escitalopram 20 mg/day. Memantine reduces alcohol cravings in preclinical studies, and alcohol dependence commonly is comorbid with major depression. The study concluded that both ttreatments significantly reduced depression and anxiety (primary outcome measures) (Muhonen et al., 2008). However, a major limitation of this study was the lack of a placebo control. Alcohol dependence may modulate the antidepressant response that is mediated via (NMDA receptors, as long-term alcohol use increases the numer (Nagy, 2004) and alters the function of glutamate NMDA receptors (Petrakis et al., 2004). Interestingly, a seven-day, placebo-controlled randomized single-blinded psychopharmacology trial study (n = 127) that utilized three different antiglutamatergic strategies (lamotrigine 25 mg 4x/day, memantine 10 mg 3x/day, or topiramate 25 mg 4x/day) for ethanol detoxification demonstrated significant improvements for acohol withdrawal symptoms and dysphoric mood (Krupitsky et al., 2007) In an effort to better understand memantine's potential antidepressant role, a recent healthy volunteer model of emotional processing attempted to assess the neuropsychologcal profile of action associated with memantine (10 mg dose; typical dose in clinical studies is at least 20 mg). Overall, the results suggest that memantine produces an early anxiogenic response in the emotion-potentiated startle similar to that seen in studies considering a single dose of the SSRI citalopram. No other significant diffference was observed with emotional or non-emotional information processing. Earlier studies have also shown that SSRI treatments initially increase the emotion-potentiated startle effect with acute administration, but that this effect is reversed after seven daily treatments (Browning et al., 2007; Grillon et al., 2007). Giventhe study only tested one dose; the authors did note that a future study (to 7 days) may help confirm the current profile of effects and provide more clinical utility. Neverthelesss, the authors also suggest that the limited neuropsychological profile associated with memantine may be consistent with the clinical data previously reported, where memantine is no more effective than placebo (Pringle et al., 2012). As already noted, similar but longer studies would help clarify some of these interpretations. Riluzole Riluzole currently is approved by the US Food and Drug Administration for treating amyotrophic lateral sclerosis. This agent crosses the blood-brain barrier and modullates the glutamatergic system by inhibiting glutamate release (via inhibitition of voltage-dependent sodium channels ) and enhancing both glutamate reuptake and AMPA trafficking and glutamate transporters. Riluzole is thought to have neuroprotective and plasticityy enhancing properties given its ability to stimulate neurotrophic factors, such as nerve growth factor (NGF), BDNF, and glial cell line-derived neurotrophic factor (GDNF) in cultured astrocytes. A number of publications also discuss ts use in neurodegenerative disorders. Combined with its glutamatergic modulating properties, riluzole has had increased investigation in off-label uses in both psychiatric and neurologic disorders (Zarate and Manji, 2008). In clinical trials, riluzole monotherapy for depression has been evaluated only in open-label trials. One trial (n = 19) with TRD and a one-week medication-free period demonstrated significant improvement in depression during weeks three through six of treatment (50-200 mg/day, mean dose = 168.8 mg/day). Improvements were also seen in scales measuring anxiety. The most common side effects were similar (e.g., headache, gastrointestinal distress, and constipation) to those seen in trials of patients with amyotrophic lateral sclerosis. Similar, positive antidepressant and anxiolytic effects were reported with riluzole (50-200 mg/day) as an augmentation antidepressant agent, but only in smaller open-label trials evaluating effects in bipolar depression, generalized anxiety disorder, and obsessive-compulsive disorder (OCD). Given some of antidepressant findings of riluzole mentioned, two double-blind, randomized, placebo-controlled studies proceeded to apply riluzole as a potential add-on strategy to maintain ketamine's rapid antidepressant effects. Both studies administered riluzole (100-200 mg/day) orally, and both trials failed to show any difference in time to relapse from placebo after a single ketamine infusion. Nevertheless, both trials did replicate earlier ketamine findings showing it to be well tolerated and having rapid antidepressant effects. Overall, double-blind, placebo-controlled clinical trials will still be necessary to confirm some of the promising observed in these open-label studies. —Neurobiology of Mental Illness, ed. Dennis S. Charney, Eric J. Nestler, Pamela Sklar, Joseph D. Baxbaum
  6. I'm sorry you're feeling this way. In some ways I know how you feel, I've felt the same things. In my eyes, as far as I can see, the truth is you are loved, you are worthy, people are not out to get you, you are deserving, you are worthy, and you have nothing to be sorry for. I hope things get better for you!
