Uncharted Territory: The treatment-resistant depressed patient who is chronically suicidal

[notamindreader]

I've had patients with similar treatment refractory presentations and often it boiled down to things like alexithymia, obsessive personalities or other personality constructs that tended to sabotage treatments before they could ever take hold. I think once we could highlight what anchored them to chronically think about suicide we were able to make some inroads. But even then, it was hard work and required a coordinated clinical team to support these people.

Relating to the psychedelic work, I seriously considered recommending a patient of mine with treatment refractory complex PTSD to join an MDMA assisted psychotherapy trial but they had medical issues that excluded them from participating. I have had patients travel to Peru for week to month long Ayahuasca workshops. As I understand it, this is serious and challenging work and very much life affirming. I monitor their care more from a cultural support angle and have to say that their experiences sound exceptionally meaningful. I've never recommended someone travel to another country for care, but as mentioned above, there are 'legally' sanctioned Ayahuasca and Peyote churches in the US.

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[clozareal]

The only study that I know that's evaluated the efficacy of treatment for individuals who've had more than 4 failed medication trials for depression is pramipexole, although it's open label. N=42. mean number of failed med trials was 6. 20% of them failed ECT. they used 2.5mg/day instead of the usual 1.5mg. half of patients remitted and another third responded. it's pretty rare to see responses like that in TRD. really wish it was placebo-controlled. Although this meta-analysis on pramipexole looks promising.

I would also consider Abilify as a meta-analysis shows that it has a high effect size (~1.3), even higher than lithium surprisingly.

I've just come across an article about when pharmacotherapy becomes futile and it's better to accept that chronic reality, then using a different approach that's used more often in chronic disease/pain management than for depression. Eventually it might be worth it to consider this approach for this patient.

 

[clausewitz2]

I've just come across an article about when pharmacotherapy becomes futile and it's better to accept that chronic reality, then using a different approach that's used more often in chronic disease/pain management than for depression. Eventually it might be worth it to consider this approach for this patient.

This article in more and explicit length gets at why I was suggesting a DBT informed approach up thread. @whopper has expressed familiarity with DBT in the past so I suggested that over ACT or anything else with a strong acceptance focus. Whether or not anything that comes in a pill bottle ultimately helps, this gentleman needs to recognize and acknowledge the current reality of his situation and be seriously examining what he will do in his life if no remission ever comes or if he keeps thinking about suicide on a regular basis.

 

[futureapppsy2]

Cluster B or other PD traits/PDs aren't necessary for DBT to helpful. Second that ACT might be helpful as well. In terms of diagnosis, sounds like persistent depressive disorder (PDD; what used to be called dysthymic disorder) rather than MDD.

 

[whopper]

I'm aware of the Pramipexole data. I was introduced to it by one of the leading experts in the field of treatment-resistant depression we worked on a case together of yet another treatment-resistant patient. There is emerging data (and I don't have a link but saw it on an APA CME lecture) that in some treatment resistant cases the reward center is being understimulated and dopamine-related meds are more specific to work better on these patients. Further an elevated CRP or IL-6 is correlated with the problem further suggesting elevated levels of these inflammatory markers would suggest a dopamine-based treatment and/or antiinflammatory treatment.

Now in the case of the specific patient I have, he was already tried on Bupropion and had a bad reaction to it. Oddly, his mother, who also has treatment-resistant depression, Bupropion worked very well for her. Pramipexole, and a CRP and IL-6 lab are next options for the patient I mentioned.

I have another treatment-resistant patient (but thankfully this guy isn't suicidal) and Bupropion was the only med that worked, but later on he developed severe tinnitus from it and it could no longer be used. In that patient I also tried Sunosi but he had a bad reaction to it. Why Sunosi? It's the ony DNRI I'm aware of other than Wellbutrin.

A problem with the antiinflammatory approach is the best meds used for it (e.g. infliximab) are meds outside the psychaitrist's comfort zone in prescribing, they're all very expensive, and insurance won't pay for this meds.

