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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 19 of 19. This is the beginning of the thread.
Posted by Mtom on August 5, 2021, at 16:12:53
Which Antidepressant have users found to be the least Activating?
I tried sertraline (Zoloft) many years ago very briefly, shot my anxiety (which was not then pre-existing) through the roof.
Then for a long period of time my depression mostly resolved on its own (still mild but tolerable).
In more recent years, depression came back and I tried citalopram (Cipralex) and it did same even at very low doses extreme anxiety-agitation-jitteriness syndrome.
Then Escitalopram (Cipralex-Lexapro) similar but to a slightly less degree so stayed with it a while, starting on very low doses and increasing slowly hoping I would adjust, but didnt. And didnt get much if any antidepressant effect, although never got quite as high as usual therapeutic dose and any benefit might have been overshadowed by the anxiety-agitation. Still, I noticed mostly in retrospect that it did seem to help with my ruminating. But I was needing to take Benzos to offset the anxiety, so that was not good.
Doctor decided switch to another class. She ruled out SNRIs because she knows these can be activating even in people less sensitive than me so figured not a good choice for me. Same with Bupropion (Wellbutrin).
So tried Mirtazapine (Remeron). Definitely less activating although becomes increasingly more so if I take more than low doses. Also has other unpleasant side effects (e.g. brain fog, lethargy, nightmares and GI issues, all of which worsen if I increase dose). And is only very modestly effective for my depression and most of that is offset by the brain fog and lethargy (not fatigue, Im not tired or sleepy but just cant get myself moving). Plus I started ruminating again.
Were working under the assumption that I would likely have the same reaction to all SSRIs based on the above. But maybe theres an SSRI out there still worth trying? Still, I read that most people tolerate Escitalopram better than most other ADs, and I didnt. Shes taken Paxil off the table too due to recent studies showing high adverse affects plus apparently the most difficult to withdraw from.
Cant take antipsychotics because genetic testing indicated gene mutations which put me at greater risk of tardive dyskinesia with these.
I should add that when trying Sertraline many years ago, I had been taking St. Johns Wort for several months including the same day I took Sertraline (no effect from the St. Johns Wort to that point). My doctor at that time had not heard of St. Johns Wort (it was just starting to be talked about as an alternative treatment back then). So even though I told her I was taking it, she discounted it as meaningless. She also started me on the regular dose and Ive since found that due to my sensitivity to these medications, I must start on very low doses and titrate up as tolerated. The combination of St. Johns Wort and Sertraline may interacted to produce the extreme agitation and other effects that I experienced (fit the description of mild Serotonin Syndrome).
Still from what Im reading it seems most people tolerate Escitalopram the best of the SSRIs, its too bad for whatever is in my genetics that I dont.
Running out of options other than Tricyclics which most articles say have more and potentially dangerous side effects than newer ADs and my Doctor seems to want to avoid these.
But are they effective for depression? When I was much younger, a PDoc I was seeing did prescribe Amitriptyline for ongoing situational stress which was resulting in increasing anxiety attacks and insomnia and the start of mild depression with concerns that would worsen. I remember him telling me he was starting me on a low dose, and increased the dose just once. I also remember mild side-effects like sudden short term dizziness and nausea, both of which resolved after a few weeks. But I also had problems waking up in the morning and did gain a lot of weight quite quickly, more than I have with Mirtazapine. I also did start feeling better and stopped Amitriptyline after about 8 months and was fine. However I also addressed my situational stress at the same time (found a new job). So I dont know if the Amitriptyline actually did anything positive or not.
I know very little about the other Tricyclics except an impression that most of the others are less effective at relieving depression. True?
Be happy to hear from anyone who can share similar experiences..
Posted by sigismund on August 5, 2021, at 17:30:14
In reply to Which antidepressants are 'less' activating?, posted by Mtom on August 5, 2021, at 16:12:53
Trimipramine in low or moderate doses is humane. Excellent for sleep which I took it for. I don't know as an AD.
Posted by linkadge on August 5, 2021, at 19:37:01
In reply to Which antidepressants are 'less' activating?, posted by Mtom on August 5, 2021, at 16:12:53
The TCAs are definitely NOT less effective than the SSRIs. Many studies show they are equivalent or superior.
More sedating antidepressants may include:
fluvoxamine
paxil
trazodone
mirtazapine
amitriptyline
trimipramine
doxepin
clomipramine (look into this one)
amoxapineDon't write off the TCAs. I found them much more tolerable (and effective) than the SSRIs. On paper (for instance) nortriptyline is supposed to be activating, but I found it much less activating than something like zoloft.
