Rash/SJS with Lamictal?

[shahseh22]

I've never noticed SJS with Lamictal, thankfully. But given, how rarely I prescribe it I would never know. I am working in a place where a lot of people tend to use it for Borderline Personality Disorder, as, frankly, it is hard to get them into DBT. I was wondering, what kind of rash/location should one worry about in order to discontinue the medication?

Also, is SJS dose dependent or time dependent? In other words, if I get someone up to 200 mg with no rash, do I just forget about looking out for it if they've been on it for a few months/years? Or is it something, that if it is going to show up, will come up in initial stages of titration?

Thanks

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[clausewitz2]

I've never noticed SJS with Lamictal, thankfully. But given, how rarely I prescribe it I would never know. I am working in a place where a lot of people tend to use it for Borderline Personality Disorder, as, frankly, it is hard to get them into DBT. I was wondering, what kind of rash/location should one worry about in order to discontinue the medication?

Also, is SJS dose dependent or time dependent? In other words, if I get someone up to 200 mg with no rash, do I just forget about looking out for it if they've been on it for a few months/years? Or is it something, that if it is going to show up, will come up in initial stages of titration?

Thanks

Any rash that extends into the mucous membranes should be deeply alarming. Generally if it is really going to go on to be SJS it is not going to be highly focal. If you are serious about trying to evaluate this you should get a good derm atlas, there is a reason they take so many pictures.

Rash is more likely with fast titration, speed of titration appears to be a bigger risk than total ultimate dose, at least within the ranges that you are ever likely to use. Vast majority of serious rxns happen early on, but as with all autoimmune things it could develop in principle at any time so you are not necessarily freed from the need of at least asking about rashes at follow-up.

 

[Crayola227]

It has greatly to deal with the rate at which you go up or down on the med, not so much the total dose. For example, doses between 400-600 are common in szs, even up to 800 has been tolerated in rare cases it's been used at those doses.

While the rash is most likely to appear while going up on the dose, there is a risk of SJS in using it, at any time, even when on a stable dose for quite some time. It's just much less than when starting. Most don't know that it can happen when dc'ing the med, so it should never be stopped suddenly, either. It's not totally understood why it all works this way, but it does.

More common is that a patient forgets to take it for a few days, leading to declining levels, and then starts right back up at the usual dose, and the drastic change in levels can trigger it.

Also, I did look this up in residency for a patient I had in the ICU who was on lamotrigine for BPAD in whom we had held all their meds, and it was said that with the half-life being what it is, that after I believe 3 days of not taking it, the safest course to being the titration ALL OVER AGAIN. The typical course I've seen takes approx 6 weeks to get to therapeutic for BPAD.

I saw a patient that had DRESS syndrome, not SJS thank God, from starting immediately at the target dose without going up gradually.

Lastly, is that rashes on lamotrigine are exceedingly common, and without a dermatologist or other highly trained individual examining the rash, which ideally would happen within 3 days of its appearance, it's hard for providers to know if it's the dreaded start of SJS etc, or just the sort of rash that you can safely continue on with. This possibly skews the data that SJS risk is higher with starting the med? Understandably, most providers just totally dc and abandon the med.

There is at least one paper about lamotrigine rechallenge after dc'ing due to rash (that is NOT SJS), and has guidelines for doing so. Not surprisingly however, the authors caution that there needs to be a pretty compelling case for the risk/benefit in pursuing this (they stated those who have a history of doing great on lamotrigine, and for whom there have been numerous drug trials that have failed or are greatly contraindicated, that was understandably the subjects in their small study).

Also, the patients in the study seemed to meet the category I mention above, of a rash of questionable dx and immediate dc.

The long and short is that rash is not uncommon with lamotrigine, but it's not clear when it's SJS, DRESS, other serious things, or fleeting and not serious, so common wisdom is a dc.

Lastly, and I'd have to review, but in my experience the rash starts/is most prominent on the face/neck/chest, but can obviously be spread over a much wider area.

No, I'm not going to quote any papers. This is what I have gathered from years of reading/education on the topic. It could be wrong. I encourage anyone not to take any of my words for anything and to possibly take my words as directions for their own further reading.

 

[whopper]

I prescribe Lamotrigine quite often. I'm guesstimating I've placed perhaps around 100 patients on it.

I've had the rash thing happen to patients maybe about less than 10% but at a percentage not too far off from it.

Lamotrigine IMHO should be prescribed more than it is. It's cheap, effective and more effective from my clinical experience than Latuda for Bipolar Depression. (I know the studies don't back this but this has been my experience). The majority of patients with Bipolar Depression get better on Lamotrigine while with Latuda from my experience it's less than 25%. It also doesn't cause weight gain or a zombie feeling associated with many Bipolar Disorder meds.

The only main problem is the SJS and that it takes 6 weeks to get to 200 mg the usual therapeutic dosage. I always warn patients about it and tell them compliance is a MUST! I have a smartphrase for it cause I want to catalog that I warned the patient about it in a thorough manner.

 

[Crayola227]

I prescribe Lamotrigine quite often. I'm guesstimating I've placed perhaps around 100 patients on it.

I've had the rash thing happen to patients maybe about less than 10% but at a percentage not too far off from it.

Lamotrigine IMHO should be prescribed more than it is. It's cheap, effective and more effective from my clinical experience than Latuda for Bipolar Depression. (I know the studies don't back this but this has been my experience). The majority of patients with Bipolar Depression get better on Lamotrigine while with Latuda from my experience it's less than 25%. It also doesn't cause weight gain or a zombie feeling associated with many Bipolar Disorder meds.

The only main problem is the SJS and that it takes 6 weeks to get to 200 mg the usual therapeutic dosage. I always warn patients about it and tell them compliance is a MUST! I have a smartphrase for it cause I want to catalog that I warned the patient about it in a thorough manner.

Agree 100%. It's a really great drug besides what you said.

 

[Crayola227]

I have to point out that while not zombifying, it can cause some sedation. I may be wrong here, but I believe in szs it is often rx'd BID, which makes sense regarding how crucial blood levels are for sz prevention. However, in BPAD, I know that it can be given once daily. So that might make qHS best for patients, and it may help just a little for sleep.

It can cause some dizziness and imbalance, so it's important that patients taking it at night are prepared for that should they have a middle of the night trip out of bed, there's a "drunken sailor" sort of thing that can happen. I had one patient catch their toe and go down like a tree in the forest. Toe was almost broken, nail ended up falling off. So watching for that and considering it the elderly/fall risks is one thing to keep in mind.

