Endogenous/"pseudoneurotic" vs Reactive psychiatric symptoms

[thelastpsych]

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Recently, I was reading Viktor Frankl's Theory and Therapy of Neurosis, and in of his chapters he describes three types of 'somatogenic pseudoneurosis', what we would call nowadays psychiatric symptoms secondary to organic causes: the "Basedow group" (latent hyperthiroidism - manifests as agorafobia, and is diagnosed as a higher rate of basal metabolism and treated with dihydroergotamine), the "Addison group" (latent hypercortisolism - manifests as despersonalization and 'psychodynamic syndrom', diagnosed when the patient has low BP and treated with desoxycortisone) and the "tethanoid group" (claustrofobia/globus hystericus; diagnosed with the Chvostek sign and serum K and Ca levels).

I know these are kinda old and archaic modalities, but I found it fascinating that they had these very specific categories. In the 1960s and 1970s the concept of endogenous depression was very popular, but it kinda disappeared from mainstream psychiatry literature nowadays. Splik made an insightful comment in another threat that the concept was debunked after careful observational and controlled trials from Paykel and colleagues, but in reviewing the literature, it seems to me that this author and his colleagues were actually advocating for the concepts existence - see Paykel ES, Klerman GL, Prusoff BA. Prognosis of depression and the endogenous-neurotic distinction. Psychol Med. 1974 Feb;4(1):57-64. doi: 10.1017/s0033291700040307. PMID: 4814478.

So, my question to more experienced clinicians is: what happened to the concept of 'organic/endogenous' depression? Was it debunked or merely forgotten? I've seen some people refer to it in a kind of conspiratorial way - that the pharmaceutical industry WANTS to blurry the line between 'true' and reactive depression, so that more and more people get prescribed SSRIs. What do you think?

 

[smalltownpsych]

Recently, I was reading Viktor Frankl's Theory and Therapy of Neurosis, and in of his chapters he describes three types of 'somatogenic pseudoneurosis', what we would call nowadays psychiatric symptoms secondary to organic causes: the "Basedow group" (latent hyperthiroidism - manifests as agorafobia, and is diagnosed as a higher rate of basal metabolism and treated with dihydroergotamine), the "Addison group" (latent hypercortisolism - manifests as despersonalization and 'psychodynamic syndrom', diagnosed when the patient has low BP and treated with desoxycortisone) and the "tethanoid group" (claustrofobia/globus hystericus; diagnosed with the Chvostek sign and serum K and Ca levels).

I know these are kinda old and archaic modalities, but I found it fascinating that they had these very specific categories. In the 1960s and 1970s the concept of endogenous depression was very popular, but it kinda disappeared from mainstream psychiatry literature nowadays. Splik made an insightful comment in another threat that the concept was debunked after careful observational and controlled trials from Paykel and colleagues, but in reviewing the literature, it seems to me that this author and his colleagues were actually advocating for the concepts existence - see Paykel ES, Klerman GL, Prusoff BA. Prognosis of depression and the endogenous-neurotic distinction. Psychol Med. 1974 Feb;4(1):57-64. doi: 10.1017/s0033291700040307. PMID: 4814478.

So, my question to more experienced clinicians is: what happened to the concept of 'organic/endogenous' depression? Was it debunked or merely forgotten? I've seen some people refer to it in a kind of conspiratorial way - that the pharmaceutical industry WANTS to blurry the line between 'true' and reactive depression, so that more and more people get prescribed SSRIs. What do you think?

Everything I’ve gathered from literature, training, and clinical experience points to a dynamic interaction between a biological/genetic tendency/vulnerability to depressed mood states and psycho/social/environmental factors. The research to parse these factors out can be very difficult because of the complex interactions. One example is a meta analysis a couple of years ago of ssri’s and efficacy in depression that found most of the effect size was in the moderate to severe range as opposed to the mild to moderate range. Right off the top of my head I can think of several hypotheses tied to this finding, but very hard to test and drug company research dollars won’t be used for it.
One flaw we have in this field is some think that because we can’t easily measure or test in a controlled experiment, then it doesn’t matter or even worse that it doesn’t exist.

 

[Ceke2002]

I am really looking forward to reading the discussion on this. Thanks to OP for posing the question. 😎

 

[aim-agm]

We certainly know that endogenous major depressive episodes occur, what do you you bipolar depressive episodes are?

A more edifying question is, what/when/how does it matter if a unipolar major depressive episode is endogenous or reactive?