 

[hamstergang]

Why Sunosi? It's the ony DNRI I'm aware of other than Wellbutrin.

There's also Methylphenidate.

Now in the case of the specific patient I have, he was already tried on Bupropion and had a bad reaction to it. Oddly, his mother, who also has treatment-resistant depression, Bupropion worked very well for her.

Is that really odd? Is there any actual evidence that we should expect some family concordance in response to psychotropic medications? I know we all basically assume it to be true but I couldn't find studies supporting this in the past.

 

[clausewitz2]

I'm aware of the Pramipexole data. I was introduced to it by one of the leading experts in the field of treatment-resistant depression we worked on a case together of yet another treatment-resistant patient. There is emerging data (and I don't have a link but saw it on an APA CME lecture) that in some treatment resistant cases the reward center is being understimulated and dopamine-related meds are more specific to work better on these patients. Further an elevated CRP or IL-6 is correlated with the problem further suggesting elevated levels of these inflammatory markers would suggest a dopamine-based treatment and/or antiinflammatory treatment.

Now in the case of the specific patient I have, he was already tried on Bupropion and had a bad reaction to it. Oddly, his mother, who also has treatment-resistant depression, Bupropion worked very well for her. Pramipexole, and a CRP and IL-6 lab are next options for the patient I mentioned.

I have another treatment-resistant patient (but thankfully this guy isn't suicidal) and Bupropion was the only med that worked, but later on he developed severe tinnitus from it and it could no longer be used. In that patient I also tried Sunosi but he had a bad reaction to it. Why Sunosi? It's the ony DNRI I'm aware of other than Wellbutrin.

A problem with the antiinflammatory approach is the best meds used for it (e.g. infliximab) are meds outside the psychaitrist's comfort zone in prescribing, they're all very expensive, and insurance won't pay for this meds.

Wellbutrin binds very weakly to DAT, so is not really great at increasing intrasynaptic dopamine. It is also not a dopamine receptor agonist, so it is unlikely to have the same effect a priori. The discrepancy in timescales between when peak neurotransmitter levels in the cleft are reached and clinical action happen means that just increasing dopamine floating around can't possibly be the mechanism by which it ultimately works.

In vitro assays suggest wellbutrin binds more weakly to DAT than sertraline does. Yes, yes, could be different in the live human and hydroxy-bupropion could be different etc. Fact is no one has published good data on this metabolite and no one has tried to patent it as a new me-too drug since it was introduced almost 50 years ago. This is suggestive to me.

@hamstergang has it right, why not stimulants if increasing dopaminergic tone is the point?

 

[clausewitz2]

I'm aware of the Pramipexole data. I was introduced to it by one of the leading experts in the field of treatment-resistant depression we worked on a case together of yet another treatment-resistant patient. There is emerging data (and I don't have a link but saw it on an APA CME lecture) that in some treatment resistant cases the reward center is being understimulated and dopamine-related meds are more specific to work better on these patients. Further an elevated CRP or IL-6 is correlated with the problem further suggesting elevated levels of these inflammatory markers would suggest a dopamine-based treatment and/or antiinflammatory treatment.

Now in the case of the specific patient I have, he was already tried on Bupropion and had a bad reaction to it. Oddly, his mother, who also has treatment-resistant depression, Bupropion worked very well for her. Pramipexole, and a CRP and IL-6 lab are next options for the patient I mentioned.

I have another treatment-resistant patient (but thankfully this guy isn't suicidal) and Bupropion was the only med that worked, but later on he developed severe tinnitus from it and it could no longer be used. In that patient I also tried Sunosi but he had a bad reaction to it. Why Sunosi? It's the ony DNRI I'm aware of other than Wellbutrin.

A problem with the antiinflammatory approach is the best meds used for it (e.g. infliximab) are meds outside the psychaitrist's comfort zone in prescribing, they're all very expensive, and insurance won't pay for this meds.

