opinions on medication management

[tr]

Yes. I usually explain Hebb's rule in lay language when I start a course of CBT.

It really helps people understand why they find their ingrained negative thought patterns so easy and convincing to believe, why new thought patterns are so difficult to generate and seem so empty and unbelievable at first, and why repeated practice will change that.

It opens them up to the idea that there may be a reason their negative thought patterns seem so convincing other than that they are God's truth, and so greatly improves buy-in to the approach.

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[Ollie123]

I don't like a strict distinction between biological and psychosocial, but I'm very confident that sometimes MDD is driven more by biological factors and sometimes more by psychosocial factors. At the very least, I think its plausible medication and behavioral treatments are more effective in one situation than the other.

In part this is just because our diagnostic system is a hot mess. That will change first.

None of this is to say its clinically useful to draw a distinction now. Just that in 100 years I think (hope?) the person who was fine until they went through a nasty divorce will not be collapsed into the same category as someone who can't remember any time they experienced pleasure all the way back to age 5 based on a symptom profile...even though they only actually have 1-2 symptoms in common. And we may end up learning some of those individuals respond better to different treatments.

It just probably won't happen soon.

 

[futureapppsy2]

I don't like a strict distinction between biological and psychosocial, but I'm very confident that sometimes MDD is driven more by biological factors and sometimes more by psychosocial factors. At the very least, I think its plausible medication and behavioral treatments are more effective in one situation than the other.

In part this is just because our diagnostic system is a hot mess. That will change first.

None of this is to say its clinically useful to draw a distinction now. Just that in 100 years I think (hope?) the person who was fine until they went through a nasty divorce will not be collapsed into the same category as someone who can't remember any time they experienced pleasure all the way back to age 5 based on a symptom profile...even though they only actually have 1-2 symptoms in common. And we may end up learning some of those individuals respond better to different treatments.

It just probably won't happen soon.

I was chatting with a physician colleague about depression chronicity or lack thereof (internist who's done a lot of research on depression in primary care and also has treated a lot of depression in primary care and hospital populations). Her opinion was that MDD is straight-up a chronic illness that almost always has a chronic course outside of a) truly situational depression (e.g., post-divorce depression), b) clearly medically-induced depression (e.g., hypothyroidism that causes depression symptoms that fully resolve with tx for the hypothyroidism), and c) post-partum depression. She just sees it as a pure chronic illness, which is why she thinks that it should fall under the broad internal medicine spectrum of care ala diabetes, HTN, COPD, etc. Thought that was a really interesting take.

 

[allantois]

I was chatting with a physician colleague about depression chronicity or lack thereof (internist who's done a lot of research on depression in primary care and also has treated a lot of depression in primary care and hospital populations). Her opinion was that MDD is straight-up a chronic illness that almost always has a chronic course outside of a) truly situational depression (e.g., post-divorce depression), b) clearly medically-induced depression (e.g., hypothyroidism that causes depression symptoms that fully resolve with tx for the hypothyroidism), and c) post-partum depression. She just sees it as a pure chronic illness, which is why she thinks that it should fall under the broad internal medicine spectrum of care ala diabetes, HTN, COPD, etc. Thought that was a really interesting take.

PCPs are the largest prescribers of psychotropic medication, as there just isn't enough psychiatrists to treat everyone with depression. Even then, it's unbelievable how many PCPs hold the view that depression and anxiety are products of a weak mind. Also, isn't a large number of first-time depression remits? Of course depression has a very heterogenous pathophysiology not all that well understood. Chronic conditions can be explained biologically for why they are chronic such as destruction of islet cells, insulin resistance, or irreversible scarring of the lung. We do not have such explanation for why depression should be a chronic condition. If anything, research would indicate the great neuroplasticity that exists in all ages.

If anything I think a great deal of psychiatric disorders arise from the mismatch between the environment that our species evolved in vs the environment we live in today.

 

[R. Matey]

an adult with significant ADHD

"Significant" is the key word here. I've regularly seen improvement in adult individuals with mild to moderate ADHD with some behavioral strategies at the UCC where I'm currently on internship. Like @Ollie123 said, I think the classification system we're all under probably hurts more than it helps. Hazarding a guess: I'll bet there is a lot of variance we are not accounting that goes into ADHD. Same story goes for depression.

 

[tr]

I don't like a strict distinction between biological and psychosocial, but I'm very confident that sometimes MDD is driven more by biological factors and sometimes more by psychosocial factors. At the very least, I think its plausible medication and behavioral treatments are more effective in one situation than the other.

How is the difference between a biological factor and a psychosocial factor defined?

 

[Fan_of_Meehl]

I don't like a strict distinction between biological and psychosocial, but I'm very confident that sometimes MDD is driven more by biological factors and sometimes more by psychosocial factors. At the very least, I think its plausible medication and behavioral treatments are more effective in one situation than the other.

In part this is just because our diagnostic system is a hot mess. That will change first.

None of this is to say its clinically useful to draw a distinction now. Just that in 100 years I think (hope?) the person who was fine until they went through a nasty divorce will not be collapsed into the same category as someone who can't remember any time they experienced pleasure all the way back to age 5 based on a symptom profile...even though they only actually have 1-2 symptoms in common. And we may end up learning some of those individuals respond better to different treatments.

It just probably won't happen soon.

Yeah...I think a lot of it in terms of a diathesis-stress model where everyone has their limits (in terms of total psychosocial/existential load they can bear). Some just reach it faster then others then clinical dysfunction precipitates as their coping patterns start to degrade/unravel and--from there--it's all 'vicious cycles' / aka positive feedback loops from there until they go into clinical disorder territory and reach some sort of dysfunctional equilibrium there. That's when they come to the office asking for help.

 

[Ollie123]

How is the difference between a biological factor and a psychosocial factor defined?

Well, I think its tough to define the biology precisely when we still have no earthly idea how it works. We seem a little further along with psychosocial factors, but even that is pretty coarse. Really, I'm just getting at the notion of multiple pathways, diathesis-stress, etc. For simplifications sake, let's say Person A has a cluster of mutations spanning 8 chromosomes that disrupts dopamine synthesis. Person B has intact dopamine synthesis, but lost much of their social life after the divorce and this disengagement decreased their dopaminergic activity despite intact synthesis...so this change is more consequence than cause. Person A responds better to Drug X, Person B responds better to BA. Again - gross oversimplification for the sake of example. Both have biological and psychosocial manifestations. The "true cause" (whatever that means) is distinct. The exact manifestations may differ at either the biological or psychosocial level - our current system is just too clunky to detect it because "Are you sad most of the day, nearly every day?" is only slightly more refined than a physical exam consisting solely of the question "How you doing?"

Its messy and still somewhat arbitrary. I know this. I'm just making the case that I think its plausible a framework like the above could shape our clinical approaches in 50 years. Its pure speculation and clinically useless right now.

