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Do you regularly prescribe TCAs for Depression?

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Blitz2006

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So as a resident, we are drilled to avoid TCAs...

But I have a few patients that I'm not sure what to do that don't response to SSRI/SNRIs/Wellbutrin/Remeron...

Should I trial a TCA or head straight to ECT land?

and if you do use TCA, do you prefer Nortryptiline, Amitryptiline?
 

Shikima

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So as a resident, we are drilled to avoid TCAs...

But I have a few patients that I'm not sure what to do that don't response to SSRI/SNRIs/Wellbutrin/Remeron...

Should I trial a TCA or head straight to ECT land?

and if you do use TCA, do you prefer Nortryptiline, Amitryptiline?
No response to any combination of SSRI/SNRI/Remeron? Then likely characterological.
 

sweetlenovo88

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I do not given lethality with OD, but for patient's I inherit, I may continue them if they have been stable.
 

MacDonaldTriad

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Take caution when using a lack of response to rule out a diagnosis. A TCA is in order, just get an EKG on anyone over 35 before and after titration and on anyone with a cardiac conduction problem. TCAs are slightly more effective than SSRIs, they are only used sparingly because this difference is slight and the drop out rate is triple that of SSRIs.
 
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splik

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yes. you need to choose patients carefully but I will routinely prescribe TCAs for melancholic/psychotic depression that has failed to respond to other treatments, or inflammatory depressions. I usually will prescribe with lithium or T3 at the get-go for augmentation, as if they have failed enough treatments to get a TCA, it just makes sense to not do SSRI monotherapy. Incidentally I've had pts who can't tolerate SSRIs who tolerate amitriptyline perfectly well! Start low and go slow usually aiming to get up to 150mg+, up to 300mg in the most severe cases (though I have never been able to get anyone to tolerate that dose!). Nortriptyline is better tolerated but I tend to go with amitriptyline as it works a bit better. desipramine is probably the best tolerated of the TCAs available in the US. I also prescribe clomipramine fairly commonly in OCD.
 
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Blitz2006

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yes. you need to choose patients carefully but I will routinely prescribe TCAs for melancholic/psychotic depression that has failed to respond to other treatments, or inflammatory depressions. I usually will prescribe with lithium or T3 at the get-go for augmentation, as if they have failed enough treatments to get a TCA, it just makes sense to not do SSRI monotherapy. Incidentally I've had pts who can't tolerate SSRIs who tolerate amitriptyline perfectly well! Start low and go slow usually aiming to get up to 150mg+, up to 300mg in the most severe cases (though I have never been able to get anyone to tolerate that dose!). Nortriptyline is better tolerated but I tend to go with amitriptyline as it works a bit better. desipramine is probably the best tolerated of the TCAs available in the US. I also prescribe clomipramine fairly commonly in OCD.

As an aside, for Lithium as an adjunct, is the target dose 300mg -600 mg for MDD?
 

MacDonaldTriad

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Even before SSRIs were around, most of us wrote for secondary Amine TCAs and almost never tertiary amines.
 
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Nortriptyline and amitriptyline have indications for pain so I sometimes use them for double duty in patients with chronic pain. However psych doses are typically rather higher than pain doses. Honestly many people don't tolerate them due to sedation, sometimes weight gain. EKG at baseline, again post-titration, and yearly thereafter.
 
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Nortriptyline and amitriptyline have indications for pain so I sometimes use them for double duty in patients with chronic pain. However psych doses are typically rather higher than pain doses. Honestly many people don't tolerate them due to sedation, sometimes weight gain. EKG at baseline, again post-titration, and yearly thereafter.
I haven't used them this way, but it would also make sense in migraineurs, although again the antidepressant dose is higher than the migraine prophylaxis dose.
 

clausewitz2

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I haven't used them this way, but it would also make sense in migraineurs, although again the antidepressant dose is higher than the migraine prophylaxis dose.

The family medicine docs who are alumni of one particular program in my neck of the woods really like using 25-50 mg amitriptyline for geris for sleep and chronic pain. I was surprised to learn this, but this program also hosts an FM/Psych residency, so now I am just curious which particular psych faculty member is the origin of this pharmacological tic.
 
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HarryMTieboutMD

Agree with OPD- even if you do ECT you need to have maintenance pharmacotherapy (in most cases). If someone fails (meaning no response at all) 2 SRI treatments (adequate dose and duration of course) then I will actually go to MAOI or ECT.

As an aside, I've found abilify to be the best augmentation agent for partial responders
 

Blitz2006

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Agree with OPD- even if you do ECT you need to have maintenance pharmacotherapy (in most cases). If someone fails (meaning no response at all) 2 SRI treatments (adequate dose and duration of course) then I will actually go to MAOI or ECT.