Also antinflammatory wise minocycline is cheap, relatively benign, and has reasonable evidence. Easy for someone employed full time doing more or less anything to pay for out of pocket.

 

[whopper]

@hamstergang has it right, why not stimulants if increasing dopaminergic tone is the point?

Already tried Methylphenidate. Only made him feel more "awake" but no other benefit.

 

[Stagg737]

@whopper , any updates on this case or with psych testing?

 

[psyguru]

How about a referral or 2nd opinion...perhaps someone who has done a fellowship in psychopharmacology, integrative psychiatrists or a specialist in mood disorders?? although the folate level was normal maybe a trial of enlyte?

 

[d2305]

I've seen levothyroxine used even with normal TFTs.

 

[clausewitz2]

I've seen levothyroxine used even with normal TFTs.

Probably safer liability wise to do so if TFTs are relatively normal, because then as a psychiatrist you are clearly treating 'depression' and not 'thyroid disease'

I would be inclined if I was going down the thyroid route to try out supraphysiologic doses, ramping up until TSH is < 0.01. The German group who publishes the most on this has studies where the median T4 dose is north of 400 mcg daily

 

[whopper]

Update: The patient is doing somewhat better but is still depressed. He was previously on Venlfaxine ER max dose, stopped it, but since the time I started this thread restarted it. Also he's on Buspirone the maximum dosage.

IL-6 and CRP were ordered. Both are in the normal range but the IL-6 was right at the borderline of normal to high. The problem here is IL-6, despite having emerging data that it's related to treatment-resistant depression, doesn't have enough information to correlate numbers as to what level should be considered related to the patient's depression. So these are not giving me any direction and I did a few lit-searches and didn't find anything helpful.

So as of right now I'm considering raising Venlafaxine ER to over the maximum, 262.5 mg or 300 mg daily.

I've referred him to a treatment resistant depression clinic headed by top researchers in the field. Thankfully we have that type of activity going on in this city, but I already know some of the people there and I don't think they'll be doing anything I'm not already doing or thinking. I've already picked their brains on cases like this and I've already heard their treatment-resistant playbook. Call it a blessing or a curse, they have me high on their pecking list of referrals. So yeah of course I'm proud of that, but darnit these are tough patients.

The patient does have prior treatment with Ketamine, only benefitted for 1 day after several treatments, each one being boosted to higher than usual dosage, but told him to reconsider and try Esketamine. As mentioned before, treating within the box hasn't worked. We got to try every option. I already told him that Ketamin and Esketamine are mostly the same but this is new territory and perhaps the Esketamine could work where Ketamine didn't.

Vitamin D levels were low but the data doesn't support, nor have I seen Vitamin D correction ever significantly improving a depressed patient. In any cause I will correct his Vitamin D levels cause there's very little I haven't already done and I don't want to leave any stone unturned.

ECT and DBS-he doesn't want to do these. TMS was already tried with no benefit. He is open to trying a hallucinogen except that we have no one we know that can provide it.

 

[robellis]

You can go up to 375 mg of Effexor per guidelines

 

[hebel]

I always wanted to just buy a stationary bike and have a patient work up a sweat on it for 45-60 minutes 3-6 days a week. Try making the guy exercise.

 

[birchswing]

I always wanted to just buy a stationary bike and have a patient work up a sweat on it for 45-60 minutes 3-6 days a week. Try making the guy exercise.

I've had a lot of ideas I haven't posted, and this was one of them! Nice to know I wasn't too far off base with that idea at least.

Also, an interesting tidbit, maybe all of you already know this, but I only learned it I think last year: endorphins are named as a portmanteau of endogenous and morphine.

But I think it's more increasing blood flow to the brain.

 

[FlowRate]

I've referred him to a treatment resistant depression clinic headed by top researchers in the field. Thankfully we have that type of activity going on in this city, but I already know some of the people there and I don't think they'll be doing anything I'm not already doing or thinking.

As you mentioned, 300mg Effexor if there's been a partial response to lower doses. Not even a TRD specialist thing, just usual depression care.