 

[Fan_of_Meehl]

Well, I think its tough to define the biology precisely when we still have no earthly idea how it works. We seem a little further along with psychosocial factors, but even that is pretty coarse. Really, I'm just getting at the notion of multiple pathways, diathesis-stress, etc. For simplifications sake, let's say Person A has a cluster of mutations spanning 8 chromosomes that span disrupts dopamine synthesis. Person B has intact dopamine synthesis, but lost much of their social life after the divorce and this disengagement decreased their dopaminergic activity despite intact synthesis...so this change is more consequence than cause. Person A responds better to Drug X, Person B responds better to BA. Again - gross oversimplification for the sake of example. Both have biological and psychosocial manifestations. The "true cause" (whatever that means) is distinct. The exact manifestations may differ at either the biological or psychosocial level - our current system is just too clunky to detect it because "Are you sad most of the day, nearly every day?" is only slightly more refined than a physical exam consisting solely of the question "How you doing?"

Its messy and still somewhat arbitrary. I know this. I'm just making the case that I think its plausible a framework like the above could shape our clinical approaches in 50 years. Its pure speculation and clinically useless right now.

It's also a 'level-of-analysis' problem (molar vs. molecular). By definition, all 'psychosocial' or 'psychological' factors occur in the context of a living and obviously biological organism.

There are clear limits to biological reductionism/determinism as applied to psychological pathology.

One of my favorite philosophers of science (Philip Kitcher) wrote an important manuscript examining the problems with a purely biological reductionist approach to the study of genetics and it's still timely, at least as applied to reductionism in psychology/psychiatry

'1953 And All That: A Tale of Two Sciences':

http://mechanism.ucsd.edu/teaching/philbio/readings/kitcher.1953andallthat.1984.pdf

 

[ERK123]

PCPs are the largest prescribers of psychotropic medication, as there just isn't enough psychiatrists to treat everyone with depression. Even then, it's unbelievable how many PCPs hold the view that depression and anxiety are products of a weak mind. Also, isn't a large number of first-time depression remits? Of course depression has a very heterogenous pathophysiology not all that well understood. Chronic conditions can be explained biologically for why they are chronic such as destruction of islet cells, insulin resistance, or irreversible scarring of the lung. We do not have such explanation for why depression should be a chronic condition. If anything, research would indicate the great neuroplasticity that exists in all ages.

If anything I think a great deal of psychiatric disorders arise from the mismatch between the environment that our species evolved in vs the environment we live in today.

At some level most disease is due to a weakness in an organ system or multiple organ systems. I don’t think it is incongruent with evidence to consider mental health illnesses a weakness as long as this does not interfere with the practitioners ability to empathize with the patient. Weakness does not imply that the patient is at fault, and even if a practitioner chooses to believe that the patient is at fault for their weakness this does not lesson the duty to treat them. I think the medical word often goes to enormous effort to manufacture a perspective that the patient’s illness is not a weakness and nobody is at fault because it makes our work feel more pure.

 

[cara susanna]

I'm open to referring people to meds. When I first started practicing I was very much "try psychotherapy first," but in the VA I've kind of developed this idea that I need to take help where I can get it. However, a lot of my patients are anti-medication and don't want to try it. Also, I am fortunate to work with psychiatrists who don't over-prescribe and also don't prescribe benzos.

All of our psychiatrists refer for therapy pretty often and honestly, although I love their respect for therapy I sometimes wish they wouldn't. Sometimes the patients aren't motivated or don't have clear goals. Sometimes it's more like "I don't know what to do with this person, help." The most egregious one is with BPD. Yes, I know that DBT works but the patient has to want to commit to the therapy. Given the above joke in this thread about the VA and motivation for therapy, of course, this is probably a VA-specific thing.

 

[clausewitz2]

How is the difference between a biological factor and a psychosocial factor defined?

Let's get away from the biological v psychosocial distinction, which is philosophically indefensible under non-dualist theories of mind, and talk instead about endogenous v. reactive. More precisely, whether the causation of the depressive symptoms is more attributable to factors external to the individual or factors internal to the individual.

The former would include a nasty divorce, unemployment, racism/pervasive oppression, narcissistic injuries etc. The later would of course include quirks of neurobiology but also the early learning history of the individual. It doesn't follow from this that meds will necessarily be better than therapy for internally caused v externally caused symptoms, but it does suggest the optimal treatments might be different and they are not the same thing.

Hebb's rule is a useful principle for predicting the behavior of neural circuits but does not actually explain anything behaviorally beyond "people learn things in way that is not 100% transient".

MDD as a unitary entity is a complete accident of history and down to the preferences of Bob Spitzer and co more than anything. Depression was seen as vastly less common than anxiety, which is why we have a bajillion anxiety disorders in the DSM and a much smaller set of Depressive disorders. Remember, the original manufacturer of clomipramine didn't want to market it because it was felt there weren't enough cases of depression to make it viable. Clearly they were talking about something other than the vague discontentment and ennui with comfort eating and poor sleep habits that can qualify for MDD at present!

 

[Ollie123]

All of our psychiatrists refer for therapy pretty often and honestly, although I love their respect for therapy I sometimes wish they wouldn't.

Absolutely not just a VA thing. I constantly get referrals like this in my AMC. I feel like its just a "Therapy is good for everyone" kinda thing. With my apologies to my neuropsych colleagues on the board, my experience is that neuropsychologists/neurologists are by far the worst. It "might" help, but they don't do it, know very little about it, but LOVE talking it up to their patients. My most frustrating referrals by far are some version of "This person thinks its unfair that normal aging-related cognitive decline is a thing. Please listen to them complain for me." or its close cousin "This person doesn't have dementia. Everyone who comes in my office who doesn't have dementia probably has anxiety/depression. Please fix their non-existent mental illness I didn't bother to evaluate once I figured out it wasn't dementia. BTW, I told them you can improve their cognition so they will fight like hell to keep seeing you until you bestow upon them superhuman cognitive powers"

Let's get away from the biological v psychosocial distinction, which is philosophically indefensible under non-dualist theories of mind, and talk instead about endogenous v. reactive. More precisely, whether the causation of the depressive symptoms is more attributable to factors external to the individual or factors internal to the individual.

This is a pretty good synopsis of what I was getting it and I think accurately captures how a lot of people feel about the topic. Biology/psychosocial has just become a shorthand.

 

[Fan_of_Meehl]

Absolutely not just a VA thing. I constantly get referrals like this in my AMC. I feel like its just a "Therapy is good for everyone" kinda thing. With my apologies to my neuropsych colleagues on the board, my experience is that neuropsychologists/neurologists are by far the worst. My most frustrating referrals by far are some version of "This person thinks its unfair that normal aging-related cognitive decline is a thing. Please listen to them complain for me." or its close cousin "This person doesn't have dementia. Everyone who comes in my office who doesn't have dementia probably has anxiety/depression. Please fix their non-existent mental illness I didn't bother to thoroughly evaluate. BTW, I told them this will improve their cognition so they will fight like hell to keep seeing you until you bestow upon them superhuman cognitive powers"





This is a pretty good synopsis of what I was getting it and I think accurately captures how a lot of people feel about the topic. Biology/psychosocial has just become a shorthand.