Linkadge
Posted by rjlockhart37 on August 6, 2021, at 0:21:01
In reply to Which antidepressants are 'less' activating?, posted by Mtom on August 5, 2021, at 16:12:53
i'm reading your post, but ill just a quick awnser : Paxil, Luvox, Remeron, and there's alot of TCA's that are sedating, but other posters know more than i do
Posted by SLS on August 6, 2021, at 2:09:46
In reply to Re: Which antidepressants are 'less' activating?, posted by linkadge on August 5, 2021, at 19:37:01
When Prozac and Zoloft had just come out, my archaic way of thinking was that the TCAs would show better than the SSRIs. My doctor did not agree. At this point, I can't cite anything that seperates these classes of drugs as far as side effects are concerned. As was mentioned, clomipramine (Anafrinil) has the reputation as having the most potent TCA. It will get more people well than does imipramine or amitriptyline. Clomipramine is definitely NOT less effective than the SSRIs. Many studies show they are equivalent or superior. In my experience, nortriptyline and trimipramine are the mildest of the TCAs that still work. Sleeplessness is probably the worst aspect of desipramine. Nortriptyline is my current best TCA.
- Scott
>
> More sedating antidepressants may include:
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> fluvoxamine
> paxil
> trazodone
> mirtazapine
> amitriptyline
> trimipramine
> doxepin
> clomipramine (look into this one)
> amoxapine
>
> Don't write off the TCAs. I found them much more tolerable (and effective) than the SSRIs. On paper (for instance) nortriptyline is supposed to be activating, but I found it much less activating than something like zoloft.
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> Linkadge
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Posted by linkadge on August 6, 2021, at 14:16:29
In reply to Re: Which antidepressants are 'less' activating?, posted by SLS on August 6, 2021, at 2:09:46
>When Prozac and Zoloft had just come out, my >archaic way of thinking was that the TCAs would >show better than the SSRIs.
I am still under the impression that TCAs are slightly more effective than the SSRIs but with a different side effect profile (perhaps more significant side effects for some patients). Some studies show superiority of TCAs in patients with higher inflammatory markers. If you could only chose between, say, amitriptyline and escitalopram, and there was no ability to drop out because of side effects, I would think that amitriptyline would do a better job at dropping depression symptoms. I think this is especially true in patients with a broader range of symptoms (i.e. insomnia, anxiety, anhedonia, energy etc). The amitriptyline group would have more side effects, however.
Apathy, for example, is a somewhat common effect of SSRIs but less so with TCAs.
Linkadge
Posted by Mtom on August 6, 2021, at 18:20:09
In reply to Re: Which antidepressants are 'less' activating? » SLS, posted by linkadge on August 6, 2021, at 14:16:29
Thank you for your comments so far. In particular those who commented research shows TCAS are not inferior to SSRIs and may be superior for efficacy. I am trying to find research so if anyone happens to have links, would be great.
There was an extensive meta-analysis published in 2018 which ranked Amitriptyline as the most efficacious antidepressant, followed by Mirtazapine although the number of studies included for these two were low in comparison to the number for several of the more popular SSRIs and others and received some criticism based on this and other biases. However in terms of acceptability and drop out rate, this study showed Amitriptyline tied for 6th with Paroxetine out of 21, and Mirtazapine ranked 11th. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)32802-7/fulltext
Almost all papers describe a significantly higher drop out rate for TCAs versus most SSRIs due to adverse effects. These are attributed to the fact that they are not selective (vs Selective SRIs and Selective NRIs) so they impact more body systems. Id say that every article or research paper Ive read mentions higher side effects with TCAs.
In addition, a large concern noted in most articles re: TCAs is the greater risk of potentially fatal heart arrythmias and possibly seizures. Also concerns about potentially fatal overdoses.
For example a 2016 article states A substantial body of evidence indicates that the cardiovascular safety profile of newer generation antidepressants is significantly improved compared to the TCAs.