 

[SmallBird]

You need a formulation. Almost certainly, the number of med trials this patient has had will have contributed to some very unhelpful beliefs around how recovery works.

 

[nexus73]

If he commits suicide you could be a high liability cause he's suicidal and you knew he was for months.

Sorry to belabor this point as it's off topic. Is someone with chronic SI really a high liability because you don't hospitalize them? Aren't we psychiatrists seeing people with SI all the time? Assessing for imminent risk? Prescribing appropriate treatments? If imminent risk is elevated you get them admitted. But if imminent risk is low you would just document to that, safety plan, and comment how inpatient care is not indicated. Whopper, as a forensic psychiatrist, would your expert opinion be that anyone with chronic SI should be admitted? How do you imagine a plaintiff's expert would argue the treating doctor acted negligently if a patient with chronic SI, but assessed to have low imminent risk, committed suicide?

 

[clausewitz2]

Sorry to belabor this point as it's off topic. Is someone with chronic SI really a high liability because you don't hospitalize them? Aren't we psychiatrists seeing people with SI all the time? Assessing for imminent risk? Prescribing appropriate treatments? If imminent risk is elevated you get them admitted. But if imminent risk is low you would just document to that, safety plan, and comment how inpatient care is not indicated. Whopper, as a forensic psychiatrist, would your expert opinion be that anyone with chronic SI should be admitted? How do you imagine a plaintiff's expert would argue the treating doctor acted negligently if a patient with chronic SI, but assessed to have low imminent risk, committed suicide?

And how does the plaintiff's expert convincingly rebut defense expert who can point to piles of published research suggesting IP hospitalization does bupkis in modifying suicide risk for chronically suicidal folks, I wonder?

 

[FlowRate]

And how does the plaintiff's expert convincingly rebut defense expert who can point to piles of published research suggesting IP hospitalization does bupkis in modifying suicide risk for chronically suicidal folks, I wonder?

Especially, IIRC, when the pt in question has been chronically suicidal and never actually attempted.

 

[whopper]

. Is someone with chronic SI really a high liability because you don't hospitalize them? Aren't we psychiatrists seeing people with SI all the time? Assessing for imminent risk?

A problem here is if the case goes to court you will not have a judge and/or jury that highly familiar with the type of case with the chronically suicidal patient that doesn't have to be hospitalized. Suicidal ideation for most people is not an understandable phenomenon. Add to this the expectations of hospitalization are also highly misunderstood. People believe hospital means complete and full quick recovery. No. Hospitalization means they're there for a few days, and if the patient simply says they're not suicidal they're almost always discharged whether they are or are not suicidal and before the duration where you even expected an antidepressant to even take effect, add to that antidepressants only work about 50% of the time.

So while a judge and jury all made of experienced mental health professionals will have better insight, you will be judged by laymen. Also there isn't a strong legal precedent (and judges understand the law, not medicine) that will protect you.

 

[clausewitz2]

A problem here is if the case goes to court you will not have a judge and/or jury that highly familiar with the type of case with the chronically suicidal patient that doesn't have to be hospitalized. Suicidal ideation for most people is not an understandable phenomenon. Add to this the expectations of hospitalization are also mostly unknown. People believe hospital means complete and full quick recovery. No. Hospitalization means they're there for a few days, and if the patient simply says they're not suicidal they're almost always discharged whether they are or are not suicidal and before the duration where you even expected an antidepressant to even take effect, add to that antidepressants only work about 50% of the time.

So while a judge and jury all made of experienced mental health professionals will have better insight, you will be judged by laymen. Also there isn't a strong legal precedent (and judges understand the law, not medicine) that will protect you.

Isn't the point of having an expert witness to explain this to the court based on their professional knowledge and experience?

 

[Stagg737]

And how does the plaintiff's expert convincingly rebut defense expert who can point to piles of published research suggesting IP hospitalization does bupkis in modifying suicide risk for chronically suicidal folks, I wonder?