LOL, I only WISH some of our (non-board certified) sortofneuropsychologists at our facility would sometimes NOT diagnose 'Mild Neurocognitive Disorder Due to Traumatic Brain Injury' in all the veterans with a history of concussion that they get referred because the veterans are self-reporting severe levels of dementia and score, basically, within normal limits. I recently asked one of them, 'just how well does someone have to do on your objective tests of neuropsychological functioning for you NOT to give them a 'neurocognitive disorder' diagnosis?

(obviously, the well-trained neuropsychs on this board would not do this and have often expressed frustration with this sort of practice in the past)

 

[futureapppsy2]

"Significant" is the key word here. I've regularly seen improvement in adult individuals with mild to moderate ADHD with some behavioral strategies at the UCC where I'm currently on internship. Like @Ollie123 said, I think the classification system we're all under probably hurts more than it helps. Hazarding a guess: I'll bet there is a lot of variance we are not accounting that goes into ADHD. Same story goes for depression.

I also think ADHD is really poorly diagnosed a lot of times, and a lot of people with the diagnosis don’t really meet the criteria, but just do lack basic organizational skills and are helped immensely by behavioral strategies and contingency management or have subclinical attention deficits that are minor enough that they can implement these strategies consistently and see marked improvement. In the adults I’ve diagnosed with unambiguous ADHD, however, and in those I’ve treated that had really solid diagnostic documentation, they’ve often pursued a lot of behavioral strategies in good faith only to not be able to implement them with any consistency and sometimes ending up worse off because people—including themselves—see them as unmotivated slackers who just won’t try. Behavioral strategies can be a helpful addition to medication in these people, but they totally need medication to see any sort of meaningful improvement in functioning, in my experience.

 

[R. Matey]

I also think ADHD is really poorly diagnosed a lot of times, and a lot of people with the diagnosis don’t really meet the criteria, but just do lack basic organizational skills and are helped immensely by behavioral strategies and contingency management or have subclinical attention deficits that are minor enough that they can implement these strategies consistently and see marked improvement. In the adults I’ve diagnosed with unambiguous ADHD, however, and in those I’ve treated that had really solid diagnostic documentation, they’ve often pursued a lot of behavioral strategies in good faith only to not be able to implement them with any consistency and sometimes ending up worse off because people—including themselves—see them as unmotivated slackers who just won’t try. Behavioral strategies can be a helpful addition to medication in these people, but they totally need medication to see any sort of meaningful improvement in functioning, in my experience.

So anyone who meets the symptom criteria clearly, regardless of the social/occupational impairment, would automatically prompt you to refer for medication prior to trialing therapy? I would be okay trialing therapy first if the case was a mild or a moderate presentation and talk to clients about their medication options. If they refused, then I'd document it and trial therapy. Out of all the ADHD referrals I've done so far over the last few years of training, I can count on one hand the number of times I've diagnosed true ADHD so I do agree with you that many people think they have it who actually just need some life skills training. We see plenty of those at the UCC too.

My experience with medication is that more severe presentations of many disorders prompt referrals for medication pretty quickly. However, I've seen plenty of improvement with milder and moderate cases with just therapy alone. Of course, in these cases, medication is discussed openly at the outset and the client usually refuses. In my mind, trialing therapy is just fine. Thinking about it in terms of symptom severity is clinically useful, even though it is philosophically indefensible. The cut points between mild, moderate, and severe for most disorders are fuzzy at best. I agree with posters who've argued that the problem lies with how we categorize some of the problems of the living with symptom presentations that are more endogenous in cause. Whether or not symptom severity is the current mansplaination of the variance in either is probably a larger philosophical debate.

 

[AcronymAllergy]

LOL, I only WISH some of our (non-board certified) sortofneuropsychologists at our facility would sometimes NOT diagnose 'Mild Neurocognitive Disorder Due to Traumatic Brain Injury' in all the veterans with a history of concussion that they get referred because the veterans are self-reporting severe levels of dementia and score, basically, within normal limits. I recently asked one of them, 'just how well does someone have to do on your objective tests of neuropsychological functioning for you NOT to give them a 'neurocognitive disorder' diagnosis?

(obviously, the well-trained neuropsychs on this board would not do this and have often expressed frustration with this sort of practice in the past)

Yeah, like you've said, it's frustrating for us as well. Because many times we end up being asked to try to undo it a few months/years later. And unfortunately, it's not always just the quasi-neuropsychologists doing it.

Also, to Ollie's point, I've certainly seen some neuropsychologists be pretty lazy when it comes to psychodiagnostic assessment, and pretty heavy-handed with the therapy referrals. For neurologists, I generally take it less as laziness and more as, "ok, this isn't neurological, please do something for this person." Obviously, I'm not going to always (or perhaps even often) be able to do an amazing job at ferreting out all the particulars of a mental health conceptualization with a pt referred to me to determine if they have dementia. But if I can't make a determination of, "yeah, this guy needs follow-up to address his previously-untreated chronic depression," vs. "this gal could probably benefit from some short-term treatment for adjustment issues pertaining to X" vs. "no, he's not depressed; sometimes getting old sucks and this guy is just processing that," I haven't done my job.

 

[Laradd]

Its clearer now. Thank you for providing the difference

 

[Ollie123]

@AcronymAllergy Just to be clear - if anyone (neuropsychology, neurology, whoever) is framing it as a referral for evaluation and possible follow-up, I would have no problem with it whatsoever regardless of how in-depth their evaluation might have been. My problem is they are clearly being referred <for treatment> and clearly being told their cognitive problems are secondary to anxiety/depression and I can fix them. I then get stuck with a patient who: A) Doesn't actually have anxiety or depression as evident from a BDI and 3-minute interview in which they deny every symptoms besides "Difficulty concentrating"; B) Only wants to take about their cognitive problems; C) Is understandably disinterested in making any other life changes; and D) Will not accept that I cannot help because they were told otherwise. Oddly enough, neurology is actually better about it here since they are more likely to frame it as evaluation. Neuropsych seems to know just enough about therapy to know that its "good" but not enough to know whether "This patient can benefit from it." (Note that I'm NOT saying all neuropsych is like that - I really think its just an artifact of 1-2 clinics here for which I have become a pipeline).

 

[PsyDr]

@AcronymAllergy Just to be clear - if anyone (neuropsychology, neurology, whoever) is framing it as a referral for evaluation and possible follow-up, I would have no problem with it whatsoever regardless of how in-depth their evaluation might have been. My problem is they are clearly being referred <for treatment> and clearly being told their cognitive problems are secondary to anxiety/depression and I can fix them. I then get stuck with a patient who: A) Doesn't actually have anxiety or depression as evident from a BDI and 3-minute interview in which they deny every symptoms besides "Difficulty concentrating"; B) Only wants to take about their cognitive problems; C) Is understandably disinterested in making any other life changes; and D) Will not accept that I cannot help because they were told otherwise. Oddly enough, neurology is actually better about it here since they are more likely to frame it as evaluation. Neuropsych seems to know just enough about therapy to know that its "good" but not enough to know whether "This patient can benefit from it." (Note that I'm NOT saying all neuropsych is like that - I really think its just an artifact of 1-2 clinics here for which I have become a pipeline).