As an aside, I've found abilify to be the best augmentation agent for partial responders

Interesting...MAO-I isn't even a topic of discussion in our program...maybe it should be!
 

Blitz2006

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Agree with OPD- even if you do ECT you need to have maintenance pharmacotherapy (in most cases). If someone fails (meaning no response at all) 2 SRI treatments (adequate dose and duration of course) then I will actually go to MAOI or ECT.

As an aside, I've found abilify to be the best augmentation agent for partial responders

I presume you use Phenelzine?

and do you dose like this: Nardil (phenelzine) dosing, indications, interactions, adverse effects, and more
 

Armadillos

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Why not TMS for people who have failed a couple antidepressants? Its going to get 20-40% of people with prior antidepressant failures better which is surely better response than a TCA in someone with multiple medication failures, and obviously much safer.
 

splik

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I presume you use Phenelzine?
I use selegiline, phenelzine and isocarboxazid (which is quite expensive unfortunately as it disappeared, but because there was a demand it got brought back for extortionate price, best to get from canada). Marplan is slighlty better tolerated than phenelzine, though I suppose if you are going to use an MAOI you should probably go for phenelzine but I give pts a choice between the 3 (not including parnate). I have not used tranylcypromine but this is popularly used by psychopharmacologists and had a small renaissance after STAR*D. It is in part metabolized to amphetamine too. Though MAOI aficionados often combine it with a stimulant and a benzo (so the pt can sleep!)

When MAOIs "work", they really work, but of course by this stage it's rare for pts to be on monotherapy. Many pts need a sleeper to sustain themselves, some B6 to avoid neuropathy, fludrocortisone if they get terrible edema or orthostasis. It is typically augmented with T3, lithium, a psychostimulant, or a low dose of a neuroleptic. Lamictal is another augmentation strategy used less often.

At the same time, they are really terrible drugs. Lots of adverse effects, a pain to use, and withdrawal is just terrible! Particularly with parnate which one of the main reasons I avoid it and stick with marplan, nardil, or selegiline. The latter can be used orally or by patch. Unfortunately the oral antidepressant dose is 30-60mg and it only comes in 5mg pills which means 12 pills a day! I am sure there is a powerful placebo effect that goes with that many drugs. I do enjoy telling patients "these drugs are so powerful if you eat smelly cheese, you'll die!" and then do the counseling (it probably won't kill you to have a small bit of cheese etc). basically you should assume if you are putting a pt on an MAOI they will take it to the death. It's really a nuisance to stop. Pts become catastrophically depressed when you stop it (if they don't become frankly delirious/psychotic from withdrawal), and it won't work if you restart it. You can imagine that on c/l the primary team is not happy when you tell them to continue the nardil etc when they come in following a hypertensive crisis!

You have got to be careful with procedures. They should really get a medalert bracelet so if they are unconscious people know they are on an MAOI. And also remember to tell people about it. One of my pts went for a screening colonoscopy - they would have given him demerol if I hadn't told him to say he couldn't have it. The NP didn't believe him!

p.s. if you really want to cause your attendings to stroke out, tell them you've started a patient on a TCA and MAOI combo! (which btw is a legit thing to do; historically trimipramine was the TCA of choice)

(wow that's a lot of exclamation marks)
 
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Blitz2006

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I use selegiline, phenelzine and isocarboxazid (which is quite expensive unfortunately as it disappeared, but because there was a demand it got brought back for extortionate price, best to get from canada). Marplan is slighlty better tolerated than phenelzine, though I suppose if you are going to use an MAOI you should probably go for phenelzine but I give pts a choice between the 3 (not including parnate). I have not used tranylcypromine but this is popularly used by psychopharmacologists and had a small renaissance after STAR*D. It is in part metabolized to amphetamine too. Though MAOI aficionados often combine it with a stimulant and a benzo (so the pt can sleep!)

When MAOIs "work", they really work, but of course by this stage it's rare for pts to be on monotherapy. Many pts need a sleeper to sustain themselves, some B6 to avoid neuropathy, fludrocortisone if they get terrible edema or orthostasis. It is typically augmented with T3, lithium, a psychostimulant, or a low dose of a neuroleptic.