They don't have to. The plaintiff's attorney just plays the sympathy card that the evil doc didn't save this patient because they just don't care enough.

Isn't the point of having an expert witness to explain this to the court based on their professional knowledge and experience?

It is, but who needs data or an expert witness when the jury places a verdict based on emotional arguments. It's the reason many of the cases where the doc is found guilty get overturned on appeal when a judge makes their ruling based on actual standards instead of emotions (like the case in this forum of the IM doc in NYC who lost and had the verdict overturned).

 

[birchswing]

Do you think his depression would lift at all knowing 75 posts have been made about him?

When I see a doctor it's usually, "What meds are you on again?" And that's the doctor prescribing the meds!

 

[Stagg737]

I forget, was psych testing ever ordered? I'm still curious about underlying personality aspects if it was (obviously you know patient best though).

The patient does have prior treatment with Ketamine, only benefitted for 1 day after several treatments, each one being boosted to higher than usual dosage, but told him to reconsider and try Esketamine. As mentioned before, treating within the box hasn't worked. We got to try every option. I already told him that Ketamin and Esketamine are mostly the same but this is new territory and perhaps the Esketamine could work where Ketamine didn't.

Vitamin D levels were low but the data doesn't support, nor have I seen Vitamin D correction ever significantly improving a depressed patient. In any cause I will correct his Vitamin D levels cause there's very little I haven't already done and I don't want to leave any stone unturned.

Esketamine's binding affinity may provide extended benefits if ketamine was actually effective. Patient could also try using some PCP or wet (kidding). I have actually had a couple of patients who had fairly significant improvements with Vit D repletion, though these were individuals with fairly severe deficiencies (<5) and they did still require other medications. Also, any trials with light therapy? I realize there's unlikely to be a seasonal affective component, but if he's got low vit D and isn't an outdoor person could be a cheap and easy attempt.

 

[futureapppsy2]

I forget, was psych testing ever ordered? I'm still curious about underlying personality aspects if it was (obviously you know patient best though).



Esketamine's binding affinity may provide extended benefits if ketamine was actually effective. Patient could also try using some PCP or wet (kidding). I have actually had a couple of patients who had fairly significant improvements with Vit D repletion, though these were individuals with fairly severe deficiencies (<5) and they did still require other medications. Also, any trials with light therapy? I realize there's unlikely to be a seasonal affective component, but if he's got low vit D and isn't an outdoor person could be a cheap and easy attempt.

Wet?

 

[Stagg737]

Wet?

Marijuana dipped "formaldehyde", which is actually liquid PCP. Very common in my geographic area.

 

[cara susanna]

So, as a DBT-trained therapist who works with a lot of people who have chronic SI, here are my thoughts.

- It sounds like you're working harder than he is. I agree with the specific questions about therapy. Has he actually tried an evidence-based protocol for depression? Did he really engage in it?
- DBT could still be helpful - it was developed to treat suicidality first and foremost.
- CBT for suicide prevention is another option, although one I know less about.
- HOWEVER - this isn't someone I'd be worried about with suicide. There is no history of suicidal behavior. He has demonstrated a repeated ability to keep himself safe despite chronic SI, even with a plan. It actually takes a lot to go from SI to behavior and not everyone will. As others have mentioned, why hasn't he done it? Part of him must want to live, and I point that out to patients like this.
- I always think of suicidal ideation as a coping mechanism and try to replace it with more effective coping skills. That's essentially what DBT does. What function is the SI serving? Is it making him feel better? I bet it must be, or he wouldn't be doing it. DBT would tell him to take suicidality off of the table, because he is never going to learn effective coping if he keeps using that.
- I also agree that an acceptance-based or third wave approach for therapy would likely be helpful, be it DBT or ACT.

 

[Mad Jack]

Some people just seem to get stuck in these thought loops, frankly I wonder if there's some OCD component to it, or something else. Or it's just a thought pattern, I think that can happen in otherwise normal individuals.

I agree about trying lithium. Perhaps his chronic depression/suicidality yet preserved function is some sort of mild variant in the bipolar realm. ..? That may make zero sense but...