 

[clausewitz2]

This is a big, complicated question. These sorts of shifts are never monocausal and always a confluence of factors but I'd argue in brief that these were some of the major factors:


1. DSM-III. The originally proposed RDC (the forerunner of the modern DSM) proposed 10 different subtypes of depression. There turned out not to be the case that there was a clear difference in response between these subtypes when treated with the state of the art of the day (TCA/MAOI + ECT). Furthermore, the whole idea of the DSM-III was that we were going to turn psychiatric diagnoses into operational definitions a la Carl Hempel. Specifically, psychiatric diagnoses had to be definable "is conceived as a rule to the effect that the term is to apply to a particular case if the performance of a specified operation in that case yields a certain characteristic result.” The specified operation here would be completion of a structured diagnostic interview that had an extremely high degree of interrater reliability and was not operator specific (modulo some basic training). It proved very difficult to turn the reactive v. endogenous distinction into something that fit this very well.

As an accident of history most of the non-specific signs of general psychological distress (sleep disruptions, changes in appetite, low energy) ended up in the MDD bucket as well.

2. The failure of the dexamethasone suppression test. There was a lot of hope that we would have a really reliable and indisputable objective marker of a functional disorder and it turns out to have bad sensitivity and specificity as a diagnostic tool. It was also complicated to perform and finicky. It was not useless and there are tantalizing suggestions of evidence that it did better and was more useful for more classic melancholic or psychotic depression but DSM making all depressions the same took the wind out of its sails.



3. Need to appease psychoanalysts. The bread and butter diagnosis of analytically oriented outpatient psychiatrists was neurosis in some form or another. Before the 70s, depression was viewed as a relatively rare and infrequent condition, because what it meant was something closer to what is sometimes called melancholic depression today. In fact, Sandoz was reluctant to allow imipramine to be trialled as an anti-depressant (it was originally a thorazine me-too attempt at an antipsychotic) because they were afraid there wasn't enough of a market for a depression drug to be commercially viable! However, DSM-III precluded making an anxiety disorder diagnosis in the presence of depressive symptoms and so the many, many anxiety disorders it did posit were not going to cut it for these outpatients. Those anxiety disorders were all really specific, which meant they were a poor fit for general problems of living. while anxiety disorders explicitly required fears be irrational and excessive, however, there was no such requirement for major depressive disorder's symptoms to be excessive or disproportionate, so it was much easier to qualify.

There was a last minute attempt to salvage neurotic depression by the inclusion of dysthymia but dysthymia/PDD immediately became the red-headed stepchild of mood disorders that it remains to this day.

4. Development of SSRIs

When MAOIs, TCAs, and ECT were your main options for treating the thing you called "depression" apart from endless analysis, it was really important to make sure that you were only treating people who were likely to benefit substantially from the treatment. They also had to be sufficiently miserable that they were willing to put up with the side effects. This ended up being much more likely to be people who couldn't easily articulate or identify reasons why everything tasted like bitter ashes in their mouths.

However, the development of medications that a) were somewhat effective for depressive symptoms and b) had side effect profiles that were much easier to sell meant that drawing these lines mattered less. You could go for more of an SSRI shotgun approach because the downsides were much smaller, so if it even looked like depression, blast it. Heck, PCPs could start people on SSRIs, it was a medication benign enough to not require specialists.


There is vastly more that could be said about this topic, including how it relates to the development of the bipolar disorder concept, but that's a first stab at some of the big factors involved.

 

[FlowRate]

I think it can be helpful for formulation purposes to have a sense of where the patient falls on the "spontaneous/endogenous" - "neurotic/poor coping/personality" and "stressor" scales. Which is basically just a restatement of bio/psycho/social domains. One issue I often debate with myself relates to patients who have severe ongoing stressors and who don't show much response to a few reasonable med trials across a few classes. When do you stop/slow on med trials as a means of even more directly focusing on the importance of resolving stressors/working on better ways of coping? (Especially when you're in not the patient's weekly therapist.)

 

[thelastpsych]

We certainly know that endogenous major depressive episodes occur, what do you you bipolar depressive episodes are?

A more edifying question is, what/when/how does it matter if a unipolar major depressive episode is endogenous or reactive?

I'd say that it is important for therapeutics. We try to investigate for bipolar depression, because the treatment goes in a very different direction - less focus on psychotherapy/SSRIs and antidepressants, and more on mood stabilizers and atypical antipsychotics.

In that sense, as Frankl sugested, maybe there are different subtypes of 'endogenous' depressions that can have vastly different treatments, such as corticoisteroids, specific antidepressants, or if there is not any sign of 'endogenous' depression, maybe that represents that patients repons better with psychotherapy, I don't know.

 

[PsyDr]

Fun fact: The FDA insert for Hydroxyzine says the medication is indicated for, "symptomatic relief of anxiety and tension associated with psychoneurosis and as an adjunct in organic disease states in which anxiety is manifested.".