 

[whopper]

I've seen that as a side effect too but it it rare. What really makes Lamotrigine stand out is the price, lack of weight gain and lack of being zombified that is so common with other Bipolar DO meds. It's also a great antidepressant augmentation med. While Abilify was over $500 a month several docs were overlooking $20 a month Lamotrigine.

 

[FatherPsychiatry]

I prescribe Lamotrigine quite often. I'm guesstimating I've placed perhaps around 100 patients on it.

I've had the rash thing happen to patients maybe about less than 10% but at a percentage not too far off from it.

What did you do in those cases? Did the patients call in telling you they had a rash, or was it something you noted on a followup? I'd like to use lamotrigine more but don't really feel too comfortable about the rash issue - I feel like if I had any inkling the patient had a rash anywhere, I'd just discontinue it which might not be the best option.

 

[birchswing]

My psychiatrist told me it was "impossible" for me to get SJS from Lamictal because of my gene report—she said I didn't have the gene type that could get it. I later looked it up, and it turned out it's merely less likely that I could get it and my gene type was actually extremely common. Unfortunately unlike YouScript, this was a Genesight report and not available online, so I'm not sure which gene it was. I vaguely recall that it tended to vary between Caucasian and Asian people, but I can't remember which race was more likely to have the gene that could lead to SJS being more likely.

I have bad skin (my PCP calls it "German skin") and so I kept questioning how I would detect the beginning of a rash from my normal skin, so I eventually decided against risking it.

I'll never know whether my psychiatrist lied to reassure me (which never works because I double-check everything) or if she really thought a genetic test could exclude the possibility of developing SJS.

 

[whopper]

What did you do in those cases? Did the patients call in telling you they had a rash, or was it something you noted on a followup? I'd like to use lamotrigine more but don't really feel too comfortable about the rash issue

I tell the patients they need to agree to be compliant on it and document it in my notes with a smartphrase where I wrote the following:
"Lamotrigine: Pt was explained the risks of the medication including the need to take as prescribed, possible rash, and Stevens-Johnson Syndrome. Patient knows if the medication is not taken consistently and as directed it cannot simply be resumed at the prior dosage and to call me to see if it can be restarted."

I also tell the patient during the meeting what SJS is but also to not be alarmed because it's rare and they will notice a small rash if they take the meds right instead of full-blown SJS should they be in the category that gets a rash from it. That's why you start small and gradually go up.

While SJS can scare a patient, that's fine. That fear will ingrain that they need to be compliant on the meds and take rashes seriously. I also tell the patient if they get a rash but know it's not from the meds, e.g. "if you pick up poison ivy in your left hand then get a rash in your left hand a few hours later it's poison ivy, its not Stevens Johnson Syndrome." When pts hear it's cheap, no weight gain, no need for labs, and usually no side effects they're very open to taking the meds especially if they've gained dozens of lbs from Seroquel or Zyprexa.

My psychiatrist told me it was "impossible" for me to get SJS from Lamictal because of my gene report

. To my knowledge the pharmacogenetic testing showing people at risk for SJS is available is only for carbamazepine and the gene that causes it is not the same ones involved in SJS with Lamotrigine.

I cannot comment on why your doc did what she did or the data she used but can say the above because it's a generalized comment concerning pharmacogenetic testing.

 

[Crayola227]

What did you do in those cases? Did the patients call in telling you they had a rash, or was it something you noted on a followup? I'd like to use lamotrigine more but don't really feel too comfortable about the rash issue - I feel like if I had any inkling the patient had a rash anywhere, I'd just discontinue it which might not be the best option.

It's sort of a bummer, because based on my reading (maybe others could find it) the determining of the more harmless rashes you can continue through, vs signs of more concerning ones that warrant d/c, is not that difficult and takes little time by a dermatologist with good experience with SJS/DRESS or lamotrigine. I read that some psychiatrists have received training be more adept in this as well.

The issue then, is how do you practically carry this out? I could imagine how one could. As said too, you'd have to get the patient in to see someone who could do this, be yourself with training or a derm, quite rapidly.

I'd have to look up the details on SJS, but I believe it is also accompanied by fever much of the time. Just another data point that might matter.

Honestly though, if you are concerned enough about SJS with a rash to dc a med, should you be concerned enough to send them to the ED where possibly they might get steroids and a derm consult more rapidly? (Assuming the ED does this and pushes derm for the consult).

I mean, frankly, SJS has such a rapid onset, is so freaking dangerous morbidity/mortality, and the need for speedy treatment (high dose steroids like yesterday), might actually warrant just this sort of management. That's playing it safe and might have the benefit of assessing the patient properly and possibly keeping them on lamotrigine in the case of harmless rash.

I mentioned the patient I had with full body rash and fever from rapid lamotrigine initiation with no titration, I did 3 things: looked up management of SJS, began high dose steroids, and called urgent consult to derm. I didn't wait for derm to start steroids. Mortality risk in SJS is greatly affected by timing of steroid initiation, much as antibotics in sepsis. Derm said this was the right thing to do, although thankfully it was DRESS just SJS.

If a rash really is the start of SJS, you don't really want to wait until that's painfully obvious. The patient's only hope of not being toast is rapid treatment.

 

[st2205]

Here are my thoughts on Lamictal. A lot of this is from personal experience, and I welcome any critiques:

Lamictal has become among one of my most prescribed medications. It’s not because I was trained this way, but rather what I’ve seen clinically, in conjunction with some small research.

For bipolar disorder I certainly use it, but not all that often. Mostly because I don’t see a gigantic amount of depressive bipolar but usually have someone with a history of mania and preventing that is the larger concern. Obviously there’s a fair share of bipolar depression that I treat, but with how rare that really is, I’m typically using Lamictal for other things.

I’ve found, clinically, Lamictal is literally one of, if not the, best tolerated of my regularly prescribed psychiatric medications. My target population that I’m using it on generally has a strong personality/irritability component, and I see them responding better to that than SSRIs or (heaven forbid) antipsychotics. And I really despise using anything like lithium, Depakote, or Tegretol for a personality disorder and sequelae. That being said, even people without personality/irritability issues who just don’t tolerate SSRIs/SNRIs usually due to feeling numb (not uncommon), then I’ll look to Lamictal, with surprising results. The doses I use in non-bipolar is typically 100-150. I explain that the largest benefit I typically see comes then, however a decent amount of people respond at 50 mg, and a very small minority at 25 mg. Overall, it’s not making people numb, they don’t feel like a zombie, it’s not sedating (95% of the time I have them take it during the day without any complaints, but give them the option of taking it however works best), no sexual side-effects, etc.