(I think we've talked in this forum about to what extent does unipolar depression vs bipolar disorder present separate illnesses with a unique basis in the brain and hence different responses to meds vs a continuum vs bipolar is like unipolar depression plus special features.... I have no idea)

in any case if his depression/suicidality isn't responding to typical treatment maybe it's time to treat it like something else.

What do you do for OCD/anxiety that aren't the meds you have used so far? I shudder to suggest benzos of course....

As far as ECT, and I don't know the best way to put this to this guy, but at some point when you're treating a disease, you have no choice. That's what it means to be sick. Like with cancer, you get left with limited choices, and none of them are good or anything you really want. If you're really fighting for your life you do whatever you have to do. I've seen some psych have this kind of tough love talk and it worked. Lithium and ECT can have some real side effects, but a lot of ppl that have held out for years and finally do it, can't believe they didn't do it sooner, even if they do suffer side effects. He also has his family to consider.

If he's otherwise compliant I don't see a reason to terminate. I understand the liability but all docs have liability and I think what people said here about CYA makes a lot of sense. I've never been sued so it's easier for me to say I'd feel better about that then terminating this guy and then later he offs himself than if he were to stay my patient and then I get blamed.

I was actually going to bring up bipolar disorder and whether he had been trialed on any mood stabilizers aside from lithium. Phenelzine also came to mind, as I've had a highly treatment resistant patient that responded to it after it was recommend by someone with much more experience than myself.

 

[Psychresy]

I was actually going to bring up bipolar disorder and whether he had been trialed on any mood stabilizers aside from lithium. Phenelzine also came to mind, as I've had a highly treatment resistant patient that responded to it after it was recommend by someone with much more experience than myself.

I remember a particular patient intern year whom was inpatient and had tried everything in the book including ECT and responded to parnate. I thought I remember hearing that MAOI actually have greater efficacy than SSRI, but the drop out rates are obviously higher (or am I making this up?)

 

[Mad Jack]

I remember a particular patient intern year whom was inpatient and had tried everything in the book including ECT and responded to parnate. I thought I remember hearing that MAOI actually have greater efficacy than SSRI, but the drop out rates are obviously higher (or am I making this up?)

We don't really divide up depression the way they used to, but this particular psychiatrist has been around a while and insisted that the more melancholic sorts of depressed patients (persistent, unrelenting depression with no identifiable triggers that was not episodic in nature) seemed to be less responsive to other medications but more responsive to MAOIs for whatever reason. No idea how good the research is on this sort of thing, I'll have to go digging

 

[Alemo]

We don't really divide up depression the way they used to, but this particular psychiatrist has been around a while and insisted that the more melancholic sorts of depressed patients (persistent, unrelenting depression with no identifiable triggers that was not episodic in nature) seemed to be less responsive to other medications but more responsive to MAOIs for whatever reason. No idea how good the research is on this sort of thing, I'll have to go digging

Well this is the “atypical” persistent depression that is sometime seen in very interpersonally sensitive people right? With hypersomnia and increased appetite?

I read an interesting study awhile back hypothesizing that this condition was similar to borderline personality and bipolar II disorder.

 

[Stagg737]

We don't really divide up depression the way they used to, but this particular psychiatrist has been around a while and insisted that the more melancholic sorts of depressed patients (persistent, unrelenting depression with no identifiable triggers that was not episodic in nature) seemed to be less responsive to other medications but more responsive to MAOIs for whatever reason. No idea how good the research is on this sort of thing, I'll have to go digging

I have 2 very experienced and excellent attendings who say the same thing, but also include that TCAs may also be a bit more efficacious for atypical depression as Alemo described (sensitive to criticism, has some happy days during periods of increased depression, hypersomnia, etc). I haven't seen data for it, but I'm guessing there is since I've also heard this before in another part of the country.

Well this is the “atypical” persistent depression that is sometime seen in very interpersonally sensitive people right? With hypersomnia and increased appetite?