If you think that psychotherapy can’t help, Dr. mittenberg would like a word.

Also behavioral therapy for adhd would like a word.

 

[Ollie123]

Psychotherapy can be very helpful for folks that actually have disturbance in functioning. It can't really do much for folks functioning perfectly fine but are concerned that it takes slightly longer to solve high-level mathematical problems at age 70 then it did at age 35. Pomodoro technique ain't gonna touch that.

If you know of treatment protocols for this, I'd love to take a look.

 

[PsyDr]

Psychotherapy can be very helpful for folks that actually have disturbance in functioning. It can't really do much for folks functioning perfectly fine but are concerned that it now takes slightly longer to solve high-level mathematical problems at age 70 then it did at age 35.

If you know of treatment protocols for this, I'd love to take a look.

I would argue you are discussing subjective complaints in the face of objectively intact cognitive functioning. Fortunately, this is exactly what mTBI/PCS is. Mittenberg outlined a CBT protocol that showed efficacy for subjective cognitive impairments without a credible mechanism of action. Caplain also showed something similar with more psychoeducation.

Caplain, S., et al. (2019). "Efficacy of Psychoeducation and Cognitive Rehabilitation After Mild Traumatic Brain Injury for Preventing Post-concussional Syndrome in Individuals With High Risk of Poor Prognosis: A Randomized Clinical Trial." Frontiers in neurology 10(929).

Mittenberg, W. (1996). "Cognitive-behavioral prevention of postconcussion syndrome." Archives of Clinical Neuropsychology 11: 139-145.

Mittenberg, W., et al. (1999). "Postconcussional syndrome: A treatment manual for patients." Anales de Psiquiatria 15: 315-323.

 

[Ollie123]

Will take a read once this grant goes in (next Fri). I'd argue there are some key distinctions between this and PCS, but its certainly far outside my usual wheelhouse so definitely worth a read.

That said...why on earth send these folks to me (SUD/Depression/Anxiety) and not rehab psych? Or even the ADHD clinic?

 

[Fan_of_Meehl]

So anyone who meets the symptom criteria clearly, regardless of the social/occupational impairment, would automatically prompt you to refer for medication prior to trialing therapy? I would be okay trialing therapy first if the case was a mild or a moderate presentation and talk to clients about their medication options. If they refused, then I'd document it and trial therapy. Out of all the ADHD referrals I've done so far over the last few years of training, I can count on one hand the number of times I've diagnosed true ADHD so I do agree with you that many people think they have it who actually just need some life skills training. We see plenty of those at the UCC too.

My experience with medication is that more severe presentations of many disorders prompt referrals for medication pretty quickly. However, I've seen plenty of improvement with milder and moderate cases with just therapy alone. Of course, in these cases, medication is discussed openly at the outset and the client usually refuses. In my mind, trialing therapy is just fine. Thinking about it in terms of symptom severity is clinically useful, even though it is philosophically indefensible. The cut points between mild, moderate, and severe for most disorders are fuzzy at best. I agree with posters who've argued that the problem lies with how we categorize some of the problems of the living with symptom presentations that are more endogenous in cause. Whether or not symptom severity is the current mansplaination of the variance in either is probably a larger philosophical debate.

My favorites are when they recommend brain games (e.g., Luminosity.com) to help with non-existent pseudo-deficits.

Will take a read once this grant goes in (next Fri). I'd argue there are some key distinctions between this and PCS, but its certainly far outside my usual wheelhouse so definitely worth a read.

That said...why on earth send these folks to me (SUD/Depression/Anxiety) and not rehab psych? Or even the ADHD clinic?

Nobody wants to deal with them. LOL. Sorry.

That being said, they comprise at least half of my caseload.

I try to contextualize it when I get frustrated with them at times (and EVERYONE gets frustrated with their clients from time to time and you can't just refer them to others who will also get frustrated with them who will refer them to someone else ad infinitum).

Think about it. You're in your 30s/40s/50s, dealing with multiple issues (financial problems, poor work history, maybe legal history, failed relationships, substances, etc.). You feel like everyone (and everything) is stacked against you; it's not your fault; you're just being persecuted/neglected/abused but...hey...at least IT ISN'T YOUR FAULT and YOU CAN'T DO ANYTHING ABOUT IT (RIGHT?).

Now the guy who's supposed to be 'helping' you (your therapist) keeps asking all these questions that make you feel like some of it may be due to your actions (or inactions) or behavioral patterns over time. He even has the audacity to suggest that maybe things could get better if you would just change (or tinker with) your own thoughts/beliefs and your behaviors. He is suggesting you make such slow, gradual changes (just to test out the theory that YOU CAN'T DO ANYTHING ABOUT HAVING A FAILED LIFE) such that it's impossible for you to come up with a reasonable counter-argument to at least TRYING to make some specific plans for the day and try to accomplish something that you yourself have said that you want to accomplish. What a jerk.

As a therapist working with folks whose lives are a catastrophe, I always have to remind myself to be careful not to blame the person for their catastrophe. It just demoralizes them and makes them want to reject therapeutic efforts. But it's challenging as hell.

 

[AcronymAllergy]

@AcronymAllergy Just to be clear - if anyone (neuropsychology, neurology, whoever) is framing it as a referral for evaluation and possible follow-up, I would have no problem with it whatsoever regardless of how in-depth their evaluation might have been. My problem is they are clearly being referred <for treatment> and clearly being told their cognitive problems are secondary to anxiety/depression and I can fix them. I then get stuck with a patient who: A) Doesn't actually have anxiety or depression as evident from a BDI and 3-minute interview in which they deny every symptoms besides "Difficulty concentrating"; B) Only wants to take about their cognitive problems; C) Is understandably disinterested in making any other life changes; and D) Will not accept that I cannot help because they were told otherwise. Oddly enough, neurology is actually better about it here since they are more likely to frame it as evaluation. Neuropsych seems to know just enough about therapy to know that its "good" but not enough to know whether "This patient can benefit from it." (Note that I'm NOT saying all neuropsych is like that - I really think its just an artifact of 1-2 clinics here for which I have become a pipeline).

The links PsyDr posted are solid, and there was recently an article that Vanderploeg et al. put out (2019 I think) showing CBT to be more effective than cognitive rehabilitation in treating PCS. If interested and you haven't already seen it, you could also look at Delis et al.'s paper on cogniform disorder, as it at least attempts to explain what may be going on with some of these patients.

Similar to chronic pain, it's a delicate line to walk: avoiding sound like you're saying, "it's all in your head" instead of, "well, everything is kind of all in our heads, and if we're distressed in one area, it can affect functioning in other areas." I also think some of these folks are more emotionally distressed than they reveal to the provider they follow-up with. I've referred numerous folks for therapy after they've told me they're essentially depressed, only for them to tell the therapist they don't know why they were referred and deny any distress, but there isn't always a whole lot we can do about that. Still, if anyone's going to effectively walk that delicate line, it's an effective therapist. There aren't many providers who specialize in addressing cognitive symptoms in folks with objectively intact cognition, rehab or otherwise.