Although interestingly, I just found a paper published in April of this year 2021 Antidepressants and Risk of Sudden Cardiac Death: A Network Meta-Analysis and Systematic Review that found through a meta-analysis that TCAs were actually associated with fewer cardiovascular events. This is contrary to all other articles Ive read on TCAs. They cited a number of limitations to their study, and also noted that CV events previously seen with TCAs may have involved higher doses plus Doctors now regularly monitor patients on TCAs and discontinue should warning signs appear. https://pubmed.ncbi.nlm.nih.gov/33922524/
One study which did not favour efficacy of TCAs: A 2014 meta-analysis of 5 studies in young people aged 7 to 25 found SSRIs produced a significantly greater response compared to TCAs. https://pubmed.ncbi.nlm.nih.gov/24998011/
Most studies cite multiple limitations (such as low numbers of participants, varying methodologies and sometimes publication bias). Theres not a lot of interest in, or maybe more importantly funding for, "large" post-marketing studies of these medications, especially extensive comparisons between the many different types. And articles indicate that Doctors now generally avoid TCAs based on adverse effects (and a perception that newer ADs are better, which may apparently be baseless). And many also reach such different conclusions that it makes your head spin.
Posted by linkadge on August 7, 2021, at 10:50:56
In reply to Re: Which antidepressants are 'less' activating?, posted by Mtom on August 6, 2021, at 18:20:09
Hi,
You raised many good points in the discussion of SSRIs vs. TCAs.
In terms of cardiac safety, there are two things to consider. The first is the norepinephrine reuptake inhibition which can increase heart rate and/or blood pressure, the second is the sodium channel inhibition. For the first effect, many newer antidepressants (venlafaxine, milnacipran, bupropion, duloxetine etc.) inhibit norepinephrine reuptake too. Venlafaxine seems to be particularly bad at raising blood pressure. Blood pressure monitoring is important in these cases.
The second effect of the TCAs is the inhibition of sodium channels. My understanding is that this effect is only really problematic in the higher / overdose situations. Again, many non-TCA drugs (i.e. antiepileptics, lithium) block sodium channels and (depending on the dose) can alter heart rhythm. Also, it is more problematic in people taking other sodium channel blockers or with genetic defects (i.e. Brugada syndrome which affects sodium channels).
Nortriptyline generally has a wide cardiac safety index in spite of some ability to block sodium channels. Also, it has been studied extensively in helping patients with post heart attack related depression. It has also been studied quite a bit in elderly with depression. It appears particularly good at treating depression related to Parkinson's disease or other comorbidities. There have been studies showing that apathy (from SSRIS) can be relieved by switching to (or adding) nortriptyline.
I tend to think that the 'cardiac safety' is more viewed in terms of safety in overdose. This may protect the doctor from lawsuit, and yes the patient from overdose, but denying the option may also keep the patient sick. I wonder too about some of the initial research comparing SSRIs to TCAS. There could be a heavy sponsorship bias. In a similar vein, initial studies show that the atypical antipsychotics were much more effective than the older ones. Later however, a large study (CATIE) showed that atypicals were no better than the older antipsychotics for core symptoms and caused more metabolic problems (but fewer movement related problems).
In terms of the lack of selectivity, this may cause more side effects but can also contribute to the therapeutic effect. For example, the antihistamine effects can contribute to reduced anxiety and/or improved sleep. The anticholinergic effects can help depression and/or anxiety (like scopolamine). The sodium channel blocking effects can reduce anxiety (similar to mood stabilizer augmentation). Drugs like amitriptyline too tend to improve sleep much better than SSRIs. I tend to think that sleep disruption from SSRIs may contribute to tachyphylaxis.
At the end of the day, your doctor should be open to trying a drug from another class if you have tried sufficient SSRIs and found them to be intolerable.
The side effects from TCAs are different and (depending on your situation) may actually be preferable. For example, I noticed zero agitation or insomnia on amitriptyline (as I do on SSRIs) as well as no sexual dysfunction. I also felt MUCH less apathetic and had more energy on amitriptyline than SSRIS. I did feel a bit more spacy and had a bit of blurred vision.
At the end of the day, your doctor should be willing to try a drug from a different class, especially if the current medications are intolerable.
I left a link below to Dr. Gillman's website. He was a psychiatrist who also did research on serotonin syndrome and MAOIs. He has some good thoughts on the TCAs.
https://psychotropical.com/tca-intro/
Linkadge
Posted by undopaminergic on August 7, 2021, at 12:49:12
In reply to Re: Which antidepressants are 'less' activating? » Mtom, posted by linkadge on August 7, 2021, at 10:50:56
>
> I left a link below to Dr. Gillman's website. He was a psychiatrist who also did research on serotonin syndrome and MAOIs. He has some good thoughts on the TCAs.
>Your use of the past tense makes it sound like he is dead. It seems he's still alive as far as I can tell.