At the same time, they are really terrible drugs. Lots of adverse effects, a pain to use, and withdrawal is just terrible! Particularly with parnate which one of the main reasons I avoid it and stick with marplan, nardil, or selegiline. The latter can be used orally or by patch. Unfortunately the oral antidepressant dose is 30-60mg and it only comes in 5mg pills which means 12 pills a day! I am sure there is a powerful placebo effect that goes with that many drugs. I do enjoy telling patients "these drugs are so powerful if you eat smelly cheese, you'll die!" and then do the counseling (it probably won't kill you to have a small bit of cheese etc). basically you should assume if you are putting a pt on an MAOI they will take it to the death. It's really a nuisance to stop. Pts become catastrophically depressed when you stop it (if they don't become frankly delirious/psychotic from withdrawal), and it won't work if you restart it. You can imagine that on c/l the primary team is not happy when you tell them to continue the nardil etc when they come in following a hypertensive crisis!

You have got to be careful with procedures. They should really get a medalert bracelet so if they are unconscious people know they are on an MAOI. And also remember to tell people about it. One of my pts went for a screening colonoscopy - they would have given him demerol if I hadn't told him to say he couldn't have it. The NP didn't believe him!

(wow that's a lot of exclamation marks)

Nice, thanks.

I just read a great review on MAO-Is: The Role of Monoamine Oxidase Inhibitors in Current Psychiatric Practice

I'm just worried about dietary restrictions with this drug and hypertensive crisis...

BTW, any reason why Moclobemide is NOT available in U.S?
 
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OldPsychDoc

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BTW, any reason why Moclobemide is NOT available in U.S?

The only reason for anything: No $$$$ in marketing it.
It entered the market during the SSRI boom--no US manufacturer wanted to take it on.

I used it twice in residency (via a Canadian pharmacy), because I had an attending who loved it.
 

michaelrack

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How about adding a TCA to an SSRI; for some of my poorer patients I have used combo of prozac 20 and Elavil 50 mg.

Any recs about adding something to vilazodone 40 mg/day; I was thinking about adding either nortripyline 25 mg or perhaps desipramine (she is not tolerating wellbutrin XL 150 mg)
 

Blitz2006

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How about adding a TCA to an SSRI; for some of my poorer patients I have used combo of prozac 20 and Elavil 50 mg.

Any recs about adding something to vilazodone 40 mg/day; I was thinking about adding either nortripyline 25 mg or perhaps desipramine (she is not tolerating wellbutrin XL 150 mg)

Yeah, but the paranoid side of me worries about serotonin syndrome (since my patients are usually on max dose of SSRI). But I know it is highly unlikely, 0.1% or something? But I guess Despiramine and Nortryptiline only really inhibit Norepi since they are secondary amines, so there should theoretically be no risk of serotonin syndrome with these TCAs....correct?

Do people commonly prescribe TCAs + SSRIs? Again, I live in a residency bubble where this is "frowned upon"...

I don't know much about Vilazodone....apart from its sell that it has no sexual side effects...
 

PistolPete

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I use selegiline, phenelzine and isocarboxazid (which is quite expensive unfortunately as it disappeared, but because there was a demand it got brought back for extortionate price, best to get from canada). Marplan is slighlty better tolerated than phenelzine, though I suppose if you are going to use an MAOI you should probably go for phenelzine but I give pts a choice between the 3 (not including parnate). I have not used tranylcypromine but this is popularly used by psychopharmacologists and had a small renaissance after STAR*D. It is in part metabolized to amphetamine too. Though MAOI aficionados often combine it with a stimulant and a benzo (so the pt can sleep!)

When MAOIs "work", they really work, but of course by this stage it's rare for pts to be on monotherapy. Many pts need a sleeper to sustain themselves, some B6 to avoid neuropathy, fludrocortisone if they get terrible edema or orthostasis. It is typically augmented with T3, lithium, a psychostimulant, or a low dose of a neuroleptic. Lamictal is another augmentation strategy used less often.

At the same time, they are really terrible drugs. Lots of adverse effects, a pain to use, and withdrawal is just terrible! Particularly with parnate which one of the main reasons I avoid it and stick with marplan, nardil, or selegiline. The latter can be used orally or by patch. Unfortunately the oral antidepressant dose is 30-60mg and it only comes in 5mg pills which means 12 pills a day! I am sure there is a powerful placebo effect that goes with that many drugs. I do enjoy telling patients "these drugs are so powerful if you eat smelly cheese, you'll die!" and then do the counseling (it probably won't kill you to have a small bit of cheese etc). basically you should assume if you are putting a pt on an MAOI they will take it to the death. It's really a nuisance to stop. Pts become catastrophically depressed when you stop it (if they don't become frankly delirious/psychotic from withdrawal), and it won't work if you restart it. You can imagine that on c/l the primary team is not happy when you tell them to continue the nardil etc when they come in following a hypertensive crisis!