And yeah, speaking from neuropsych's perspective, we definitely understand that lots of these folks can be difficult to work with, and many probably won't stick it out for a course of therapy. But we still may catch a few who get better. And them just agreeing to a referral is a small victory in itself.

 

[Ollie123]

The links PsyDr posted are solid, and there was recently an article that Vanderploeg et al. put out (2019 I think) showing CBT to be more effective than cognitive rehabilitation in treating PCS. If interested and you haven't already seen it, you could also look at Delis et al.'s paper on cogniform disorder, as it at least attempts to explain what may be going on with some of these patients.

Similar to chronic pain, it's a delicate line to walk: avoiding sound like you're saying, "it's all in your head" instead of, "well, everything is kind of all in our heads, and if we're distressed in one area, it can affect functioning in other areas." I also think some of these folks are more emotionally distressed than they reveal to the provider they follow-up with. I've referred numerous folks for therapy after they've told me they're essentially depressed, only for them to tell the therapist they don't know why they were referred and deny any distress, but there isn't always a whole lot we can do about that. Still, if anyone's going to effectively walk that delicate line, it's an effective therapist. There aren't many providers who specialize in addressing cognitive symptoms in folks with objectively intact cognition, rehab or otherwise.

And yeah, speaking from neuropsych's perspective, we definitely understand that lots of these folks can be difficult to work with, and many probably won't stick it out for a course of therapy. But we still may catch a few who get better. And them just agreeing to a referral is a small victory in itself.

Starting to think we may be discussing different things here. I'm not in any way talking about the stereotypical mTBI "I bumped my head getting into the car once 10 years ago and now I need disability" folks I know many of you see. Those folks I could certainly see getting referred. I'm not the best spot, even within our institution (heck, within our clinic) but I get that.

The folks I'm complaining about are usually quite clear they are doing fine, just noticing very subtle cognitive changes that are probably irrelevant unless you are trying to win a nobel prize or run a major corporation. They're usually pretty well-adjusted and not objectively distressed about this beyond mild frustration that their memory "ain't what it used to be". More analogous to the olympic athlete who tears their ACL and its still "not quite right" a year later because they worked their butt off and still came in 3rd. Chances are pretty damn good something is actually wrong but ortho/radiology/etc. aren't really set up to detect and fix problems that bring someone from the 99.99th percentile to the 99.98th percentile. My impression is this is just folks turfing patients to avoid having to do 5 minutes of psychoed during which they admit their field isn't perfect and there isn't a lot we can do.

Anyways, sorry for the thread derail!

 

[PsyDr]

@Ollie123 that is exactly what that literature is about... giving psychoed literally helps outcome. This isn’t an issue of faking. It’s people coming in, scared. The empirical literature shows that psychoed and/or cbt helps with just this sort of thing.

 

[futureapppsy2]

On the topic of mTBI/PCS, one of the most fascinating studies I've ever seen presented was a prospective study of high school athletes where participants were extensively and thoroughly screened out for any past mTBI/concussion (treated or not) at baseline, given PCS/cognitive testing pre-season, and tested again post-season, along with data on any sustained concussions during the season. Weirdly, participants who sustained one or more concussions during the season had higher PCS-like symptoms at baseline, when the concussions hadn't yet been sustained. Fascinating, odd finding.

 

[WisNeuro]

On the topic of mTBI/PCS, one of the most fascinating studies I've ever seen presented was a prospective study of high school athletes where participants were extensively and thoroughly screened out for any past mTBI/concussion (treated or not) at baseline, given PCS/cognitive testing pre-season, and tested again post-season, along with data on any sustained concussions during the season. Weirdly, participants who sustained one or more concussions during the season had higher PCS-like symptoms at baseline, when the concussions hadn't yet been sustained. Fascinating, odd finding.

Well, not that odd when you consider that the PCS is simply a list of non-specific symptoms that exist across a wide continuum of medical and mental disorders.

 

[Fan_of_Meehl]

Well, not that odd when you consider that the PCS is simply a list of non-specific symptoms that exist across a wide continuum of medical and mental disorders.

There are two (often co-occurring) implicit and incorrect assumptions that cause so many people to misinterpret findings pertaining to this population.

1) As you point out, measures of 'post-concussion syndrome' are merely self-report checklists of extremely common emotional/behavioral, cognitive, and somatic/medical symptoms that--in and of themselves--are not specific to ANY medical or psychiatric diagnosis or condition and are typically elevated across all kinds of samples (undergrads, medical patients, non-brain injured psychological patients)

2) This one I very rarely see mentioned but it is absolutely critical, in my opinion. All of the studies in the VA system (which make up a huge number of the studies on mTBI) are conducted using samples of people who go through their (primary) screening for TBI process (generally in primary care) which consists of a few brief self-report yes/no questions. If they screen positive, they are sent to a '2nd level evaluation' which, at our site, is a half-day evaluation where they are interviewed by members of an interdisciplinary team. Being the psychologist on the team, it's my role to do a brief mental health screening interview (I only have about 20 min/ patient due to the logistics of the clinic). What I've found interesting is that at least 19 out of 20 (95%) of the veterans coming through these clinics either already have mental health diagnoses (clinical depression, severe substance abuse, PTSD, etc.) or they produce elevated scores on the PHQ-9. This is NOT representative of the universe of people (even veterans) who have sustained a concussion in the past. That is, the majority of people who have sustained concussions (in the population) do NOT have clinically significant (or diagnosed) mental illness. The next time you pick up an article on mTBI/concussion that used VA samples, see how they composed the sample. It's from this population of folks who almost all are reporting significant psychopathology. So, the fundamental assumption that we all learned in undergrad experimental psych courses (that the sample of the study constitutes a random representative sample of the population to which the results are supposed to apply) is clearly violated.

Why? My guess is:

1) You start with the population of all servicemembers/veterans who have ever actually sustained one or more concussions

2) Then, you select out all of the veterans who DON'T use the VA system

3) Then, you select out all of the veterans in primary care who don't want to play the 'I have brain damage so where is my money game' in primary care (at the screening level)

4) Then, you throw in all of the veterans in primary care who (despite never having had a concussion) DO want to play the 'I have brain damage so where is my money (or 'why don't my wife stop nagging me to get a job') game' in primary care (at the screening level)

5) Then, you only include all of the veterans actually motivated enough to attend the half-day '2nd level screening' process such that they formally end up with the diagnosis (in the VA system/database) of 'personal history of concussion / mTBI'

6) Then, your study is done on #5 and the results are (mis)interpreted or generalized to #1

Now as to the 'why?' I think that the fact that veterans get paid and/or get some form of secondary gain from over-reporting both neurocognitive and psychopathological symptoms in our current system is a likely contributor to the problem but, of course, it's so politically incorrect to even acknowledge it (despite the data, whenever the issue is examined, being pretty clear) that no one can openly acknowledge it, let alone examine it formally by way of further research.

