I'll be honest, I hadn't heard of it before this thread. I did some looking into it, and I can't find a real justification for it. I think that's one of my biggest problems here -- so much of psychiatry seems arbitrary already and I hate that, especially when presenting our field to others. IMO, this is one of the problems we have in getting respect from other fields and the public and in attracting med students.
So, without recommending that I read an entire book, why is it that the Kraeplin Dichotomy is reasonable and useful?
So I personally think every psychiatrist should read the
Dementia Praecox and
Manic Depressive Insanity with someone who knows Kraepelin well and can highlight the salient parts (not an easy read). Fortunately our program director/associate PD are true Kraepelinians and go through both texts with us our intern year. But I will try to summarize why I think it is vital. First, as I have said numerous times, we do not have external validators (yet), so we have to rely upon clinical observation, longitudinal course, family studies, and delimitation from other illnesses. Our modern concept of Schizophrenia is most closely tied to Kraepelin's Dementia Praecox, whereby he describes psychic functioning in terms of cognition, emotion, and motivation, which is interestingly how many neuroscientists today conceptualize the mind in terms of respective brain systems. Anyway, after much arduous and time consuming clinical observation and meticulous research, Kraepelin surmised that hallucinations and delusions do NOT define the illness; it is really a destruction the emotional and motivational systems resulting in a premature dementia, the degree of which can vary from patient to patient, which today we conceptualize as negative symptoms. Kraepelin noted that basic cognitive abilities are largely intact and that the debilitation is caused chiefly by emotional and volitional problems (though we now know that chronic SCZ is associated with many deficits that are strictly speaking, cognitive in nature- working memory, attention, etc). The hallucinations and delusions, are merely symptoms but not completely diagnostic (though they can be suggestive in certain circumstances). One of Kraepelin's most brilliant feats was thus saying that this unifying feature was common to all different clinical forms, which Pre DSM 5 were subtypes: Simplex (negative symptoms), Silly dementia (hebephrenia or disorganized), Circular/Agitated/Periodic (prominent affective components), Paranoid (paranoid), and Catatonic (catatonic). Recent GWAS studies have supported grossly this classification system (though catatonia is another issue that is probably not an individual SCZ subtype given its predominance in BPAD). Also, untreated positive symptoms can definitely come and go, which is why the inter episodic period is so vital for diagnosis.
The Manic Depressive Insanity, conversely, does not result in a terminal state of weak mindedness or dementia, and the patients may make full recovery and are stable for discharge. And Kraepelin describes their non-episodic debilitation as more temperamental in nature (ie, manic temperament sounds like ASPD, irritable temperament sounds like Borderline, etc), but generally their social, emotional, and motivational functioning remains intact when they are not in episodes, which is the principle delimitation criterium from the Dementia Praecox. Also, mania is conceptualized as an over activation of the volitional (impulsive behavior, incr goal directed activity), emotional (lability, elevation of affect), and cognitive (flight of ideas) spheres, whereas depression is conceptualized as an underactivation. Mixed states can either exist as a transition between the two or independent states (one are where DSM V probably improved from DSM IV).
The point is that cross sectionally, Bipolar and schizophrenia are not discernable by descriptive psychiatry alone, which is why longitudinal course is so vital. Kraepelin notes that the ultimate delimitation is based on issue, or terminal state, and that the true diagnosis can only be made at the end of the disease course (ie, did the patient become weak minded/demented/stably encephelopathic?. This is the most difficult feature of Kraepelin's system: without knowing the terminal state, how does one make the diagnosis? Thus, diagnoses can certainly change, but given the critical feature of weakmindedness that is necessary for SCZ but absent from BPAD, they are absolutely mutually exclusive. I will relay this dilemma with several examples of cases in which I was involved (just using clinical course so I don't break HIPAA)- and in all of these cases organic and substance causes were ruled out.
1) High functioning patient first had depressive episode in 20s and was diagnosed with MDD, treated and recovered. Shortly thereafter had a manic episode and then recovered. Diagnosis changed to BPAD Had several more presentations of psychosis without affective symptoms and when treated responded somewhat well but has been frequently noncompliant. Also has experienced significant downward drift. Largely asocial on mental status exam even with treated psychosis. After much discussion diagnosis was changed to SCZ.
2) Patient presented very disorganized and delusional; did not have clear signs of mania (or depression). Lack of reliable history prompted diagnosis of SCZ. When florid psychosis was treated with D2 blockade, patient became manic (classic picture). When mania was treated with Lithium, patient displayed normal affect, intact social engagement, appropriate grooming and hygiene. More history revealed that patient has definitely met criteria for mania, but this has never been aggressively treated, and the patient is chronically noncompliant. I left the diagnosis as Schizoaffective Bipolar type because I don't have objective documentation of history, but in discussion with multiple attendings, this patient is most likely severe Bipolar.
3) Patient with long history of Bipolar with both severe manic and depressive episodes with excellent inter episodic functioning but marred by noncompliance- patient had frequent presentations with the most florid mania one could imagine. Consequently the patient was observed in clinic to have inter episodic psychosis (at a late decade in life) and diagnosis was changed to schizoaffective disorder; however, when looking back carefully at the inter episodic psychosis, the patient was irritable, not sleeping, had inhibition of activity (and was likely in a mixed state). Kraepelin's longitudinal diagrams show similar clinical courses of Manic Depressive Insanity.
4) Very high functioning patient who had first break psychosis with very intricate, complex delusions; some elements of downward drift (quit job, stopped talking to friends) but at first history did not discern if this was truly prodromal or unnoticed mania. Patient was hypertalkative and elevated on exam, though did not appear to be floridly manic. Patient was lost to follow up but then re presented with impulsive behavior, delusions of persecution, hypertalkativity, some question of decreased need for sleep. Importantly she had appropriate social engagement with normal/possibly elevated affect and appeared cognitively intact. More rigorous history taking revealed a true prodromal phase absent manic criteria, and when observed on the inpatient unit the patient did not meet true criteria for mania. The patient had significant downward drift and avolition compared to previous level of functioning, so the diagnosis of Schizophrenia was made.
The catch with all of this is that in order for the Kraepelinian Dichotomy to make sense patients should be followed prospectively with clear descriptions of symptoms and medication changes noted. Kraepelin charted out the courses of all of his patients from his clinical observations, which provided the data from which he drew is inferences and deductions.
And I'm post call and somewhat delirious now...