You have got to be careful with procedures. They should really get a medalert bracelet so if they are unconscious people know they are on an MAOI. And also remember to tell people about it. One of my pts went for a screening colonoscopy - they would have given him demerol if I hadn't told him to say he couldn't have it. The NP didn't believe him!

p.s. if you really want to cause your attendings to stroke out, tell them you've started a patient on a TCA and MAOI combo! (which btw is a legit thing to do; historically trimipramine was the TCA of choice)

(wow that's a lot of exclamation marks)

How come the MAO-I doesn't work once stopped and re-started?
 

st2205

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Pts become catastrophically depressed when you stop it [...], and it won't work if you restart it.
Is there evidence for this?

Edit: also, I'm glad to see that "do you masturbate regularly" is listed below as a similar thread.
 
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splik

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Is there evidence for this?
Depends what you mean by evidence. It's not the sort of thing you study. This is what I learned from very senior psychiatrists who had been around when MAOIs were more of a thing, and my medical school was the place where the concept of atypical depression for MAOIs originated. I have no personal experience of this as I have never taken a patient off an MAOI.
 
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splik

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How about adding a TCA to an SSRI; for some of my poorer patients I have used combo of prozac 20 and Elavil 50 mg.

Any recs about adding something to vilazodone 40 mg/day; I was thinking about adding either nortripyline 25 mg or perhaps desipramine (she is not tolerating wellbutrin XL 150 mg)
I dont think we know enough about what combos w/ vilazodone work. But I don't see any contraindication so give it go and see what happens!

As for the TCA +SSRI thing, the data is not great. The main thing to be aware of is not serotonin syndrome (which is highly unlikely if not using the serotonergic TCAs like clomipramine, and even then I will use luvox + clomipramine in refractory OCD cases because clomipramine inhibits n-demethylation of fluovoxamine given an overall powerful combo) but that SSRIs will often increase TCA levels so you may need to use lower doses. I am more inclined to check TCA levels in pt is on an SSRI. It is probably more likely that increasing the TCA levels from the interaction causes any therapeutic benefit than the actual combination itself.
 
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st2205

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Depends what you mean by evidence. It's not the sort of thing you study. This is what I learned from very senior psychiatrists who had been around when MAOIs were more of a thing, and my medical school was the place where the concept of atypical depression for MAOIs originated. I have no personal experience of this as I have never taken a patient off an MAOI.
Not necessarily anything published as research, but just curious if there's more to it than a truism stemming from someone staring in to a Magic Eye and thinking there's a pattern.

I guess my biggest concern in managing a patient s/p hypertensive crisis that you're balancing an established risk (hypertensive crisis) against a theoretical risk (it won't work if you restart it) based on contemporary truism.

I've had one patient come off MAOI (they were on max dose and were taking way more than prescribed). They had been on it as long as I've been alive. They've done just as poorly off it as they did on it.
 
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clausewitz2

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The only reason for anything: No $$$$ in marketing it.
It entered the market during the SSRI boom--no US manufacturer wanted to take it on.

I used it twice in residency (via a Canadian pharmacy), because I had an attending who loved it.

Well, not marketing even so much as money to do the studies you need to get it approved by the FDA. Can't off-label if there is no label, and "the EU thinks it's fine and it's been used for decades" is insufficient.
 
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Why not TMS for people who have failed a couple antidepressants? Its going to get 20-40% of people with prior antidepressant failures better which is surely better response than a TCA in someone with multiple medication failures, and obviously much safer.

Because it's exorbitant. Even for those who are lucky enough to have insurance coverage, the copay can come out to hundreds of dollars per session and you need to have a session every week for weeks on end.
 

Armadillos

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Because it's exorbitant. Even for those who are lucky enough to have insurance coverage, the copay can come out to hundreds of dollars per session and you need to have a session every week for weeks on end.

Maybe insurance coverage is better around here.


But to be devils advocate, what is it exorbitant in comparison to when your dealing with a serious treatment resistant consition?

I think even people paying straight out of pocket cash around here is something like $100/session x 30 sessions so 3K total. (The TMS clinics here may be cheaper here than elsewhere) Many people rack up bills greatly in excess of that over a year in the course of trying to recover from treatment resistant depression.

I'm not saying it's a first line treatment, but if someone's failed a cbt trial and a couple antidepressants your looking at a pretty slim chance of getting them better with a side effect ridden and dangerous medication vs a likely more effective and clearly safer alternative.
 