 

[WisNeuro]

I agree that the VA studies have their own can or worms, you throw any symptom checklist at that population and it will be elevated compared to controls, even samples of vets from other countries due to the SC system. But, we also see the "PCS" pattern in peds/adolescent samples. So, it's not the concussion "causing" the symptoms to persist. It's normal variability coupled with pre-existing conditions in most cases.

 

[Sanman]

I agree that the VA studies have their own can or worms, you throw any symptom checklist at that population and it will be elevated compared to controls, even samples of vets from other countries due to the SC system. But, we also see the "PCS" pattern in peds/adolescent samples. So, it's not the concussion "causing" the symptoms to persist. It's normal variability coupled with pre-existing conditions in most cases.

This is true, but I can still see the case for self-selection bias in concussion cases. Outside of football and soccer (and the military) who is sustaining these concussions? Are the people sustaining more concussions playing harder and more likely to get injured due to increased levels of aggression compared to the mean? Does this account for some or all of the elevation in PCS symptoms?

 

[Fan_of_Meehl]

This is true, but I can still see the case for self-selection bias in concussion cases. Outside of football and soccer (and the military) who is sustaining these concussions? Are the people sustaining more concussions playing harder and more likely to get injured due to increased levels of aggression compared to the mean? Does this account for some or all of the elevation in PCS symptoms?

I think what bothers me the most about how all this is handled in the contemporary 'scientific' literature is how the common threats to validity issues that we all learned (e.g., Cook and Campbell) in grad school are so routinely and thoroughly ignored by most of the people publishing in this area.

• Campbell, D. & Stanley, J. (1963). Experimental and quasi-experimental designs for research. Chicago, IL: Rand-McNally.
  
  
• Cook, T. D., & Campbell, D. T. (1979). Quasi-experimentation: Design and analysis issues for field settings. Boston, MA: Houghton Mifflin Company.

 

[WisNeuro]

This is true, but I can still see the case for self-selection bias in concussion cases. Outside of football and soccer (and the military) who is sustaining these concussions? Are the people sustaining more concussions playing harder and more likely to get injured due to increased levels of aggression compared to the mean? Does this account for some or all of the elevation in PCS symptoms?

Possibilities, from what I've seen, pre-existing risk factors for elevated PCS symptoms, with or without a concussive event are diagnoses of anxiety or depression, female gender, poor social support, and proneness to somatization. Remember, you see these elevations regardless of whether or not someone plays a sport, or suffers a concussion.

 

[Therapist4Chnge]

The folks I'm complaining about are usually quite clear they are doing fine, just noticing very subtle cognitive changes that are probably irrelevant unless you are trying to win a nobel prize or run a major corporation. They're usually pretty well-adjusted and not objectively distressed about this beyond mild frustration that their memory "ain't what it used to be". More analogous to the olympic athlete who tears their ACL and its still "not quite right" a year later because they worked their butt off and still came in 3rd. Chances are pretty damn good something is actually wrong but ortho/radiology/etc. aren't really set up to detect and fix problems that bring someone from the 99.99th percentile to the 99.98th percentile. My impression is this is just folks turfing patients to avoid having to do 5 minutes of psychoed during which they admit their field isn't perfect and there isn't a lot we can do.

This is the group that I tend to take for follow-up, as they usually just tread water in traditional CBT when they aren't pushed on specifics and given clear factual information about recovery. It ends up being a ton of education and managing expectations of recovery, which starts from the intake. Anxiety &/or depression are present in 99.98% of these cases....though the patient rarely if ever is straight-up about it. Some don't recognize that is what is going on, others do but give a "I don't have time for that!" response, and then the last group are usually in denial about it. It happens with your local plumber to professor to professional athlete. It's amazing what proper education and setting expectations can do for a case...shout out to Dr. Mittenberg for the original research.

 

[futureapppsy2]

Well, not that odd when you consider that the PCS is simply a list of non-specific symptoms that exist across a wide continuum of medical and mental disorders.

Yes, that was discussed as well, but the group who sustained concussions also showed objective cognitive deficits at baseline on neuropsych testing. Again, high school athletes, so not a VA sample.

 

[WisNeuro]

Yes, that was discussed as well, but the group who sustained concussions also showed objective cognitive deficits at baseline on neuropsych testing. Again, high school athletes, so not a VA sample.

Ah, missed that part of your statement. Depends on the measure, though. If they used the ImPACT, it's hard to trust much of that data, terrible test re-test reliability, and no real measure of effort. They could just be capturing noise in some of those studies, or poor effort. We still get plenty of poor effort outside of the VA.

 

[Therapist4Chnge]

Ah, missed that part of your statement. Depends on the measure, though. If they used the ImPACT, it's hard to trust much of that data, terrible test re-test reliability, and no real measure of effort. They could just be capturing noise in some of those studies, or poor effort. We still get plenty of poor effort outside of the VA.

I wish IMPACT was designed differently. I rarely if ever use it even as a reference bc kids (and college/pro) already know how to manipulate it via the baseline scoring.

I don't see a ton of sports-related concussions these days outside of a handful of pro athlete referrals I get each year. For those, it's whatever I think will be most effective, so I skip IMPACT all together.

 

[beginner2011]

You mean active placebo? (Nocebo = "I shall harm," like if we were to yell at our patients, tell them our treatments are ineffective, and fill our offices with cacophonous noise and noxious odors. I assume that's not what you mean.)

I don't see how an active placebo is preferable to an SSRI. Anything that has identifiable side effects is by definition having some kind of physiological effect. I can't think of what you could give people that would be both biologically active and safer than an SSRI. What is the purpose of choosing a different biologically active agent that expressly lacks antidepressant efficacy?

The reason SSRIs became so widely prescribed is because of their safety and generally benign side effect profile. TCAs and MAOIs are somewhat more effective but much more dangerous, hence rarely used now.

Came across an open-label placebo trial for MDD (Open-Label Placebo for Major Depressive Disorder: A Pilot Randomized Controlled Trial). Participants in the open placebo condition (n=11) reported reduced HAM-D scores (d=0.54, p=0.26) relative to wait-list control – very similar to the estimated effect of antidepressant meds. Unfortunately, it looks like this line of research has dropped off and a trial with adequate statistical power hasn't been reported. The lead author of the study appears not to be doing research anymore. I also don’t see any evidence of a clinical trial in the pipeline looking at open-label placebos for the treatment of depression other than this one which is several years behind schedule (and may have died on the vine from the looks of it): Open-Label Placebo for the Treatment of Depression - Full Text View - ClinicalTrials.gov.

Hopefully there's more research done on this. I'd love to have data on how open-label placebo compares with antidepressants. With adequate evidence to support effectiveness I'd like to see non-prescribers able to offer open-label placebo to patients who are medication averse.

 

[PikminOC]

Private practice is different from the integrated hospital systems. I have seen therapists not want to lose patients so they don't refer for medication management. They aren't on salary like in a hospital system.

 

[tr]

Came across an open-label placebo trial for MDD (Open-Label Placebo for Major Depressive Disorder: A Pilot Randomized Controlled Trial). Participants in the open placebo condition (n=11) reported reduced HAM-D scores (d=0.54, p=0.26) relative to wait-list control – very similar to the estimated effect of antidepressant meds.