-undopaminergic
Posted by linkadge on August 7, 2021, at 14:52:01
In reply to Re: Which antidepressants are 'less' activating?, posted by undopaminergic on August 7, 2021, at 12:49:12
Oh yes, sorry. He is alive and IS a psychiatrist. However I think he has retired from regular practice. My use of past tense was meant to reflect this, but I should have phrased it differently.
Linkadge
Posted by SLS on August 9, 2021, at 13:30:46
In reply to Re: Which antidepressants are 'less' activating? » SLS, posted by linkadge on August 6, 2021, at 14:16:29
> >When Prozac and Zoloft had just come out, my >archaic way of thinking was that the TCAs would >show better than the SSRIs.
>
> I am still under the impression that TCAs are slightly more effective than the SSRIs but with a different side effect profile (perhaps more significant side effects for some patients). Some studies show superiority of TCAs in patients with higher inflammatory markers. If you could only chose between, say, amitriptyline and escitalopram, and there was no ability to drop out because of side effects, I would think that amitriptyline would do a better job at dropping depression symptoms. I think this is especially true in patients with a broader range of symptoms (i.e. insomnia, anxiety, anhedonia, energy etc). The amitriptyline group would have more side effects, however.
>
> Apathy, for example, is a somewhat common effect of SSRIs but less so with TCAs.
>
> Linkadge
Nice, post.I think psychomotor retardation is a hallmark symptom that leaves TCAs to be a better choice than SSRIs. I am thinking that Prozac (fluoxetine) might be a better choice of SSRI after one failed trial of another SSRI. I would gravitate towards Lexapro or Zoloft as the first choice, but that is more of a subjective impression than a statistical appraisal.
1. Which drug - of any class - would be your first pick for the average case of Major Depressive Disorder (atypical)?2. What would be your first choice of a pro-serotoninergic drug for treating "atypical" depression presenting WITHOUT psychomotor retardation?
3. Which drug - of any class - would be your first choice for treating "endogenous" or "melancholic" depression presenting WITH psychomotor retardation?
4. How would you characterize Prozac *clinically*, and what place would it have in your treatment algorithm?
5. Why am I annoying you with so many questions?
Your opinions carry great with me. Of course, you don't have to answer all of my questions, but if you feel strongly about any of them, your input would be greatly appreciated.Thanks,
- Scott
Posted by linkadge on August 10, 2021, at 15:14:03
In reply to Re: Which antidepressants are 'less' activating?, posted by SLS on August 9, 2021, at 13:30:46
>I think psychomotor retardation is a hallmark >symptom that leaves TCAs to be a better choice >than SSRIs. I am thinking that Prozac
>(fluoxetine) might be a better choice of SSRI >after one failed trial of another SSRI.That makes sense.
>I would gravitate towards Lexapro or Zoloft as >the first choice, but that is more of a >subjective impression than a statistical >appraisal.
I think this was the conclusion too of some meta-analysis looking at dropout rates and overall efficacy. These are safe first choices for garden variety depression.
>Which drug - of any class - would be your first >pick for the average case of Major Depressive >Disorder (atypical)?
Zoloft may be worth a try too as a first agent. After that maybe effexor or imipramine. Failing that I might try an MAOI (if the patient is willing).
>2. What would be your first choice of a pro->serotoninergic drug for treating "atypical" >depression presenting WITHOUT psychomotor >retardation?
It's hard to say. I'd have to dig into the symptoms a bit more. If the patient was mostly anhedonic (perhaps with overeating and oversleeping) than sertaline, effexor or prozac might be worth a try.
>3. Which drug - of any class - would be your >first choice for treating "endogenous" or >"melancholic" depression presenting WITH >psychomotor retardation?
Imipramine or amitriptyline. Effexor may be a good option too.
>4. How would you characterize Prozac >*clinically*, and what place would it have in >your treatment algorithm?
I tend to think that prozac is a bit better with energy and apathy than other SSRIs. I would probably put it as a second option if escitalopram or zoloft didn't work. If low energy or apathy were prominent, or if the patient was not a candidate for NE boosting meds, then it might be a good first option.
It's really hard to tell for some of these as the categories are pretty broad. I would probably first rate the patient on a scale of 1-10 on interest, anxiety, insomnia, energy, low self esteem, hopelessness etc. and then go from there.