H

HarryMTieboutMD


I use selegiline, phenelzine and isocarboxazid (which is quite expensive unfortunately as it disappeared, but because there was a demand it got brought back for extortionate price, best to get from canada). Marplan is slighlty better tolerated than phenelzine, though I suppose if you are going to use an MAOI you should probably go for phenelzine but I give pts a choice between the 3 (not including parnate). I have not used tranylcypromine but this is popularly used by psychopharmacologists and had a small renaissance after STAR*D. It is in part metabolized to amphetamine too. Though MAOI aficionados often combine it with a stimulant and a benzo (so the pt can sleep!)

When MAOIs "work", they really work, but of course by this stage it's rare for pts to be on monotherapy. Many pts need a sleeper to sustain themselves, some B6 to avoid neuropathy, fludrocortisone if they get terrible edema or orthostasis. It is typically augmented with T3, lithium, a psychostimulant, or a low dose of a neuroleptic. Lamictal is another augmentation strategy used less often.

At the same time, they are really terrible drugs. Lots of adverse effects, a pain to use, and withdrawal is just terrible! Particularly with parnate which one of the main reasons I avoid it and stick with marplan, nardil, or selegiline. The latter can be used orally or by patch. Unfortunately the oral antidepressant dose is 30-60mg and it only comes in 5mg pills which means 12 pills a day! I am sure there is a powerful placebo effect that goes with that many drugs. I do enjoy telling patients "these drugs are so powerful if you eat smelly cheese, you'll die!" and then do the counseling (it probably won't kill you to have a small bit of cheese etc). basically you should assume if you are putting a pt on an MAOI they will take it to the death. It's really a nuisance to stop. Pts become catastrophically depressed when you stop it (if they don't become frankly delirious/psychotic from withdrawal), and it won't work if you restart it. You can imagine that on c/l the primary team is not happy when you tell them to continue the nardil etc when they come in following a hypertensive crisis!

You have got to be careful with procedures. They should really get a medalert bracelet so if they are unconscious people know they are on an MAOI. And also remember to tell people about it. One of my pts went for a screening colonoscopy - they would have given him demerol if I hadn't told him to say he couldn't have it. The NP didn't believe him!

p.s. if you really want to cause your attendings to stroke out, tell them you've started a patient on a TCA and MAOI combo! (which btw is a legit thing to do; historically trimipramine was the TCA of choice)

(wow that's a lot of exclamation marks)

Nice, thanks.

I just read a great review on MAO-Is: The Role of Monoamine Oxidase Inhibitors in Current Psychiatric Practice

I'm just worried about dietary restrictions with this drug and hypertensive crisis...

BTW, any reason why Moclobemide is NOT available in U.S?

Yes, I use Nardil because it's the easiest to dose. I'm trying to convince a patient to go on Parnate because it is somewhat less sedating and possibly more activating than nardil. The biggest problem in my experience (which is limited compared to Splik's) is sleep disturbance, which can sometimes be transient, but I've had good responses with Klonopin or Seroquel. I have never had use midodrine or fludrocortisone because of orthostatsis; lowering the dose helped

Also, the original "rocket fuel" (before Stahl) was simultaneously starting an MAOI and TCA (other than clomipramine), which my older attendings do not infrequently.

Hypertensive crisis is an issue, but MOST patients do not have trouble adhering to the diet (it's less restrictive than you might think). Our oldest attending with 50+ years of experience said of the 1000s of patients he's treated, one has had a hypertensive crisis because the patient had a passion for aged cheeses.
 
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Pts become catastrophically depressed when you stop it [...], and it won't work if you restart it.

I interestingly had a patient become manic when we started her on isocarboxazid. The working theory was that none of the antidepressants worked because she was actually bipolar and finally converted with a MAO-I. Some would call that a substance-induced mania, but she sure did respond to lamotrigine after that. She had been trialed on multiple SSRIs, SNRIs,lithium and TCAs with no results prior to flipping with the MAO-I, which we did stop.

I had an attending in residency who was very big on using TCAs and MAO-Is, and he operated primarily in a treatment-resistant clinic, where most individuals had failed multiple SSRI medications. We pretty much jumped from maxed-out Cymbalta to nortriptyline to either amitritptyline or clomipramine and then to isocarboxazid. I definitely saw patients not get better until we made the jump to a tertiary amine or to the MAO-I.
 

PistolPete

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I interestingly had a patient become manic when we started her on isocarboxazid. The working theory was that none of the antidepressants worked because she was actually bipolar and finally converted with a MAO-I. Some would call that a substance-induced mania, but she sure did respond to lamotrigine after that. She had been trialed on multiple SSRIs, SNRIs,lithium and TCAs with no results prior to flipping with the MAO-I, which we did stop.