With regard to SJS, I explain that it’s not necessarily uncommon to develop a rash (reports say 10-15% but I honestly see this far less than 5% of the time). If they develop a rash, they are instructed to stop and call me. I then explain SJS and that if they have a rash that is accompanied by any unusual physical symptom (fever, flu-like symptoms, wide-spread or painful rash, muscle or joint pains beyond what’s normal, etc.), then they are to seek emergency evaluation.

Other mood stabilizers I sometimes consider in personality is Trileptal (see a lot of hyponatremia with this, though), but I don’t see this being helpful for depression, more just irritability. I utilize this fairly infrequently. I don’t ever use Depakote or lithium for anything that’s not Axis I. I really never use Tegretol for anything.

That’s my bias on mood stabilizers. Maybe one day I’ll post my biases on Effexor and Risperdal.

 

[Crayola227]

Here are my thoughts on Lamictal. A lot of this is from personal experience, and I welcome any critiques:

Lamictal has become among one of my most prescribed medications. It’s not because I was trained this way, but rather what I’ve seen clinically, in conjunction with some small research.

For bipolar disorder I certainly use it, but not all that often. Mostly because I don’t see a gigantic amount of depressive bipolar but usually have someone with a history of mania and preventing that is the larger concern. Obviously there’s a fair share of bipolar depression that I treat, but with how rare that really is, I’m typically using Lamictal for other things.

I’ve found, clinically, Lamictal is literally one of, if not the, best tolerated of my regularly prescribed psychiatric medications. My target population that I’m using it on generally has a strong personality/irritability component, and I see them responding better to that than SSRIs or (heaven forbid) antipsychotics. And I really despise using anything like lithium, Depakote, or Tegretol for a personality disorder and sequelae. That being said, even people without personality/irritability issues who just don’t tolerate SSRIs/SNRIs usually due to feeling numb (not uncommon), then I’ll look to Lamictal, with surprising results. The doses I use in non-bipolar is typically 100-150. I explain that the largest benefit I typically see comes then, however a decent amount of people respond at 50 mg, and a very small minority at 25 mg. Overall, it’s not making people numb, they don’t feel like a zombie, it’s not sedating (95% of the time I have them take it during the day without any complaints, but give them the option of taking it however works best), no sexual side-effects, etc.

With regard to SJS, I explain that it’s not necessarily uncommon to develop a rash (reports say 10-15% but I honestly see this far less than 5% of the time). If they develop a rash, they are instructed to stop and call me. I then explain SJS and that if they have a rash that is accompanied by any unusual physical symptom (fever, flu-like symptoms, wide-spread or painful rash, muscle or joint pains beyond what’s normal, etc.), then they are to seek emergency evaluation.

Other mood stabilizers I sometimes consider in personality is Trileptal (see a lot of hyponatremia with this, though), but I don’t see this being helpful for depression, more just irritability. I utilize this fairly infrequently. I don’t ever use Depakote or lithium for anything that’s not Axis I. I really never use Tegretol for anything.

That’s my bias on mood stabilizers. Maybe one day I’ll post my biases on Effexor and Risperdal.

Is bipolar depression all that uncommon? I read somewhere that an overwhelming majority of BPAD no matter the type, when not euthymic, have more depressive episodes than manic ones, and more time spent that way on average compared to manic episodes. I may be wrong. I don't deny the need to use other mood stabilizers with a more anti-manic effect, but I still see a role for lamotrigine as an adjunct for a good deal of BPAD.

I'm surprised you're using it more for conditions besides bipolar depression than for bipolar depression. That isn't to say I'm rebutting any other uses you're describing.

 

[Crayola227]

Is there evidence for efficacy in any psychiatric condition at doses below 200 mg (I think we established in a thread elsewhere that was the FDA studied dose for BPAD? I could be wrong) ?

I'm honestly just interested. It's a great drug so I think it's worth thinking about other indications.

 

[st2205]

Is bipolar depression all that uncommon? I read somewhere that an overwhelming majority of BPAD no matter the type, when not euthymic, have more depressive episodes than manic ones, and more time spent that way on average compared to manic episodes. I may be wrong. I don't deny the need to use other mood stabilizers with a more anti-manic effect, but I still see a role for lamotrigine as an adjunct for a good deal of BPAD.

I'm surprised you're using it more for conditions besides bipolar depression than for bipolar depression. That isn't to say I'm rebutting any other uses you're describing.

You’re correct on the depression part of BPD, however, it’s not as often (in my current setup) that they’re presenting for that. I’ve also found the idea of antipsychotics having benefit for bipolar depression fairly interesting, as I’ve seen them be effective clinically in those situations less than placebo, but that’s another discussion (I actually see antipsychotics inducing depression in a two-fold manner, by 1) quelching the elevation from the mania and 2) making them more lethargic and numb, which is even more accentuated in combination with #1, on top of the actual depression kicking in).

My point about it being rare is more about how rare bipolar is (real bipolar). For plenty of people with “bipolar,” I see medications approximate a more by-the-book pattern, but actual bipolar depression I find tougher to treat and a lot of the truisms don’t end up holding so true. I still use Lamictal quite a bit for BP depression, it’s just that it’s so rare and, when I see it, Lamictal is one of a few options, so the volume is quite low.

 

[splik]

Is bipolar depression all that uncommon? I read somewhere that an overwhelming majority of BPAD no matter the type, when not euthymic, have more depressive episodes than manic ones, and more time spent that way on average compared to manic episodes. I may be wrong. I don't deny the need to use other mood stabilizers with a more anti-manic effect, but I still see a role for lamotrigine as an adjunct for a good deal of BPAD.

I'm surprised you're using it more for conditions besides bipolar depression than for bipolar depression. That isn't to say I'm rebutting any other uses you're describing.

well the evidence for use in bipolar depression is pretty weak. of the 5 RCTs that evaluated the use of lamictal in bipolar depression, 4 were negative. Only when you did a pooled analysis of all 5 studies did lamictal come out statistically better than placebo, and even then the NNT was 11 which is not particularly impressive, and less than the NNT for typical interventions for depressions (antidepressants in unipolar depression have an NNT of 7 by way of comparison).

Although many psychiatrists do use lamictal in the treatment of bipolar depression, this comes from a misunderstanding or misinterpretation of the actual literature, which shows it has some benefit compared to lithium in preventing depressive relapses in bipolar I disorder.

lamictal is very commonly used in the treatment of borderline personality disorder. there is a little bit of data supporting this (not great). the most popular and convincing theory is that because of its titration schedule it has an added placebo effect as patients continue to get improvement each time you increase the dose.