Did you read the paper? The result is no difference between open-label placebo and waitlist control. Also the improvement on the HAMD from open-label placebo was 1.64 points. Compare to Kirsch's report of 6.8 points in the STAR*D and 14.4 points in comparator placebo-controlled trials. (Clinical Trials Grossly Overestimate Antidepressant Efficacy). See table pasted below.

The authors correctly report that "improvement on the HAM-D-17 was relatively small as compared to the improvement typically seen in MDD RCTs ... our findings do not support the hypothesis that open-label placebo is effective for MDD."

Unfortunately, it looks like this line of research has dropped off and a trial with adequate statistical power hasn't been reported. The lead author of the study appears not to be doing research anymore. I also don’t see any evidence of a clinical trial in the pipeline looking at open-label placebos for the treatment of depression other than this one which is several years behind schedule (and may have died on the vine from the looks of it): Open-Label Placebo for the Treatment of Depression - Full Text View - ClinicalTrials.gov.

Hopefully there's more research done on this. I'd love to have data on how open-label placebo compares with antidepressants.

I'm guessing the lack of larger follow-up trials is due to the disappointing results from the pilot. The NIH is not going to hand out $5M to test something at scale that hasn't been at least suggested to work in pilot studies.

With adequate evidence to support effectiveness I'd like to see non-prescribers able to offer open-label placebo to patients who are medication averse.

If you want to tell your clients to take, like, some vitamin C, explaining that it will have no biological effect of relevance to depression but might help them by the placebo effect, be my guest. I don't think anyone can take away your license for that.

 

[beginner2011]

I'll admit I didn't read it very closely when I saw the sample size was so small. My intention was to point out that others have considered this question worth investigating.

However, after looking at it more closely I think you're also misinterpreting the results and grossly misrepresenting the implications.

Did you read the paper? The result is no difference between open-label placebo and waitlist control. Also the improvement on the HAMD from open-label placebo was 1.64 points. Compare to Kirsch's report of 6.8 points in the STAR*D and 14.4 points in comparator placebo-controlled trials. (Clinical Trials Grossly Overestimate Antidepressant Efficacy). See table pasted below.

The authors correctly report that "improvement on the HAM-D-17 was relatively small as compared to the improvement typically seen in MDD RCTs ... our findings do not support the hypothesis that open-label placebo is effective for MDD."


View attachment 309920



I'm guessing the lack of larger follow-up trials is due to the disappointing results from the pilot. The NIH is not going to hand out $5M to test something at scale that hasn't been at least suggested to work in pilot studies.



If you want to tell your clients to take, like, some vitamin C, explaining that it will have no biological effect of relevance to depression but might help them by the placebo effect, be my guest. I don't think anyone can take away your license for that.

First, the severity for the sample on the HAM-D (HAM-D=18) was WAY below the typical minimum threshold (HAM-D=24), reducing the room for change.

Second, the control comparison was at two-week follow up, which is two weeks less than any follow-up length in the Kirsch trial. Kirsch only included trials with between 4-8 week follow up.

Third, as you (and I) mentioned, the wait-list control comparison was not statistically significant. There was an effect of comparable size to antidepressant medication (d=.54), but the actual effect in raw HAM-D units was below what is typical (Difference=2.30).

Fourth, you neglected to report the pre-post results (n=20, collected 4 weeks after intervention, consistent with Kirsch), which were statistically significant for all three outcomes; HAM-D (d=.56, p=.03), QIDS (d=.76, p=.005), SDQ (d=.41, p=.02).

I'm pretty disappointed by how you cherry-picked here, based on my read. You quoted the author stating that, "our findings do not support the hypothesis that open-label placebo is effective for MDD," when what they were saying with that statement is they didn't have a sufficient sample size to have a statistically significant result. The full quote for your cherry-picked excerpt says:

"To our knowledge, this is the first RCT to test the efficacy of open-label placebo for MDD. Despite the fact that we observed a medium-sized effect for the main outcome measure, our findings do not support the hypothesis that open-label placebo is effective for MDD. However, the results were in the predicted direction, and this pilot study was limited by small sample size, low statistical power, and short duration."

If that's "disappointing results" that don't justify a moderately sized follow up investigation with a larger sample size and later follow-up with an actual comparison condition then that does not reflect very positively on NIH funding priorities, in my opinion. I think you'll acknowledge that clearly there's evidence to suggest that people benefit from open-label placebo that is delivered in this fashion. The most obvious future directions are: (a) what is the actual effect size, (b) how does it compare to antidepressant medications, (c) how long does it last/take to show up, (d) is the effect different for people with different levels of severity. These are reasonable questions to ask. The fact that this hasn't happened in the last 8+ years is a little bewildering.


Edit: To reframe this a bit, imagine if there were a chemical compound that Pfizer had patented with results like this (ZERO side effects, comparable d effect size to antidepressant meds, potential to massively reduce health care costs). You think they'd be interested in running a large RCT to further investigate? Somehow, I think they'd find a way.

 

[DynamicDidactic]

Just no. SSRIs are among the safest available pharmaceuticals.

I have been thinking about this a lot recently. Safety is a relative term. For the longest time I hear that SSRIs are safe. However, I have only recently started thinking about what the term safe indicates. The psychopharm field is actually saying is that SSRIs are safer (not safe) than the previous medications for depression. However, this message of "safe" makes others think there are no problems from using them, which is not true.

Can we agree that the majority of individuals that take an SSRI (for the required time period to experience a benefit) will experience a side effect (plenty of literature on this)?
Can we agree that the majority of side effects will be mild (again, plenty of research on this)?
Can we agree that a small minority of people will experience a severe adverse effect?

The adverse effect I am most worried about is mood switching (SSRI-induced hypomania or mania), particularly for young people. Mood switching occurs in 6-8% of individuals taking SSRIs with (what is believed to originally be) unipolar depression. This rate is twice as high for SSRIs as it is for placebo. Juveniles are at higher risk for mood switching.

Now, I am going to get away from the empirical literature. We have all likely worked with people that have been diagnosed with a slew of disorders and have tried different therapies and drug cocktails. These are the consumers that tax the mental health system the most. What are the chances that a large chunk of these individuals' problems are due to the iatrogenic effects of SSRIs (and potentially other drugs marketed as being antidepressants)?

Let's not forget other side effects that concern me: emotional blunting and increased suicidailty in teens and young adults.

I am not an anti-pharma person but my concern is this consistent banging of the drum that SSRIs are "safe" without context. This leads to the overprescribing of SSRIs (particularly from PCPs) for individuals that really shouldn't be taking them (the NICE guidelines support this "should" statement ). My view is that SSRIs (and other meds) are being treated as a panacea and doled out like Tylenol. The consequence is that maybe a small subset of people then become a major toll on the mental health system.