I had an attending in residency who was very big on using TCAs and MAO-Is, and he operated primarily in a treatment-resistant clinic, where most individuals had failed multiple SSRI medications. We pretty much jumped from maxed-out Cymbalta to nortriptyline to either amitritptyline or clomipramine and then to isocarboxazid. I definitely saw patients not get better until we made the jump to a tertiary amine or to the MAO-I.

I guess technically that's drug-induced mania but I'd still conceptualize this patient as having underlying bipolar disorder.
 

2amfrappucino

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just curious if there's more to it than a truism stemming from someone staring in to a Magic Eye and thinking there's a pattern.

To take this off topic for a moment, and if I am reading correctly that you doubt what people see in Magic Eye images, in a past life I was a graphic designer and did work for a very well-known 3D artist who, among other things, created Magic Eye images (technically they are called random dot stereograms). Making these images is a very technical endeavor, and although I could do the work in Photoshop to create the images under his direction, I could not see what he was seeing. To me it was just a bunch of dots. It was very frustrating to have him look at the image as I was making it for him, with him going, "oh yes, this is looking great"!

A few weeks later after finishing the project with him and looking at the images over and over, it finally happened -- I saw what he saw. These images are based on how our eyes and brain make sense of what we are looking at to perceive depth and dimension. My lay understanding is that our eyes converge in an inverted V shape to focus, and we use the info coming from each eye to knit together the data to perceive 3D. What a random dot stereogram does is it creates image data for the left eye and right eye separately. The trick to seeing them is letting the eyes relax so that they do not converge in the V but rather stay straight. The data in the image for the left eye and right eye is there, the brain then puts it together as 3-d and that's when you can see the image. It's pretty cool and it's actually a relaxing exercise for eyestrain.
 
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Liquid8

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A few weeks later after finishing the project with him and looking at the images over and over, it finally happened -- I saw what he saw. These images are based on how our eyes and brain make sense of what we are looking at to perceive depth and dimension. My lay understanding is that our eyes converge in an inverted V shape to focus, and we use the info coming from each eye to knit together the data to perceive 3D. What a random dot stereogram does is it creates image data for the left eye and right eye separately. The trick to seeing them is letting the eyes relax so that they do not converge in the V but rather stay straight. The data in the image for the left eye and right eye is there, the brain then puts it together as 3-d and that's when you can see the image. It's pretty cool and it's actually a relaxing exercise for eyestrain.

Interesting. When I tried Magic Eyes, for some reason I always saw the images inverted, as in instead of the image popping out, it sunk into the dots. Probably not doing it right!

As for using TCAs and MAOIs, I've not found that I've had to rely on these treatment options too heavily. If monotherapy is insufficient, I'd probably look at augmentation with Lithium or Abilify, Venlafaxine/Mirtazapine combination or TMS/ECT first. At present, TMS seems to be shaping up as a cheaper option for inpatients although it's still a relatively new service at our hospital and it's probably only organisational and logistical issues still being worked out that are limiting use.

Of the MAOIs, I've had more experience using parnate, prescribed in divided doses with the last at lunchtime to reduce the chances of insomnia. Our usual process is to get a second opinion and start it as an inpatient, which allows for close monitoring and also gives access to a dietician. With Nardil I remember seeing being used once before I started training, and the consultant prescribing it made a point about most of the new psychiatrists never having being exposed to it as part of their training.
 

st2205

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To take this off topic for a moment, and if I am reading correctly that you doubt what people see in Magic Eye images, in a past life I was a graphic designer and did work for a very well-known 3D artist who, among other things, created Magic Eye images (technically they are called random dot stereograms). Making these images is a very technical endeavor, and although I could do the work in Photoshop to create the images under his direction, I could not see what he was seeing. To me it was just a bunch of dots. It was very frustrating to have him look at the image as I was making it for him, with him going, "oh yes, this is looking great"!

A few weeks later after finishing the project with him and looking at the images over and over, it finally happened -- I saw what he saw. These images are based on how our eyes and brain make sense of what we are looking at to perceive depth and dimension. My lay understanding is that our eyes converge in an inverted V shape to focus, and we use the info coming from each eye to knit together the data to perceive 3D. What a random dot stereogram does is it creates image data for the left eye and right eye separately. The trick to seeing them is letting the eyes relax so that they do not converge in the V but rather stay straight. The data in the image for the left eye and right eye is there, the brain then puts it together as 3-d and that's when you can see the image. It's pretty cool and it's actually a relaxing exercise for eyestrain.
[video]
 
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nancysinatra

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Great thread. I didn't realize there were many people interested in using these older drugs. I always have them in mind when patients are not doing well on the usual meds. But here's my question for all of you who use TCAs, MAOIs, and even ECT - who are these treatment resistant depressed patients? In my experience 99% of the patients who fail the common meds have a comorbid condition, either substance abuse, a personality disorder, PTSD, or maybe a somatoform disorder or chronic pain. Rather than treatment failure, there's usually a misdiagnosis.