 

[Crayola227]

You’re correct on the depression part of BPD, however, it’s not as often (in my current setup) that they’re presenting for that. I’ve also found the idea of antipsychotics having benefit for bipolar depression fairly interesting, as I’ve seen them be effective clinically in those situations less than placebo, but that’s another discussion (I actually see antipsychotics inducing depression in a two-fold manner, by 1) quelching the elevation from the mania and 2) making them more lethargic and numb, which is even more accentuated in combination with #1, on top of the actual depression kicking in).

My point about it being rare is more about how rare bipolar is (real bipolar). For plenty of people with “bipolar,” I see medications approximate a more by-the-book pattern, but actual bipolar depression I find tougher to treat and a lot of the truisms don’t end up holding so true. I still use Lamictal quite a bit for BP depression, it’s just that it’s so rare and, when I see it, Lamictal is one of a few options, so the volume is quite low.

You are totally spot on, I think, with the "deflation" effect of antipsychotics in BPAD, and moreso with initiation, I think. I know of a few psychiatrists that think so, and I'm inclined to agree based on observation and discussion with patients. Not to mention I think there's an association with a depressive episode following a manic one even when medications aren't used to terminate it. Something about brain chemicals. Specific there, I know.

Thank you for expounding on your views.

 

[Crayola227]

well the evidence for use in bipolar depression is pretty weak. of the 5 RCTs that evaluated the use of lamictal in bipolar depression, 4 were negative. Only when you did a pooled analysis of all 5 studies did lamictal come out statistically better than placebo, and even then the NNT was 11 which is not particularly impressive, and less than the NNT for typical interventions for depressions (antidepressants in unipolar depression have an NNT of 7 by way of comparison).

Although many psychiatrists do use lamictal in the treatment of bipolar depression, this comes from a misunderstanding or misinterpretation of the actual literature, which shows it has some benefit compared to lithium in preventing depressive relapses in bipolar I disorder.

lamictal is very commonly used in the treatment of borderline personality disorder. there is a little bit of data supporting this (not great). the most popular and convincing theory is that because of its titration schedule it has an added placebo effect as patients continue to get improvement each time you increase the dose.

Thank you for these points, and as always presenting results from literature.

I would wonder, if it has some benefit compared to lithium in preventing depressive relapses in BPAD 1, wouldn't that be a significant (as in meaningful) use for it then? I think of depression in BPAD as sort of the great bane of the illness as far as patient experience and its treatment.

Given how effective Li is for management of mania, and I know it has this mortality benefit, and I know that suicidality in BPAD is much more complicated than just "straightforward" tx of mania/depression. It's not clear to me how all these things are linked, and from what reading I've done my impression is it's difficult to sort out in these studies?

I don't know the explanation for why the mortality benefit is seen with Li, just that it is. Is that believed to be more related to its antimanic effect or something else? Possibly it's not even that simple?

If that benefit seen with Li is related mostly to an effect on depression, I would then wonder if lamotrigine would have a similar effect, and if it does have some superiority to Li in preventing depressive relapse, would it then possibly have a similar benefit to that seen with Li regarding mortality? That hasn't been seen in studies? Do we just not have good answers to these questions?

I see what you're saying that lamotrigine isn't that great, and what you're saying with comparing it to Li. I'm just wondering if there are any other conclusions we might wonder or even have support for?

You bring up NNT for BPAD and lamotrigine, and for unipolar depression with other agents. I've heard different things from different psychiatrists, and even articles. Some maintain that bipolar depression is fundamentally a different beast on the biochemical level, and therefore different than unipolar depression and therefore supports the different treatments that we see between the two (of course part of this has to do with how mania is managed which you don't see in unipolar). Others maintain it's the same and that for some reason we see mania in the patients we see mania in, but the depressive aspect is fundamentally the same, and treatable with the same agents.

The question is, do the agents have similar effectiveness from unipolar depression to bipolar? And either viewpoint we take on all this, rather than comparing lamotrigine's NNT for depression in bipolar to other agents in unipolar, my real question is how does that NNT stack up with the other ways we actually try to treat bipolar depression?

Sort of an apples to apples comparison, I guess. If you told me that lamotrigine's NNT was 12, but it was 11 for Seroquel and 10 for Li (for the sake of argument), then that wouldn't seem so bad.

To be fair, we give all sorts of way more toxic drugs with worse SEs to what might be seen as less deadly or incapacitating conditions, with similar NNTs, all the time. So just for the sake of argument wondering how bad NNT for lamotrigine would be if you really thought it was of enough benefit to that lucky person out of 11. However I understand that if the data's weak on that benefit actually existing, this might be mental masturbation.

Just my thoughts, I appreciate any input direction education on it.

 

[Crayola227]

If this isn't the thread for this, let me know. Thank you.

 

[splik]

you have made the same error that many psychiatrists make, which is conflating preventing depressive relapse with treatment of acute bipolar depression. both are noble goals. however the data primarily supports using lamictal for the former, not the latter. if you are choosing maintenance therapy for a bipolar patient who has a lot of depressive episodes, lamictal might be a good part of the combo; for acute depression not so much. the other problem is the slow titration limits its utility in bipolar depression. the NNT for quetiapine in bipolar depression is about 5, and for the olanzapine/fluoxetine combo it is 5, and for lurasidone it is 7 cf. 11 for lamictal. it wasnt really an apples to oranges comparison because i would hope that our interventions for bipolar and unipolar depression might be similarly efficacious (even if the treatments are different).

in terms of the difference between bipolar and unipolar depression, the key distinction (at least in european psychiatry) is recurrence of episodes rather than the presence of mania/hypomania. there is a world of difference between patients with unipolar depression who have recurrent episodes vs. those who have one lifetime episode and depression is split 50:50 between those with one off episodes and those with a recurrent pattern. those with recurrent depressive illness share much more in common with patients with bipolar disorder than do patients who have a single depressive episode. there are other differences (in general bipolar depressive episodes are much shorter, tend to begin earlier in life, and are more likely to have psychotic or atypical features). but in general I would say the more important distinction is not about manic/hypomanic episodes but recurrence. we even use lithium and atypical antipsychotics for recurrent depressive illness much like bipolar disorder.

as for lithium's anti-suicidal properties, this is independent of any effect it has on mood. lamictal does not confer any antisuicidal properties (and there is some data associated AEDs in general with increased suicidal ideation).

lamictal has its place. it is probably underused in bipolar disorder. but it should not be a first, second, or third choice in the treatment of acute bipolar depression.