  7. ROFL! I'm laughing so hard right now!! I love this website. It's so wonderful!
  8. I'm looking at the diagram in Stahl's Essential Psychopharmacology on pg. 278 that discusses reduced positive affect and increased negative affect. Norepinephrine and dopamine (Wellbutrin) target reduced positive affect. Symptoms related to reduced positive affect include depressed mood; loss of happiness, interest, or pleasure; loss of energy or enthusiasm; decreased alertness; and decreased self-confidence. Reduced positive affect may be hypothetically related to dopaminergic dysfunction, with a possible role of noradrenergic dysfunction as well. Serotonin and norepinephrine (Prozac) target increased negative affect. Symptoms of increased negative affect include depressed mood, guilt, disgust, fear, anxiety, hostility, irritability, and loneliness. Increased negative affect may be linked hypothetically to serotonergic dysfunction and perhaps also noradrenergic dysfunction. Norepinephrine and dopamine dysfunction can potentially be fixed by Wellbutrin and stimulants like methylphenidate (Ritalin), dexmethylphenidate (Focalin), mixed amphetamine salts (Adderall), or dextroamphetamine (Dexedrine). Serotonin and norepinephrine dysfunction can potentially be targeted by SSRIs, especially Prozac (which targets serotonin, dopamine, and norepinephrine), and Paxil (which targets serotonin and norepinephrine.) Zoloft, which affects serotonin and dopamine, can potentially target increased negative and decreased positive affect (by affecting dopamine and serotonin dysfunction), as well as SNRIs, and tricyclics (TCAs). MAOIs can target dysfunction of serotonin, norepinephrine, and dopamine, increasing positive affect and decreasing negative affect.
  9. My pdoc finally took me off of Vraylar. I was on just 1.5 mg and still having akathisia from hell and insomnia. I was at one point up to 4.5 mg to see if it would help my depression better, but it just flattened me out and made me practically mute—I didn't talk much anymore, I had "poverty of speech," I think it was practically inducing negative symptoms... Not to mention the akathisia was so bad I had to text my pdoc and ask for Cogentin, which she gladly prescribed, thankfully. But even with 2 mg Cogentin/day, I was having breakthrough akathisia, so she lowered me to 1.5 mg, and even with 2 mg Cogentin/day, I was still having akathisia. So at my next appointment, rather than letting me try something else, she just took me off of Vraylar and said, "let's see how you do without an antipsychotic for now." So my meds are: Amphetamine salts (Adderall) 10 mg 1 po bid (20 mg) prn Titrating off Emsam (selegiline transdermal system) 6 mg/24 hr 1 TD as per titration schedule Lamotrigine (Lamictal) 25 mg 1 po bid (50 mg) (up-titrating) Pramipexole (Mirapex) 0,25 mg 1 po qid (1 mg) Titrating on to tranylcypromine (Parnate) currently on 10 mg 1 po bid (20 mg) Zonisamide (Zonegran) 100 mg 1 po q AM + 2 po qhs (300 mg) Alprazolam (Xanax) 2 mg 1 po qd prn Benztropine (Cogentin) 2 mg ½-1 po bid prn
  10. Yes I do this when my akathisia is acting up and I'm not up pacing around. It's my sign to take a Cogentin.
  11. (Glad it is having a positive effect for you! I was going to suggest that you could probably try a different antipsychotic which blocks only presynaptic dopamine receptors, like low dose sulpiride (50-200 mg), or low dose flupenthixol 1-2 mg?), then that might help too.
  12. In my non-educated opinion, I'd say yes, you are.
  13. That's right—by blocking certain serotonin receptors and partially agonizing certain serotonin receptors, you get serotonin, dopamine, norepinephrine, even acetylcholine and histamine release.
  14. Viibryd is an "SMS" (serotonin modulator and stimulator) aka "SPARI" (serotonin partial agonist and reuptake inhibitor), same class as Trintellix (SMS). It achieves 100% SERT occupancy at 10 mg?! Where did you see this?
  15. Yes, I can't find any information about it, but I have read that weight-loss doctors will use fluoxetine along with phentermine to potentiate the phentermine and therefore the weight loss effects. My mom was on phentermine 37.5 mg and her doctor put her on fluoxetine and ramped it up to 80 mg to potentiate it, and she lost a lot of weight on that combo. Yes, some SNRIs like Effexor, Pristiq, and Cymbalta can cause weight loss. I experienced weight loss on Pristiq and Cymbalta, no weight loss or gain on Fetzima, and actually weight gain on Effexor, strangely enough.