It's similar with OCD. I believe I have seen one - ONE - legitimate case of this disorder in my entire career to date. Yet I've probably seen hundreds of patients who have it listed in their chart. The ONE patient I ever saw who I really thought had it, I put him on clomipramine and he did amazingly, but then he had a syncopal episode that was initially thought to be secondary to an arrhythmia. I couldn't get a clear answer from cardiology about whether there was something to worry about or not, so I just stopped it. However I kind of regret that because I think we are overly conservative with TCAs, and it was really helping him.

He was the only patient I've ever seen who actually had irrational obsessions and unavoidable compulsions. Every single other person I've ever seen who claims to have OCD actually has either some garden variety anxiety disorder or OCPD. Depression obviously is not quite that rare, but treatment resistant major depressive disorder where there's not a comorbid condition has been rare in my experience. Is that just me??
 
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HarryMTieboutMD

Great thread. I didn't realize there were many people interested in using these older drugs. I always have them in mind when patients are not doing well on the usual meds. But here's my question for all of you who use TCAs, MAOIs, and even ECT - who are these treatment resistant depressed patients? In my experience 99% of the patients who fail the common meds have a comorbid condition, either substance abuse, a personality disorder, PTSD, or maybe a somatoform disorder or chronic pain. Rather than treatment failure, there's usually a misdiagnosis.

It's similar with OCD. I believe I have seen one - ONE - legitimate case of this disorder in my entire career to date. Yet I've probably seen hundreds of patients who have it listed in their chart. The ONE patient I ever saw who I really thought had it, I put him on clomipramine and he did amazingly, but then he had a syncopal episode that was initially thought to be secondary to an arrhythmia. I couldn't get a clear answer from cardiology about whether there was something to worry about or not, so I just stopped it. However I kind of regret that because I think we are overly conservative with TCAs, and it was really helping him.

He was the only patient I've ever seen who actually had irrational obsessions and unavoidable compulsions. Every single other person I've ever seen who claims to have OCD actually has either some garden variety anxiety disorder or OCPD. Depression obviously is not quite that rare, but treatment resistant major depressive disorder where there's not a comorbid condition has been rare in my experience. Is that just me??

I agree that the idea of TRD itself is overly reductionist and in practice ignores a lot of psychiatric comorbidity (see this all the time in our TRD clinic). Secondly, as Kendler says psychiatric nosology attempts to "carve nature at its joints," but for TRD do the joints even exist? I generally find operational criteria useful, but I find fallacy in attempting to define/categorize depression by treatment failure. Here is a recent editorial on the subject that attempts to use the STAR*D structure, but again, is this really defining a clinically useful entity? Toward an Evidence-Based, Operational Definition of Treatment-Resistant Depression (one of the authors is one of my attendings, and I brought this up with him) Depression is such a complex, heterogeneous syndrome that a more person centered approach (however far away we may be from that notwithstanding; right now there are a few predictors for ECT and CYP pharmacogenetic testing) to difficult to treat cases.

I think the model works better for schizophrenia (assuming the diagnosis is correct)- patient fails D2 blocking antipsychotic adequately dosed for an adequate duration, then fails clozapine with adequate blood levels/time, then fails ECT augmentation, etc (you are SOL at this point but the good news is over time they pay less attention to positive symptoms and *might* be more receptive to cognitive enhancement therapy

OCD can be tricky. I actually find OCD to be under-diagnosed in my patients, and in my experience, I have made the diagnosis when 1) I think the established diagnosis is wrong or doesn't completely explain psychopathology and 2) OC symptoms better explain the patient's impairment. For example, I have a patient who was previously diagnosed as ASPD+cocaine (hasn't used in many years)+ marijuana "use disorders" (still smokes weed) and labeled as "unspecified depression", all of which are true (is baseline dysregulated, immature, etc), but she was very behaviorally underactivated and sat at home all day (MJ notwithstanding). When I asked her why she mentioned that she doesn't like taking public transportation because of thoughts of contamination (though described it in an ego dystonic, obsessional manner) and when I went through the YBOCS questionnaire this was chronic and pervasive. She actually responded somewhat well to SRI treatment.