Linkadge
Posted by rjlockhart37 on August 10, 2021, at 15:23:46
In reply to Re: Which antidepressants are 'less' activating?, posted by linkadge on August 10, 2021, at 15:14:03
yeah prozac is stimulating in some aspects, not totally a NE med, but it does increase NE at higher doses. Some people can't take 60-80mg, the standard dose usally is 20-40mg. At 40mg i found it activating many years ago before we increased to 80. Some people get dulled out by prozac, at higher doses, because it can treat OCD. But 80mg is moderantly stimulating, but not as a stimulant, more antidepressant elevation.
Posted by Lamdage22 on August 27, 2021, at 7:21:24
In reply to Re: Which antidepressants are 'less' activating?, posted by rjlockhart37 on August 10, 2021, at 15:23:46
Even the less activating antidepressants activate me enough. Tend to tolerate them much better. I actually take Trazodone in the daytime without any sleepyness.
Posted by Mtom on August 27, 2021, at 10:06:26
In reply to Re: Which antidepressants are 'less' activating?, posted by Lamdage22 on August 27, 2021, at 7:21:24
> Even the less activating antidepressants activate me enough. Tend to tolerate them much better. I actually take Trazodone in the daytime without any sleepyness.
So interesting and inexplicable how we all react so hugely differently to the same medication. I took very low dose Trazodone briefly about 5 years ago when going through a period of nightly insomnia (waking at 2 and unable to get back to sleep). Doctor said dose was too low to have any antidepressant side effects, but I did. I slept through the night but upon waking my anxiety skyrocketed, felt spacey (not tired) all day, really intense Tinnitus and other stuff I cant remember.SSRIs, even at low doses, also skyrocket my anxiety even more along with agitation and jitteriness. Also cause Tinnitus (not quite as intense as Trazodone) and at moderate doses sleep disturbances, nightmares, restless legs at night, and others.
Mirtazapine is somewhat more tolerable, if I keep the dose low. But still get a variety of side effects, and only partial response. Higher (still quite low) doses make me feel ill in a way thats difficult to describe, and also increase my anxiety I suspect the Norepinephrine/Noradrenaline affect kicks in too much when I increase the dose. Or maybe the Serotonin effect gets too strong (considering my intolerance to SSRIs).
I wonder if in some of us Serotonin is not the issue at all and if so, increasing Serotonin activity not only is ineffective but brings on adverse effects.
Also Im sure individual genetics come into play. Interestingly I had Genetic testing for medications 3 years ago, I am an intermediate metabolizer for the liver P450 CYP2D6 enzyme (1 active and 1 inactive allele) which, puzzlingly, is not thought to be the main metabolic route for Citalopram or Escitalopram which I could not tolerate, but is the major enzyme metabolizing Mirtazapine which I tolerate better.
One important enzyme in metabolism of about 60% of all drugs is CYP3A4 and they did not test for that. Explanation was that there are too many variations/mutations in the populace for this enzyme and inadequate data on most of them to draw any conclusions. This is the enzyme that is inhibited by Grapefruit and thus why people on certain medications are told to avoid grapefruit or juice.
Many drugs are also inhibitors of the various P450 CYP Enzymes which effectively could increase drug concentrations by slowing down their metabolism. Im reading increasing numbers of papers discussing drug interactions (not just with Antidepressants), and the general lack of knowledge about these.
The Genetic report did not show I would have any issues with Citalopram or Escitalopram, which I did. Data was pretty limited though e.g. as above they dont test for or even yet know all the genes involved in drug metabolism and adverse effects.
My Doctor spoke to others at Conferences about these genetic tests, and while they show great promise for the future of personalized medicine, she found the consensus generally seems to be that right now theyre not quite ready for prime time. Two PDocs I talked to a couple of years ago didnt even know these tests existed.
Posted by linkadge on August 27, 2021, at 14:32:07
In reply to Re: Which antidepressants are 'less' activating? » Lamdage22, posted by Mtom on August 27, 2021, at 10:06:26
Yeah, responses to psychiatric meds are influenced by so many different factors. I am getting gene testing done for my variant of the serotonin transporter. This is mostly for informational purposes.
People with the SS variant apparently have poor responses to serotonin reuptake inhibiting meds. The theory is that their serotonin reuptake is already particularly low. People with the LL or LS variant have better responses.
The more I read, the more I realize there is no such thing as clearly defined bipolar, unipolar or anxiety. There are hundreds (if not thousands) of genes involved in the pool of psychiatric disorders. Each SNP has several variants. Doing the math on combinations, there are an astronomical number of different versions of 'depression' or 'anxiety' that we're talking about.