I read an interesting study awhile back hypothesizing that this condition was similar to borderline personality and bipolar II disorder.

Would love to read that if you can find it easily.

 

[Alemo]

Something like this...

Are atypical depression, borderline personality disorder and bipolar II disorder overlapping manifestations of a common cyclothymic diathesis?

The constructs of atypical depression, bipolar II disorder and borderline personality disorder (BPD) overlap. We explored the relationships between these constructs and their temperamental underpinnings. We examined 107 consecutive patients who met DSM-IV ...

www.ncbi.nlm.nih.gov

 

[clausewitz2]

I have 2 very experienced and excellent attendings who say the same thing, but also include that TCAs may also be a bit more efficacious for atypical depression as Alemo described (sensitive to criticism, has some happy days during periods of increased depression, hypersomnia, etc). I haven't seen data for it, but I'm guessing there is since I've also heard this before in another part of the country.



Would love to read that if you can find it easily.

The original papers delineating a difference in treatment response between atypical and melancholic depression came down on MAOIs being more useful for atypical depression thus described and TCAs being more useful for melancholic depression. There is some work suggesting TCAs best SSRIs for really severe depression and certainly plenty of clinical experience in that regard. I wouldn't put much stock in the reality of a clear differentiation between these types but at the same time if I encounter someone with a lot of psychomotor slowing, intermittent nihilistic fixed ideas who has stopped eating and is wearing out the floorboards pacing at 3 AM ruminating about how awful they are as a person Pamelor had a good chance of being my first stop.

MAOIs are pretty well tolerated and apart from a very, very limited number of medications (SSRIs/SNRIs, tramadol, demerol, methadone) they have virtually no drug interactions and minimal side effects. Main problem is people who get too orthostatic at reasonable dose but this can be addressed. Certainly people seem to tolerate them better than high doses of most TCAs. Parnate can be a little tricky because people often start sleeping way less but it doesn't actually seem to induce manic switching any more than placebo. Cannot be said about TCAs.

Then again there is no reason you cannot combine most TCAs and MAOIs and as has been discussed before on this board nortriptyline + parnate used to be a fairly standard TRD sort of combo. For the truly bold the old school folks will suggest Ritalin + MAOI.

 

[clausewitz2]

Something like this...

Are atypical depression, borderline personality disorder and bipolar II disorder overlapping manifestations of a common cyclothymic diathesis?

The constructs of atypical depression, bipolar II disorder and borderline personality disorder (BPD) overlap. We explored the relationships between these constructs and their temperamental underpinnings. We examined 107 consecutive patients who met DSM-IV ...

www.ncbi.nlm.nih.gov

Did Perugi and Akiskal ever meet a condition that they didn't think was 'soft bipolar'?

 

[mmms85]

Have you thought about prescribing l-methylfolate calcium salt? I'm not sure how well supported this is in literature, but anecdotally I had a treatment resistant patient try 15mg QD (brand name in the USA is Denovo) and it significantly improved his depression to the point he was able to work and get off of SSI. With a refractory patient such as this, even long shots like this are worth as try in my opinion.

(Apologies if I somehow break a rule, I'm new to this forum and just getting my bearings)

 

[whopper]

I've already tried L-Methylfolate, no success.

The patient is somewhat improved. Instead of severe depression with suicidal ideation he's improved to moderate depression almost bordering the severe side with passive SI and no intent to act upon it.

And per him (and prior psychiatrists who treated him, some of whom are renown) that's the best he gets.

I hate saying it but it's like the STAR*D says. While the overwhelming majority will at least get some benefit from pharmacotherapy there is a small percentage where nothing works, or very little improvement.

If you got a rep for being good, oh yeah the respect, the prestige, all happens, and then they toss you the hardest cases.

 

[Onions]

Psychedelics. Give him the mushroom.

 

[birchswing]

Psychedelics. Give him the mushroom.