The issue really is research (which is currently dried up in this area). Instead of treating depressive disorders as homogenous and thinking either meds or therapy will work equally well for everyone, there is a need for more research to identify who is more or less likely to get better from the numerous different treatments we have (e.g., meds, therapy, exercise) and the heterogeneity of depression etiologies. I think they new catch phrase in healthcare is precision medicine? Either way, we know very little about who is going to benefit from a different type of therapy. More precisely, the cause of your depression is likely to influence the efficacy of the treatment. At the moment, all we have is a band aid no matter the injury.

My current thinking about safety is the following: Penicillin is safe yet every medical provider will ask me if I am allergic to it. SSRIs may be "safe" but we have no way of identifying those that would be metaphorically allergic to it (meaning, it is iatrogenic).

Final thought, I don't think responsible researchers and clinicians should be using the term safe for meds without more context.

 

[deleted343839]

Second, the control comparison was at two-week follow up, which is two weeks less than any follow-up length in the Kirsch trial. Kirsch only included trials with between 4-8 week follow up.

what they were saying with that statement is they didn't have a sufficient sample size to have a statistically significant result

This is a pilot study, so any hypothesis testing is suspect anyway. I do think it's weird that they went with this multiple baseline design. Why didn't they at least wait 4 weeks for the waitlist group? I'd have rather seen them pilot a crossover or parallel group trial. If this is a test run for a full-scale RCT, they need to rethink their approach.

The Role and Interpretation of Pilot Studies in Clinical Research

Pilot studies represent a fundamental phase of the research process. The purpose of conducting a pilot study is to examine the feasibility of an approach that is intended to be used in a larger scale study. The roles and limitations of pilot studies are ...

www.ncbi.nlm.nih.gov

Ted Kaptchuk, one of the authors, has done more sophisticated work on placebo response in other settings, so this was a disappointing read overall. Thanks for sharing, though.

 

[DynamicDidactic]

@beginner2011
I here from clinicians often that they are satisfied with providing a therapeutic effect no better than placebo. I find this to be a failure. I feel/believe that relying on placebo is the game of pseudoscientific treatments. I'd prefer to leave that to the homeopaths, acupuncturists, and chiropractors.

For mental health (across the allied professions), I'd prefer we keep working toward finding treatments that work above and beyond a placebo effect. For example, SSRIs for severe depression (not for mild depression). We have very effective exposure treatments (e.g., for panic and specific phobia). That shouldn't stop us from continuing to find and support bona fide treatments.

 

[DynamicDidactic]

The most succinct and accurate summary is a comment in the second thread:
"Antidepressants have an effect size of 0.3. Proponents and opponents argue whether that counts as "working.""

I think there was a more detailed discussion of this elsewhere on this forum but I'll address this now anyway. Also, I am not saying this is the stance of @tr

I don't want to be overly semantical about it but is there any strong evidence to support any putative mechanism of any medication for depression? For example, SSRIs have an effect above that of placebo but by most people's interpretation that effect has no clinical/real-world significance. More importantly, the effect is unrelated to changing the serotonin activity in individuals. An abundance of data indicates SSRIs do not decrease depressive symptoms through an alteration of serotonin activity and that depression is not caused by reduced serotonergic activity. As I highligth before, this could be due to the heterogeneity of depressive etiologies. So, maybe it is from some but not the average person.

Just to be clear, not anti-psychopharm here but I am in support of science. For example, its abundantly clear for me, from the literature, that neither meds or behavioral strategies alone are effective (above an beyond a credible placebo) to treat ADHD improve functional outcomes in ADHD. However, their combination works best (for adults) and improves academic outcomes for children. This is also ignoring the problem with poor diagnostics in the community and potential iatrognesis from stimulant medication.

 

[hamstergang]

Let's not forget other side effects that concern me: emotional blunting and increased suicidailty in teens and young adults.

I've got to say, it's not clear to me that the suiciadality risk is something real. The trials which found the increase over placebo didn't find any actual suicides, and the rate of suicides in the US were dropping when SSRIs hit the scene, not increasing.

That's not to say SSRIs are risk free, but the black box warning is not one of the things I truly worry about when prescribing these meds (I'm a child/adolescent psychiatrist, for the record).

For example, its abundantly clear for me, from the literature, that neither meds or behavioral strategies alone are effective (above an beyond a credible placebo) to treat ADHD.

What? The literature is abundantly clear that meds treat ADHD very well.

 

[DynamicDidactic]

2) Almost all data suggests that medication + psychotherapy produce synergistic effects. Why wouldn’t you want that for a patient?

This is a very strong statement. Can you please provide citations? For example, there are studies indicating that medication may actual reduce the effectiveness of other treatments. For example:

Exercise alone beats out exercise+meds in maintenance stage of depression treatment with no differences at end of Tx

https://www.mentalhealthexcellence.org/wp-content/uploads/2013/10/2000_Psychosomatic-Medicine_62_633-8.pdf

Studies indicating benzos reduce the effectiveness of exposure treatments (I can find cites later).​

Here is just some data indicating that combination treatment does not provide better outcomes:

This recent meta indicates that globally speaking meds+psychotherapy work better than psychotherapy alone (ES = .35). HOWEVER, there is no difference at follow-up/maintenance. When comparing CBT, the effect was even smaller (ES = .15). To be fair, I can't imagine that having any real-world significance. Particularly, in light of potential harm from medications.

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onlinelibrary.wiley.com

Social Anxiety Disorder doesn't but I always forget the citations for this meta. I have the data. Basically, the ES are as follows: Sham treatments = .63; Psychodynamic = .62; SSRI = .91; Ind CBT = 1.19; Meds+therapy = 1.30. While CBT was statistically better than SSRI, meds+therapy were NOT statistically different.​

I could look for more.

 

[DynamicDidactic]

What? The literature is abundantly clear that meds treat ADHD very well.

Sorry sorry sorry, I meant to say improve academic performance. Each post takes forever to write (and I made a mistake) since I have become a full time daycare

My take on ADHD is poorly written. I meant to say that meds are very good at targeting symptoms but poor at increasing functional outcomes such as academic performance in children or other functional outcomes in adults.

 

[DynamicDidactic]

I've got to say, it's not clear to me that the suiciadality risk is something real. The trials which found the increase over placebo didn't find any actual suicides, and the rate of suicides in the US were dropping when SSRIs hit the scene, not increasing

This gets under my hide. I never (nor does the research) state that it increases suicide attempts. The increase is in suicidality or more specifically suicidal thinking. The evidence is very strong and clear that this is happening.

The correlation of a drop in suicide and the use of SSRIs is just that, a correlation. We have no strong controlled evidence to indicate that SSRIs decrease suicide attempts. Here is a recent paper on the common tactics some are using to try to conceal the increase in suicidal thoughts:

Frontiers | Duty to Warn: Antidepressant Black Box Suicidality Warning Is Empirically Justified

The United States Food and Drug Administration issued a Black Box warning in October 2004 after placebo-controlled trials of antidepressant medications found...

www.frontiersin.org

As I have stated above, there is wayyyyy to much misrepresentation about the purported safety of medications marketed to treat depression. I have no problem with the medication but I have a problem with the lack of information provided to individuals about their medication.