06Chapter 4. Kraepelin and Bleuler: How the Word Was Born

In the sixth edition of his famous Textbook of Psychiatry, published in Leipzig in 1899, Emil Kraepelin (1856–1926), a professor at the University of Heidelberg, quietly sparked a revolution. At the time, no one grasped its full magnitude, but it was within the pages of this book that a concept was first presented in a complete and systematic form—a concept that would define psychiatry for the next hundred years.

Kraepelin grouped three seemingly distinct illnesses under a single term: dementia praecox, or “early dementia.” These conditions had previously been described by his predecessors as separate entities. Hebephrenia, identified by Ewald Hecker in 1871, was characterized by bizarre, childlike behavior in young patients with disordered thinking. Catatonia, delineated by Karl Ludwig Kahlbaum in 1874, involved states of immobility, mutism, waxy flexibility, and episodes of motor agitation. The paranoid form featured delusions and hallucinations, leading to profound personality deterioration.

Kraepelin looked at these three syndromes and asked a question that no one had posed before him: Is this one illness manifesting itself in different ways? And if so, what is the common thread that ties them together?

What united them, according to Kraepelin, was the fate of the patients. Whether they were hebephrenics, catatonics, or paranoids, all began to fall ill in their youth, often between the ages of fifteen and twenty-five. All deteriorated steadily over time. All eventually reached a state Kraepelin termed “mental weakness”—a collapse of will, emotional impoverishment, and loss of critical judgment. This was early dementia, in contrast to senile dementia, which was already recognized at the time and occurred in old age as a result of organic brain damage.

Kraepelin had a method. He called it the clinical-catamnestic approach. Simple? Yes. Now try doing it. You must observe. For years. For decades. Every symptom—written down. Every shift in the course of the illness—tracked. The progression. Step by step. Day by day. And then—the endpoint. Fifteen years. Twenty. The patient reaches their final condition. Kraepelin opens the old notes. The first pages. The first weeks. The first symptoms. And asks one question: What at the onset of the illness hinted at this outcome?

It was along this path that Kraepelin arrived at the idea: these different clinical pictures were one process, one illness, one inevitable outcome.

And then Kraepelin drew a second line. The one that changes everything. Opposite dementia praecox—the disintegration, the irreversibility, the end—he placed another group of endogenous psychoses. Its name: manic-depressive psychosis. This is where the key lies hidden. In dementia praecox, there is a rupture. The fabric of personality tears, and it cannot be stitched back together. The end. Here, it’s the opposite. Episodes of agitation or depression. Severe ones. Extremely so. The person struggles within them, as if caught in a storm—and it feels like it will last forever. But afterward—remission. Often nearly complete. The patient returns to normal. To themselves. To life. Until the next episode.

What modern psychiatry refers to as bipolar affective disorder is a descendant of Kraepelin’s original concept.

Thus, at the end of the 19th century, Kraepelin introduced a dichotomy to psychiatry that endured nearly to the present day: endogenous psychosis with a progressive course (dementia praecox) versus endogenous psychosis with an episodic course and remissions (manic-depressive illness). The former was destined to worsen. The latter was not.

Many contemporary psychiatrists question this dichotomy—we will explore this further in the following chapters. However, without Kraepelin, modern diagnostics simply wouldn’t exist. His “Manual” is the cornerstone from which everything we now recognize as “scientific psychiatry” originates.

But Kraepelin was a clinician. Nothing more. He observed with care. He classified with precision. He never tried to explain what was actually happening inside the patient.

Someone else has taken on this task.

Zurich. The Burghölzli Clinic. One of Europe’s most renowned psychiatric institutions at the turn of the century. Here, Eugen Bleuler worked. 1857–1939. A Swiss psychiatrist. The polar opposite of Kraepelin. Kraepelin, a Prussian by birth, was as cold as a scalpel. Strict. Systematic. Patients were mere objects of observation to him—faceless units in a clinical chart. He observed them through a glass wall. Bleuler, a Swiss to the core, tore down that wall. Warm-hearted. Inquisitive. A humanist. To him, patients were not things. They were interlocutors to be understood. He peered into their fear-distorted minds and heard not delirium, but a cry for help. Two temperaments. Two approaches. Two views on madness. Which of them saw the truth?