Just saw this today:

Newly decriminalized psychedelics intrigue travelers seeking therapies

The palm-fringed beachfront and breezy cabanas at MycoMeditations are the stuff of glossy...

www.chron.com

 

[hebel]

Hey @whopper, any further updates?

Came across this thread again when looking for ideas for a patient I've been dealing with.

 

[psychma]

Wrong thread

 

[hebel]

Wrong thread

?

 

[psychma]

?

I responded in the wrong thread and couldn’t delete.

 

[whopper]

I forgot to add...
Same patient I mentioned above was tried on Auvelity. It worked wonders. PHQ-9 went from high teens to low 20s to about 7 points. (Error, low 20s to low teens). He said he felt SO MUCH BETTER.

So this is like 4 months ago.

Then like 3 months ago he said it still helps but PHQ-9 is back up to the mid teens. WTF happened I don't know.
Only thing odd with his labs and I did every freaking lab I could think of, even the labs with low links to depression such as EBV is he has a chronic EBV antibody level. I speculate now he might have chronic EBV that's causing fatigue and depression. The problem, however, is that WTF to do about it? There are no good treatments and frankly that's outside my area.

So I referred him to a university infectious disease doctor. The doctor told me him he agreed there's some chronic EBV going on, but basically told him there's nothing that can be done about it.

 

[nexus73]

I forgot to add...
Same patient I mentioned above was tried on Auvelity. It worked wonders. PHQ-9 went from high teens to low 20s to about 7 points. He said he felt SO MUCH BETTER.

So this is like 4 months ago.

Then like 3 months ago he said it still helps but PHQ-9 is back up to the mid teens. WTF happened I don't know.
Only thing odd with his labs and I did every freaking lab I could think of, even the labs with low links to depression such as EBV is he has a chronic EBV antibody level. I speculate now he might have chronic EBV that's causing fatigue and depression. The problem, however, is that WTF to do about it? There are no good treatments and frankly that's outside my area.

So I referred him to a university infectious disease doctor. The doctor told me him he agreed there's some chronic EBV going on, but basically told him there's nothing that can be done about it.

I know I read not personality disorder, but this seems exactly like the profound placebo response we see in patients with BPD, come back a month after a new med feeling amazing, then another month goes by and it's back to feeling bad like nothing is working, rinse and repeat. And we'd expect a more notable placebo with Auvelity because I assume people consciously feel something when their serum concentration of DXM skyrockets.

 

[annoyedpsychiatrist]

I know I read not personality disorder, but this seems exactly like the profound placebo response we see in patients with BPD, come back a month after a new med feeling amazing, then another month goes by and it's back to feeling bad like nothing is working, rinse and repeat. And we'd expect a more notable placebo with Auvelity because I assume people consciously feel something when their serum concentration of DXM skyrockets.

i agree, this case seems like personality disorder to me. Placebo response, chronic suicidality.... Ill be that negative/brutally honest guy. In my experience it isnt the ones who continuously endorse SI who actually do it, its the one that leave a not after the fact or say nothing at all and just do it. Often when people claim SI its for attention, an aspect of facticious disorder, or because they dont want to harm themself and they're just scared of how they feel/cry for help. Not everyone is that way, but occurs quite often.

From another standpoint, if he did try something, how could anyone blame you? Youve been documenting his SI, and im sure youve followed standard of care. You didnt cause him to have SI, nothing you did or didnt do contributed to his SI because he has had SI the entire time I get a lot of people like this on my caseload and it use to stress me out but realistically what can you do? Often times the people you worry about doing something arent the ones who actually do it. In our field you just dont know what can happen, because people often surprise you so all i do is document and follow standard of care (which is often debateable in itself) the best that I can.

I think that's why our job is stressful because we want things to be predictable and the minute we start thinking things are predictable, people surprise us.

/endrant

 

[whopper]

If he has a personality disorder it's not cluster B. Guy is polite. Another theory that crossed my mind is he hates his job, but won't leave it. I've seen toxic jobs really harm someone's mood and when they get out of the job they feel much better.