 

[Crayola227]

you have made the same error that many psychiatrists make, which is conflating preventing depressive relapse with treatment of acute bipolar depression. both are noble goals. however the data primarily supports using lamictal for the former, not the latter. if you are choosing maintenance therapy for a bipolar patient who has a lot of depressive episodes, lamictal might be a good part of the combo; for acute depression not so much. the other problem is the slow titration limits its utility in bipolar depression. the NNT for quetiapine in bipolar depression is about 5, and for the olanzapine/fluoxetine combo it is 5, and for lurasidone it is 7 cf. 11 for lamictal. it wasnt really an apples to oranges comparison because i would hope that our interventions for bipolar and unipolar depression might be similarly efficacious (even if the treatments are different).

in terms of the difference between bipolar and unipolar depression, the key distinction (at least in european psychiatry) is recurrence of episodes rather than the presence of mania/hypomania. there is a world of difference between patients with unipolar depression who have recurrent episodes vs. those who have one lifetime episode and depression is split 50:50 between those with one off episodes and those with a recurrent pattern. those with recurrent depressive illness share much more in common with patients with bipolar disorder than do patients who have a single depressive episode. there are other differences (in general bipolar depressive episodes are much shorter, tend to begin earlier in life, and are more likely to have psychotic or atypical features). but in general I would say the more important distinction is not about manic/hypomanic episodes but recurrence. we even use lithium and atypical antipsychotics for recurrent depressive illness much like bipolar disorder.

as for lithium's anti-suicidal properties, this is independent of any effect it has on mood. lamictal does not confer any antisuicidal properties (and there is some data associated AEDs in general with increased suicidal ideation).

lamictal has its place. it is probably underused in bipolar disorder. but it should not be a first, second, or third choice in the treatment of acute bipolar depression.

thank you for clarifying all these points!!

 

[clausewitz2]

in terms of the difference between bipolar and unipolar depression, the key distinction (at least in european psychiatry) is recurrence of episodes rather than the presence of mania/hypomania. there is a world of difference between patients with unipolar depression who have recurrent episodes vs. those who have one lifetime episode and depression is split 50:50 between those with one off episodes and those with a recurrent pattern. those with recurrent depressive illness share much more in common with patients with bipolar disorder than do patients who have a single depressive episode.

Not limited to European psychiatry, Nassir Ghaemi has been saying the same thing for years. For all that he is an arch-bipolar imperialist, the man makes some good points.

 

[PistolPete]

you have made the same error that many psychiatrists make, which is conflating preventing depressive relapse with treatment of acute bipolar depression. both are noble goals. however the data primarily supports using lamictal for the former, not the latter. if you are choosing maintenance therapy for a bipolar patient who has a lot of depressive episodes, lamictal might be a good part of the combo; for acute depression not so much. the other problem is the slow titration limits its utility in bipolar depression. the NNT for quetiapine in bipolar depression is about 5, and for the olanzapine/fluoxetine combo it is 5, and for lurasidone it is 7 cf. 11 for lamictal. it wasnt really an apples to oranges comparison because i would hope that our interventions for bipolar and unipolar depression might be similarly efficacious (even if the treatments are different).

in terms of the difference between bipolar and unipolar depression, the key distinction (at least in european psychiatry) is recurrence of episodes rather than the presence of mania/hypomania. there is a world of difference between patients with unipolar depression who have recurrent episodes vs. those who have one lifetime episode and depression is split 50:50 between those with one off episodes and those with a recurrent pattern. those with recurrent depressive illness share much more in common with patients with bipolar disorder than do patients who have a single depressive episode. there are other differences (in general bipolar depressive episodes are much shorter, tend to begin earlier in life, and are more likely to have psychotic or atypical features). but in general I would say the more important distinction is not about manic/hypomanic episodes but recurrence. we even use lithium and atypical antipsychotics for recurrent depressive illness much like bipolar disorder.

as for lithium's anti-suicidal properties, this is independent of any effect it has on mood. lamictal does not confer any antisuicidal properties (and there is some data associated AEDs in general with increased suicidal ideation).

lamictal has its place. it is probably underused in bipolar disorder. but it should not be a first, second, or third choice in the treatment of acute bipolar depression.

Thanks for this awesome response! I don’t use lamotrigine all that often, but I think I’ll start doing so. Like one of the above posters, derm has never been my strong Suite so that’s been the biggest detractor for my using it up until now.

 

[NickNaylor]

At our institution, it's the general practice to stop lamotrigine if ANY type of rash develops following initiation of treatment. The downside of this is that we are probably including a lot of people that we label as "failing" treatment due to adverse effects when they may have had only a very minor drug-related rash or simply a rash that was completely unrelated to the initiation of the medication.

I tend to agree with @clausewitz2 in that any rash on mucosa is very concerning and I would stop lamotrigine immediately for anything on or near mucosa. Other rashes - e.g., on the trunk - I would evaluate and likely continue with cautious observation and extensive warning for the patient unless it was a very serious rash.

 

[whopper]

I've treated the most sickest patients. I've treated patients that didn't need a psychiatrist but really just needed psychotherapy. (Meaning they didn't need meds but it really was a personality disorder or they just needed someone to listen to them.

I've done jails, prisons, geriatric, acute adult inpatient, forensic unit, long-term inpatient (pts that were treatment resistant and at their best couldn't be discharged), outpatient, private inpatient, well pretty much everything.

The meds highly varied per treatment setting. E.g. I almost never treated ADHD on inpatient units. It's almost (emphasis on almost) never an inpatient issue.

In inpatient units I tended to give Depakote, Lithium, Risperidone and Olanzapine more so. Why? Cause these people had severe illness and those meds are more efficacious. I hardly ever gave Lamotrigine because it'd take weeks to get to the right dosage and it's not effective in treating mania. (It can prevent mania but once it's on Lamotrigine isn't effective).

In outpatient I hardly give out Depakote, Lithium, Risperidone, or Olanzapine. Why? Cause most of my patients in outpatient are stable and their mental illness rarely gets severe. They can be stabilized with lower-efficacy meds with better side effect profiles. I give out Lamotrigine much more in this situation. Also I have many ADHD patients in this type of clinical situation.

If one, for example, only works acute inpatient they all of a sudden get this bias that Lamotrigine is useless, that ADHD doesn't exist, that everyone should be treated on the high-efficacy meds with worse side effect profiles, etc. If one, for example, only works outpatient without many severe patients they'll get an impression Lithium is always too toxic for the risk.