Linkadge
Posted by SLS on August 27, 2021, at 23:26:46
In reply to Re: Which antidepressants are 'less' activating?, posted by linkadge on August 10, 2021, at 15:14:03
Hi, Linkadge.
Thank you.
We share opinions here. You are spot-on as far as I'm concerned. I like your selections of drugs and the algorithms to place them in order. Choosing antidepressants is no longer blind trial and error.
> >I think psychomotor retardation is a hallmark >symptom that leaves TCAs to be a better choice >than SSRIs. I am thinking that Prozac
> >(fluoxetine) might be a better choice of SSRI >after one failed trial of another SSRI.
>
> That makes sense.
>
> >I would gravitate towards Lexapro or Zoloft as >the first choice, but that is more of a >subjective impression than a statistical >appraisal.
>
> I think this was the conclusion too of some meta-analysis looking at dropout rates and overall efficacy. These are safe first choices for garden variety depression.
>
> >Which drug - of any class - would be your first >pick for the average case of Major Depressive >Disorder (atypical)?
>
> Zoloft may be worth a try too as a first agent. After that maybe effexor or imipramine. Failing that I might try an MAOI (if the patient is willing).
>
> >2. What would be your first choice of a pro->serotoninergic drug for treating "atypical" >depression presenting WITHOUT psychomotor >retardation?
>
> It's hard to say. I'd have to dig into the symptoms a bit more. If the patient was mostly anhedonic (perhaps with overeating and oversleeping) than sertaline, effexor or prozac might be worth a try.
>
> >3. Which drug - of any class - would be your >first choice for treating "endogenous" or >"melancholic" depression presenting WITH >psychomotor retardation?
>
> Imipramine or amitriptyline. Effexor may be a good option too.
>
> >4. How would you characterize Prozac >*clinically*, and what place would it have in >your treatment algorithm?
>
> I tend to think that prozac is a bit better with energy and apathy than other SSRIs. I would probably put it as a second option if escitalopram or zoloft didn't work. If low energy or apathy were prominent, or if the patient was not a candidate for NE boosting meds, then it might be a good first option.
>
> It's really hard to tell for some of these as the categories are pretty broad. I would probably first rate the patient on a scale of 1-10 on interest, anxiety, insomnia, energy, low self esteem, hopelessness etc. and then go from there.
Posted by Mtom on September 6, 2021, at 9:50:33
In reply to Re: Which antidepressants are 'less' activating? » linkadge, posted by SLS on August 27, 2021, at 23:26:46
This thread evolved to include considerable discussion on Tricyclics (TCAs) and the fact that Doctors seem to rarely consider them these days (in my experience) despite some (mostly older) data that they may be as effective, or possibly more so, than newer antidepressants. This was discussed earlier in the thread.
In medical literature, side effect burden is often cited as a reason to make other choices. As well as higher toxicity.
Many, many years ago I was prescribe Amitriptyline, I believe a low(ish) dose, for intense situational stress which was leading to panic attacks and early symtpoms of depression. My anxiety and depression did resolve fairly quickly, however that might have been due to the fact that I took other specific steps to change the stressful circumstances. Or, although I didn't sense this at the time, it is possible that the Amitriptyline played a role in my ability to make these changes. There is no way to know for certain.
I discontinued the Amitriptyline after about 7 to 8 months.
The adverse effects I remember were initial occasional bouts of dizziness or light-headedness accompanied by a kind of brain fog feeling which resolved over a relatively short period of time. More difficult to deal with were somnolence (difficulty waking up in the morning) and fairly significant weight gain.
Is anyone currently taking a Tricyclic or has taken one in past? What were your specific experiences regarding efficacy and adverse effects?
Thank you!
Posted by undopaminergic on September 6, 2021, at 16:14:57
In reply to Is anyone now taking or has taken TCAs? Results?, posted by Mtom on September 6, 2021, at 9:50:33
>
> Is anyone currently taking a Tricyclic or has taken one in past? What were your specific experiences regarding efficacy and adverse effects?
>I'm taking trimipramine (Surmontil) 50+100 mg (morning+evening). It is my first experience with a tricyclic, and it is working better than any other drug classified as an "antidepressant" that I've taken (including 4 SSRIs). I would expect sedation, but I'm taking other sedative drugs, so it does not seem to make a difference. Possibly, there is some cognitive impairment from the anticholinergic action.
-undopaminergic
This is the end of the thread.
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