Psychiatric clinicians don't tend to know their history, or if they do, it's often superficial. A classic example is the work of Emil Kraepelin, who gave us the concepts of schizophrenia (which he called dementia praecox) and manic-depressive illness. Typically, colleagues often will misstate what Kraepelin believed, and then criticize him as being wrong for it.
It's important to know our history, and to understand Kraepelin's ideas correctly, if we are to have a better present. In this post, I'll address a few common mistakes or matters of controversy.
There are two key distinctions in Kraepelin’s basic ideas:
first, the dichotomy between dementia praecox and manic-depressive insanity (MDI);
and second, and more importantly in my view, Kraepelin’s refusal to divide MDI into bipolar illness and unipolar depression.
Most modern psychiatrists do not know the second point. They don’t realize that Kraepelin’s MDI is not bipolar illness, but rather bipolar illness plus unipolar depression. If this point is not understood, no one can discuss Kraepelin’s ideas accurately.
DSM-III onward is NOT neo-Kraeplinian. It is neo-Leonhardian because it rejects Kraepelin unitary MDI model in favor of the split into bipolar illness and unipolar depression (a view promoted by Karl Leonhard, a mid 20th century critic of Kraepelin). It is neo-Leonhardian, as opposed to purely Leonhardian, becuase it also waters down the concept of unipolar depression to "major depressive disorder” (MDD), which is not the same thing since it combines the manic-depressive unipolar patients with "neurotic depression”, which had never been seen as being the same as MDI. This is a major critique that the Austrian/British psychiatrist Martin Roth always made in the late 20th century, but that the psychiatric profession has not understood.
So all in all, we cannot critique Kraepelin validly if we see him through the distorted lens of DSM-III onward concepts, like bipolar illness and MDD.
The claim, for instance, that dopamine blockers are "antidepressants” is not meaningful, because those studies are done in "MDD”, which is not a diagnostically meaningful concept, and certainly not the same thing as unipolar depression or MDI. Dopamine blockers improved mixed states. Most mood episodes, whether in bipolar illness or in unipolar depression, are mixed states. That’s a major reason why Kraepelin’s unitary MDI concept makes sense; there is no pure polarity for most patients. Hence improvement for depressive symptoms in mixed states is not an "antidepressant” effect, but an anti-mixed effect. We think it’s antidepressant because the DSM definition of "MDD” is so broad that it includes most mixed states.
Our vision is distorted by DSM, even when we criticize DSM.
Another example: Historians sometimes say that Kraepelin talked of a "firewall” between schizophrenia and MDI. Instead, he really spoke of two spectra of illnesses that didn’t overlap much. The small overlap, in my view, is consistent with the schizoaffective picture.
I think Kraepelin was enough of a biologist to have been suffused with Darwin’s anti-essentialism about species. Kraepelin’s entomologist older brother I’m sure would have taught him this fact also: there are no firewalls in nature. There are variations on dimensions everywhere, with small amounts of overlap. That overlap is where nature gets the flexibility to evolve via natural selection.
So I am willing to believe that a number of different diseases and/or etiologies comprise the schizophrenia concept, and so too for MDI, but I’m convinced by the evidence we have that the overall schizophrenia group is quite different than the overall MDI group, although by different I mean relatively, and not absolutely, consistent with the Darwinian nature of dimensional variability in all aspects of nature.
Sometimes critics cliam that the concept of spectrum conditions conflicts with Kraepelin’s nosology, but I think spectra are consistent with it: MDI was one large spectrum from full mood recurrent mood episodes to mild chronic affective temperaments. Dementia praecox was a spectrum from severe chronic psychosis to mild "schizothymia” as Kretschmer later put it. As I described above, these spectrum concepts are part and parcel of Darwinian biology and were well-known to Kraepelin, and accepted by him.
I suppose I think Kraepelin was right on both counts, much as it’s unpopular to think we haven’t figured things out better than the Old Man.
I also often hear colleagues invoke Kraepelin’s last edition of his textbook, or other articles in the last years of his life in the 1920s, and use those writings to contradict his earlier statements. They feel that such reference is sufficient to prove their point. In fact, it isn’t.
Just because someone says something when he is older doesn’t mean that he is more correct than what he said when he was younger.
This phenomenon is common especially with great thinkers, in whom there always is an Early, Middle, and Late thinker. The assumption in these critics of the Kraepelinian system often is that the Late Kraepelin is the Right Kraepelin, or the Best Kraepelin. But how do we know that?
Is the late Marx the best Marx? Or is the early Marx, who was much more liberal and humanistic, a „better” Marx? Is the late Freud the best Freud? Or are his early works on sexual repression more meaningful and closer to clinical reality? Is the late Heidegger the best Heidegger? Or is the early Heidegger of Being and Time much more original and influential? The late Sartre vs the early Sartre? The late Jaspers vs the early Jaspers? The late Einstein vs the early Einstein? The late Nietzsche vs the early Nietzsche?
I personally think that if one had to generalize, the best phase of a thinker is his or her most mature phase, which usually is in the middle of one’s life. The middle Marx who wrote Kapital is the mature Marx. The middle Freud who wrote Ego and Id is the mature Freud. The middle Heidegger, the middle Jaspers, those are the core thinkers. The middle Kraepelin of 1896 to about 1910 is the mature Kraepelin.
Later is not necessarily better.
Lastly, colleagues often turn to studies of diagnoses like schizophrenia and bipolar illness, and report a great deal of symptom overlap, and then conclude that such data argue against the view that they are different illnesses.
But overlap in symptom studies is common in medicine, and it is the least meaningful nosologically. If you did a symptom study of primary asthma versus cigarette-related chronic obstructive pulmonary disease (COPD), you would find alot of symptom overlap.
I really don’t understand why we psychiatrists keep talking about symptoms so much. This was indeed one of Kraepelin’s key insights, lost again in our false DSM ideology: symptoms overlap in medicine and psychiatry. That’s nothing new or interesting. You have to use some other criterion to establish diagnostic validity – not symptoms, but something else: pathology, course of illness, laboratory tests, genetic markers.
In fact, if you sue genetics, looking at classic genetic studies of the schizoaffective question, like the Roscommon family study, the diagnostic overlap between schizophrenia and affective illness is quite small, and completely consistent with the statistical likelihood of random comorbidity of those two conditions in the same family lineage.
So I see no need to invoke the ever-present favorite ghost of the pre-Kraepelinian and anti-Kraepelin unitary psychosis model. That would be like saying that since I can’t see beyond the horizon, I will return to the theory that the earth is flat. There are other explanations.
It is the psychiatric profession, not Kraepelin, who has created false categories, before and after DSM-III, and then confusedly wondered what is what. As in the old saying: Men first raise a dust, and then complain they cannot see.