I remember graduating from residency hardly ever treating ADHD and thinking it was in general BS. I don't think this anymore.

I also remember working in a jail, putting a patient on Olanzapine and the patient having no access to food in his cell other than the scheduled breakfast, lunch and dinner actually fainted from hunger. Then I remember seeing another, then another, then another faint. This virtually never happens in regular outpatient psychiatry where patients have easy access to food.

I remember seeing the British version of Kitchen Nightmares (the US version blows) and Gordon Ramsay was trying to fix up a low-key restaurant. Despite being used to working in the finest of eating establishments, he was able to adjust gears and get a place that wasn't trying to get fine dining. He'd tell the chef to focus on simple plus good approaches and tell the management they need to focus not on making huge amounts of money per customer but quick service, good food and then get people in and out very quickly. On another episode he was working in a very expensive restaurant where he told the management to focus on making the meals incredible dining experiences where they'd charge huge amounts per meal. He knew how to change his approach for the right situation.

 

[whopper]

I mentioned the patient I had with full body rash and fever from rapid lamotrigine initiation with no titration,

And this begs the question. WTF was the doctor who did this bold (not in a good way) and foolhardy treatment thinking? I never do rapid titration of it. There's a reason why you titrate this med slowly.

"Oh by the way we titrate this med very slowly because it can cause a fatal condition but for you we're going to do the special treatment. We're going to put your life at risk by not doing the recommended slow titration."

This is by no means a reason to be scared of this med. The doctor who did a rapid titration either wasn't thinking or there was some type of very out-of-the-norm exception that could've warranted this approach.

"Oh and by the way I pioneered a new approach before surgery to instead of washing your hands, do a rectal exam, don't wash your hands, and then do surgery. What do you think of my brilliant new approach?"

One time a neurologist in the hospital I worked at put a patient on Lamotrigine 400 mg daily starting day one then transferred her to my unit with no written justification to what he did. I called him asking him his rationale and he wouldn't return my phone calls. I documented what happened, and thankfully there was no SJS but I was majorly ticked off. Yes I could've stopped the Lamotrigine but the patient suffered severe and chronic seizures, this was the only seizure med the neurologist ordered and when I ordered a neurology consult they refused to show up to the unit to check up on that patient.

 

[hamstergang]

I also remember working in a jail, putting a patient on Olanzapine and the patient having no access to food in his cell other than the scheduled breakfast, lunch and dinner actually fainted from hunger. Then I remember seeing another, then another, then another faint. This virtually never happens in regular outpatient psychiatry where patients have easy access to food.

Is it actually possible to have a hunger induced syncopal episode when the issue isn't inadequate food intake but instead artificially elevated hunger? I mean, I get the point of your post regardless, but I don't know what mechanism you believe to be at play here.

 

[birchswing]

Is it actually possible to have a hunger induced syncopal episode when the issue isn't inadequate food intake but instead artificially elevated hunger? I mean, I get the point of your post regardless, but I don't know what mechanism you believe to be at play here.

I've been on both Zyprexa and Seroquel and they are a beast with making you need to eat. I've fallen asleep mid-bite of food and woken a second later choking. I have Zyprexa stretch marks. 60 lbs in a couple of months.

IIRC insulin resistance increases nearly immediately on Zyprexa as does insulin production. This happens before people ever gain weight on the drugs (and it explains why they gain the weight—your cells are starving so you need higher and higher blood glucose levels). I've never had an insulinoma, but I wonder if it's similar. I used to try going to sleep on Seroquel (I didn't take it for sleep but had to take it at night because couldnt stay awake in day on it) not giving in to the hunger and it would make me have massive hypnic jerks as I fell asleep if I didn't give in to the eating—almost seizure-like. And while they had extremely powerful sedating effects (an effect I hated), the hunger-inducing effects competed with it and I'd lose the fight about an hour after falling asleep and stagger to the kitchen eating anything with carbs.

It does weird stuff to you. Because of having been on those meds, I now believe that people who are massively obese (like 600 plus pounds) must have a medical condition beyond a lack of moral fortitude. Being off Zyprexa, I could not physically will myself to gain the weight I did when I was on it if I wanted to. And on it, I could not will myself not to eat what that drug made me feel I had to eat. It's not just a lack of satiety (though it is that), but it's also an awful feeling in your head if you don't give in to it.

They used to give psychiatric patients overdoses of insulin on purpose to cause seizures. I can't say that I had seizures, but the effect is definitely awful if you don't give in to the cravings. I used to get most of my calories for the day after my evening dose of Seroquel, which I took for years. It was a very strong effect, but by the time I woke up the next day, the cravings were gone. It made me eat combinations of things I would never consider eating not on it--just going for the maximum punch of carbs and fat, no matter how weird the food combinations were.

Anyhow, all that is to say, I could imagine bad neuroglycopenic type symptoms happening giving someone a drug that increases insulin, insulin resistance, and not letting them eat ad libitum.

EDIT: I actually just had a friend who I used to talk to on the phone at night, and the Seroquel effect was so regular all I had to say was "it's hitting" and she knew I just had minutes before I was going to go out. She knew all about the eating. Her SO was just put on Seroquel and she called me asking what to do because he's night-eating and gaining a lot of weight (but otherwise generally much better). They're trying to find snacks that are less caloric. I swear, it's almost like you need some sawdust to fill the first 90% of that bottomless pit so you could get some fullness without the calories, but even then you'd need 10% (probably more) to get that glucose up that your body is demanding. I used to try to think up things that would take up space but not be terribly caloric, but it never really worked out. You don't really want celery sticks in that state.

 

[st2205]

Is it actually possible to have a hunger induced syncopal episode when the issue isn't inadequate food intake but instead artificially elevated hunger? I mean, I get the point of your post regardless, but I don't know what mechanism you believe to be at play here.

I think it would be taking what the patient says at face value. I’d be more inclined to suspect supratentorial origin or malingering, but I thought the rest of the post was all solid points. I think that’s one of the things more interesting about psychiatry training (on average), and other specialties where you’re the go-to for the subject matter (as opposed to a specialty that is setting-based like EM, CC, or anesthesia) — it’s fascinating how seeing the whole spectrum influences your decision-making abilities at any point along that spectrum. I was recently speaking with a med school friend who’s an anesthesiologist about issues in medicine and the stark difference in our approach was interesting to me, much of which I felt was the lack of understanding of longitudinal care on an outpatient basis, and not understanding what those challenges are. Unfortunately, that can’t be taught in medical school or residency unless one does it. But I’m getting off tangent.