Nevertheless, I have seen things mistakenly called OCD but usually in the context of untreated primary affective or psychotic pathologies (which the classic phenomenologists have long described as featuring prominent obsessions) that resolve when the primary mood/psychotic disorder is treated. I've also seen it mistaken for autistic rigidity (I think in DSM IV it was very difficult to make separate diagnoses for the two), though I've seen and have several patients who have both ASD and separate OCD.

Some of the experts (one of my attendings included) think OCPD and OCD are on the same spectrum with some work showing trait manifestations in childhood predict the development of actual OCD later on, yet others in the field debate this.
 
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Ceke2002

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Interesting. When I tried Magic Eyes, for some reason I always saw the images inverted, as in instead of the image popping out, it sunk into the dots. Probably not doing it right!

Off topic for a sec, but it sounds like you're using cross-eyed instead of parallel viewing to try and see them. It's difficult to explain, but you kind of have to look through the image, like your focusing about half a metre or so away from the image but looking at it at the same time (same as if you hold your finger in front of your face and focus past it you'll see a double image, that's what you should be going for).
 

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interesting thread. reminds me a colleague wants to refer a patient actually the patient asked to see another psychiatrist. Haven't seen said patient yet, don't even know if he will show up, But he is supposedly on Parnate 70 mg BID, Desipramine 300 mg at noon, as well as Lithium 1200 mg a day, Risperdal 2 mg bid and Seroquel 500 mg hs! I rarely prescribed Parnate but have any of you seen this high dosing?
 

thoffen

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Like just about everything, OCD is simultaneously under diagnosed and improperly diagnosed. Many patients are extremely distressed by their obsessions and do anything not to let it out including talking around symptomatology. Whenever I see significant isolation of affect, avoidance of eye contact, and especially when they report doing ok but then seemed panicked that you aren't going to up their medicine, I look intently for OCD.

RE: TCAs, I think there's definitely a role for them, but I also would not restrict someone from ECT, etc. if they haven't first failed a TCA. I stick to secondary amines except for clomipramine and doxepin (for sleep).
 

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yes. you need to choose patients carefully but I will routinely prescribe TCAs for melancholic/psychotic depression that has failed to respond to other treatments, or inflammatory depressions. I usually will prescribe with lithium or T3 at the get-go for augmentation, as if they have failed enough treatments to get a TCA, it just makes sense to not do SSRI monotherapy. Incidentally I've had pts who can't tolerate SSRIs who tolerate amitriptyline perfectly well! Start low and go slow usually aiming to get up to 150mg+, up to 300mg in the most severe cases (though I have never been able to get anyone to tolerate that dose!). Nortriptyline is better tolerated but I tend to go with amitriptyline as it works a bit better. desipramine is probably the best tolerated of the TCAs available in the US. I also prescribe clomipramine fairly commonly in OCD.
T3? Do you really use that?
 

splik

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Im not sure what you are asking? I have already said I prescribe T3 augumentation for TCAs and MAOIs (the evidence does not really support its use with SSRIs/SNRIs). the way the literature has evolved we use T3 augmentation in unipolar depression and T4 augmentation in bipolar depression. I have not heard a convincing explanation of this. Endocrinologists hate it when we rx cytomel but whatevs.Personally I prefer to use lithium augmentation as its much better but some patients can't take it or don't want to, in which case I'll give it a go. Usually well tolerated, need to watch out for suppressing endogenous thyroxine production. I had one patient develop auditory hallucinations on T3 that disappeared with discontinuation, but most patients tolerated it very well. Start at 25mcg and increase to 50mcg.

For further reading: http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2011.10030402
 
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HarryMTieboutMD

Im not sure what you are asking? I have already said I prescribe T3 augumentation for TCAs and MAOIs (the evidence does not really support its use with SSRIs/SNRIs). the way the literature has evolved we use T3 augmentation in unipolar depression and T4 augmentation in bipolar depression. I have not heard a convincing explanation of this. Endocrinologists hate it when we rx cytomel but whatevs.Personally I prefer to use lithium augmentation as its much better but some patients can't take it or don't want to, in which case I'll give it a go. Usually well tolerated, need to watch out for suppressing endogenous thyroxine production. I had one patient develop auditory hallucinations on T3 that disappeared with discontinuation, but most patients tolerated it very well. Start at 25mcg and increase to 50mcg.

For further reading: http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2011.10030402

I have never heard of any psychiatrist actually using synthroid in bipolar depression- even on the west coast I doubt this is common practice
 

clausewitz2

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I have never heard of any psychiatrist actually using synthroid in bipolar depression- even on the west coast I doubt this is common practice

I promise you if you do a Google scholar search for "synthroid bipolar depression" you will find papers. I might post a link a bit later if I have time.
 
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