 

[Crayola227]

And this begs the question. WTF was the doctor who did this bold (not in a good way) and foolhardy treatment thinking? I never do rapid titration of it. There's a reason why you titrate this med slowly.

"Oh by the way we titrate this med very slowly because it can cause a fatal condition but for you we're going to do the special treatment. We're going to put your life at risk by not doing the recommended slow titration."

This is by no means a reason to be scared of this med. The doctor who did a rapid titration either wasn't thinking or there was some type of very out-of-the-norm exception that could've warranted this approach.

"Oh and by the way I pioneered a new approach before surgery to instead of washing your hands, do a rectal exam, don't wash your hands, and then do surgery. What do you think of my brilliant new approach?"

One time a neurologist in the hospital I worked at put a patient on Lamotrigine 400 mg daily starting day one then transferred her to my unit with no written justification to what he did. I called him asking him his rationale and he wouldn't return my phone calls. I documented what happened, and thankfully there was no SJS but I was majorly ticked off. Yes I could've stopped the Lamotrigine but the patient suffered severe and chronic seizures, this was the only seizure med the neurologist ordered and when I ordered a neurology consult they refused to show up to the unit to check up on that patient.

I didn't make it clear that the patient who had fever, full body rash after lamotrigine initation, admitted for concern for SJS, later found to have DRESS - the patient was given the Rx and instructions for slow titration. The prescribing doc had done due diligence in writing it and explaining that a titration should occur and how, and about rash being serious. This was reported by the patient. I don't know that the doc made a point to scare them about the risk for SJS and its deadly-ness. Perhaps they should have, not sure it would have made a difference given what the patient and SO reported next.

However, the patient just started taking it at the target dose day 1. When asked why, just sorta shrugged. SO was collateral, they both seemed to support, and I believe, this was legitmately an idiotic brain fart that no one could explain otherwise, and not a suicide/self harm attempt.

It seemed too, that the patient's SO was typically in charge of overseeing the patient's med management (not because he lacked capacity, my understanding was that the SO was just better at tracking, clearly) and that in this instance he took some initiative for once and didn't really think about/account for titrating, and bad stuff happened.

We all know patients who make these sorts of errors.

I pointed it out, because sometimes patients do wrong things and rash happens (too quick to get to target as in this case, or forget to take and then restart at target (I saw rash here, med was dc'd and then the protocol for rechallenge was done) or rapid d/c (have not seen this)) are all not exactly uber rare scenarios in what patients can do with any med. It's just more dangerous with some meds than others, clearly.

Given that, if I were counseling a patient I would cover all 3 points: titrate slowly, don't forget, if you forget for longer than 3 days you should stop taking it and we will have to talk about a restart, and don't stop taking it all of a sudden, we should taper. Basically, not being consistent and any major changes in the levels in your body, could trigger life threatening rash. That's rare, so we don't have to be scared, we do need to be careful.

My take on it anyway.

 

[whopper]

Thanks for the information on the SJS case. I've seen some (idiot) doctors not warn patients about the SJS or not tell the patient to titrate the dosage up like it's supposed to be done.

Is it actually possible to have a hunger induced syncopal episode when the issue isn't inadequate food intake but instead artificially elevated hunger? I mean, I get the point of your post regardless, but I don't know what mechanism you believe to be at play here.

I'm not sure either. I don't think they were faking it either. Trust me on that. The situation I was in at that jail was extremely unethical. E.g. by professional guidelines jails are supposed to have agreements with local hospitals to take their patients. This jail not only didn't have it, but the local politicians weren't interested in following professional guidelines, and although I was attached to a university and told the university this was unacceptable my superiors at the university did nothing to address the issue. The only times they mentioned the jail much was in regards to the money they were paid by the jail to provide a psychiatrist (and the money was very good-but it wasn't going into my pocket, I just got usual attending wages while they took the money, put it in their pockets and got paid as much as the next guy and the next guy wasn't making good money for the department).

So even though the university was paid to provide the jail with attendings, they wouldn't agree to take the jail's patients if inpatient admission was needed.

In effect it was next to impossible to get patients admitted. If we had ambulances bring a patient to a local hospital the hospital literally would discharge the patient despite being in acute danger. (E.g. pt bashed their head in pretty badly and the ER refuses to admit the patient. Another patient was about to be tossed out of the ER and literally asphyxiated himself to the point of unconsciousness in the ER forcing them to admit him and they were ticked off with us for sending him to them in the first place).

Point is that malingerers hardly ever got anything out of their malingering cause guess what? Even the REAL PATIENTS couldn't get out of that jail if they needed to go to the hospital! That was usually what malingerers were trying to attempt by faking symptoms in the jail.

This as a major killing blow to me being in academia. The entire situation was unethical with the university having a part in the situation. If we are aware that our partner is not following guidelines then we were supposed to demand they be fixed but the university was making no action to fix the situation despite that I made it clear that I thought this was unethical and possibly even illegal. I demanded the situation be fixed but a year later literally no actions were taken. I just wasn't sounding off. I told everyone involved actions we needed to take and I'd do the work to make them happen but was told no on all of the orders I gave by my superiors. Also despite this horrendous issue (which just by itself would've been enough to make any reasonable attending leave) it was only one of several problems at that place with several other horrendous issues that were going on all of which would make any reasonable person leave.

Another point I was trying to make above is depending on the clinical scenario very very different things happen.

I don't think those patients were malingering. Faking fainting is not on the usual list of suspected malingering symptoms and when it happened, trust me, in the jail the nurses would do things nurses in a hospital would not. E.g. chest rubs that bordered on assault, smelling salts (never given in the hospital but it was given in a jail several times), placing patients in Ferguson smocks, etc. I suspect that perhaps their blood sugars dropped.

I've seen patients that were sincerely suicidal and didn't tell me cause they didn't want to be placed in a Ferguson smock and a high security room where they were locked in a small cell, 23 hrs a day, with no sunlight, and the hour they could spend outside the cell was in a room with no sunlight that looked like an unfinished basement with poor lighting.

 

[hamstergang]

I don't think they were faking it either. Trust me on that.

I wasn't suggesting faking, I was suggesting that they weren't fainting as a result of hunger.

 

[Crayola227]

I've been on both Zyprexa and Seroquel and they are a beast with making you need to eat. I've fallen asleep mid-bite of food and woken a second later choking. I have Zyprexa stretch marks. 60 lbs in a couple of months.

IIRC insulin resistance increases nearly immediately on Zyprexa as does insulin production. This happens before people ever gain weight on the drugs (and it explains why they gain the weight—your cells are starving so you need higher and higher blood glucose levels). I've never had an insulinoma, but I wonder if it's similar. I used to try going to sleep on Seroquel (I didn't take it for sleep but had to take it at night because couldnt stay awake in day on it) not giving in to the hunger and it would make me have massive hypnic jerks as I fell asleep if I didn't give in to the eating—almost seizure-like. And while they had extremely powerful sedating effects (an effect I hated), the hunger-inducing effects competed with it and I'd lose the fight about an hour after falling asleep and stagger to the kitchen eating anything with carbs.

It does weird stuff to you. Because of having been on those meds, I now believe that people who are massively obese (like 600 plus pounds) must have a medical condition beyond a lack of moral fortitude. Being off Zyprexa, I could not physically will myself to gain the weight I did when I was on it if I wanted to. And on it, I could not will myself not to eat what that drug made me feel I had to eat. It's not just a lack of satiety (though it is that), but it's also an awful feeling in your head if you don't give in to it.

They used to give psychiatric patients overdoses of insulin on purpose to cause seizures. I can't say that I had seizures, but the effect is definitely awful if you don't give in to the cravings. I used to get most of my calories for the day after my evening dose of Seroquel, which I took for years. It was a very strong effect, but by the time I woke up the next day, the cravings were gone. It made me eat combinations of things I would never consider eating not on it--just going for the maximum punch of carbs and fat, no matter how weird the food combinations were.

Anyhow, all that is to say, I could imagine bad neuroglycopenic type symptoms happening giving someone a drug that increases insulin, insulin resistance, and not letting them eat ad libitum.

EDIT: I actually just had a friend who I used to talk to on the phone at night, and the Seroquel effect was so regular all I had to say was "it's hitting" and she knew I just had minutes before I was going to go out. She knew all about the eating. Her SO was just put on Seroquel and she called me asking what to do because he's night-eating and gaining a lot of weight (but otherwise generally much better). They're trying to find snacks that are less caloric. I swear, it's almost like you need some sawdust to fill the first 90% of that bottomless pit so you could get some fullness without the calories, but even then you'd need 10% (probably more) to get that glucose up that your body is demanding. I used to try to think up things that would take up space but not be terribly caloric, but it never

in the interest of being off topic and space

Spoiler: Massive OT Rant on Atypicals, the pancreas, and seroquel munchies

A few points here.

One of the first case studies I ever did in medical school, was one on Abilify and a patient who presented with extremely elevated glucose, and I can't recall if it was HHS or DKA. With a normal BMI! Moving forward they were insulin-dependent.

Quite a bit of the presentation was looking at primary data on the interactions Abilify has, not only on peripheral tissue and insulin resistance, but also in how the drug interacts with the pancreas directly, on beta and alpha cells. If I do recall correctly, this was more or less true for at least most of the drugs in the class, and I do recall a list ranking the risk of metabolic syndrome/diabetes for each of the commonly used ones.

A big take home that I know that they wanted us to get, is that even with atypicals not renown for weight gain, and at normal BMI, these drugs act peripherally and on the pancreas itself, and all that do carry risk of glucose intolerance, diabetes, pancreatitis. Also that metabolic syndrome can be present without obesity.

What I don't recall, was whether or not Abilify or others, were directly toxic to beta cells, or if it was more due to increase in insulin production, which itself can be toxic to them, that can happen at the level of the cell being stimulated directly, vs peripheral factors like insulin resistance and glycemic load. I'm not sure I recall exactly, but if I had to guess I would say directly toxic given the risk of pancreatitis with many of the agents.

If we want to get into the weeds, I know that there is a whole body of literature about how insulin works in the brain. We know there's receptors in there, and other stuff going on with it. NO, peripheral insulin doesn't go in there. Anyhow, so there was some question that if atypicals affect insulin production/metabolism peripherally, might they also do so centrally? And what would the effect be? Now, this isn't to say the actions of them on dopamine, serotonin, isn't the main thing.

Now, all this may be old hat to you all, or just a really crappy recollection of outdated or erroneous pseudo-points. I find it interesting to consider atypicals either beyond their psychiatric effects or actions in the brain that may not be fully understood/off the beaten path.

Especially as someone outside psych, consideration of everything it does outside the brain seems like a good direction (not that one should not consider its psychiatric or neurological effects if outside the specialty, nor that psychiatrists don't consider the whole body).

Lastly, I'll address the very real craving for food with something like Seroquel. Here's what I do know, is that seroquel is a pretty strong antihistamine, which is part of what makes it so soporific. I couldn't tell you why, except that it's very real, but Benadryl is notorious for causing "munchies" and I've seen it and severe weight gain in patients regularly using it for sleep, especially as they gain tolerance and use higher and higher self-dosing. I don't know why it does this. Some think that what is similar between the two, "munchies" and being antihistamine, is the connection there, but I couldn't say why it seems a side effect of antihistamines.

Also +1 to the "munchies" of quetiapine "hitting" when a patient feels it kick in. A lot of patients certainly take it at night because of the sleepy factor. I also know patients who feel the onset of swallowing difficulty at that point. Sounds to me like an EPS sorta thing, but what do I know? So I've also seen the phenomenon of the patient taking their meds, and then stumbling out of bed not long after, to try to choke down some food, and also fall asleep with it in their mouths, and wake up choking. I also know patients who have woken up in the middle of the night and raided the fridge, and have no memory beyond being told they did this, finding food out, or in their mouths.

I don't know how all these things are connected. I'm actually inclined to think the "munchies" of seroquel have nothing to do with other metabolic effects it has. But despite having different MOAs as I think they do, giving a drug that BOTH gives one a compulsive need to eat, and a tendency to gain weight, is a recipe for massive gain.

 

[Crayola227]

it was someone somewhere else who brought up the dreaded M-word (malingering)

 

[whopper]

I wasn't suggesting faking,

Wasn't you, someone else I believe mentioned malingering.

But I don't think it was fainting due to an issue like hypotension. In each case the nurses reported the patient was suffering from extreme hunger. Further I've prescribed Olanzapine thousands of times and never saw healthy young males faint from even low dosages like I did at the jail. Only times I've seen people get major hypotension to the point of almost fainting was if mega dosages were given very quickly. E.g. an agitated patient punching people in the ER but even then I'd rarely see it.

Again this is a phenomenon we usually don't see in usual clinical cases cause unlike a jail or prison people usually have free access to food.