In 1911, Bleuler published a book that reshaped psychiatry: “Dementia Praecox, or the Group of Schizophrenias”.

The very name he chose carried an entire program. Bleuler did not reject Kraepelin’s concept. He accepted it but renamed and deepened it. Why schizophrenia? The word was compound, derived from ancient Greek roots: schizo—“to split,” “to cleave”—and phren—“soul,” “mind.” Literally: a split mind.

What exactly did Bleuler mean? Something entirely different from what the uninitiated have grown accustomed to thinking. “Schizophrenia” is not “split personality.” Not two personalities locked in one cage of flesh. Bleuler meant something far subtler and far more terrifying. A splitting between the psychic functions within a single person. Feelings — one thing. Thoughts — another. Will — a third. Behavior — a fourth. In a healthy mind these functions are woven into a single neural knot, beating in harmonious accord. In the schizophrenic, that knot is torn apart. The functions operate independently. Each on its own route. Each by its own remorseless logic.

Hence the strange reactions. Hence the astonishing paradoxes of behavior. Hence what would later be termed affective dissociation: the patient recounts the death of a loved one with a smile or laughs while describing terrifying hallucinations. Not because they don’t understand. But because their emotional response is detached from the content of their thoughts.

Bleuler’s main contribution was his famous “four A’s” — the four primary, fundamental symptoms of schizophrenia. In German, all four began with the letter “A”:

Associations — a disturbance of associative thinking. The patient’s thoughts slip, lose their connections, jump from one to another. Logic breaks down. What emerges is what psychopathology calls a “formal thought disorder.

Affect — a disturbance of emotionality. Emotions are either flattened, incongruous with the content, or internally contradictory.

Ambivalence — the coexistence of opposing feelings, thoughts, and desires toward the same object. A patient loves and hates their mother at the same time. Wants and fears. Affirms and denies. This is not indecision; it is simultaneity.

Autism — a withdrawal into one’s own inner world. But careful: it was here that Bleuler introduced the term “autism,” and only later, in 1943, did Leo Kanner apply the word to a completely different childhood disorder that we today call “autism.” Bleuler meant something else — a walling-off from reality, a fixation on one’s own fantasies and thoughts.

Alongside these four primary symptoms, Bleuler also described secondary, or accessory, ones — hallucinations, delusions, catatonic symptoms, and others. An important detail: Bleuler did not consider hallucinations and delusions to be the most essential signs of schizophrenia. What mattered most to him was the splitting of the psychic functions themselves. Delusions and hallucinations can occur in other illnesses too. The splitting — only in this one.

Today most of Bleuler’s specific theoretical constructs are no longer used in their pure form in modern psychiatry. The concept of the “four A’s” remains a pedagogical and historical monument — psychiatry students study it, but contemporary diagnosis of schizophrenia rests on other, stricter criteria, set out in the DSM-5 and the ICD-11.

Yet Bleuler’s philosophical contribution remains enormous. He brought into psychiatry something Kraepelin lacked: an attempt to grasp the inner logic of the patient’s experience. Kraepelin observed and classified. Bleuler listened and tried to decipher.

And here is an important point that is often overlooked. Bleuler was the first major psychiatrist to take Sigmund Freud’s ideas seriously and apply them to the psychoses. Carl Gustav Jung worked at his Burghölzli clinic, not yet fallen out with Freud. Together they discussed association tests and tried to understand what exactly was happening in the inner world of a patient with schizophrenia.

Freud himself, in 1914, reflecting on the history of psychoanalysis, wrote:

“Bleuler showed that a number of purely psychiatric cases can be explained by the intervention of processes that psychoanalysis describes for understanding dreams and neuroses (‘Freud’s mechanisms’). Jung, having successfully applied the method of analytical interpretation to the strangest and most incomprehensible phenomena, demonstrated that such phenomena originate in the lives and fears of patients. From that moment on, it became impossible for psychiatrists to ignore psychoanalysis. Bleuler’s major work on schizophrenia (1911), in which the psychoanalytic and the clinical-systematic aspects are treated as equals, finally brought him success.”

Thus Bleuler — the Swiss clinician — became the bridge between Kraepelin and Freud. Between classical descriptive psychiatry and depth psychology. Between the attempt to see and the attempt to understand.

But this is exactly where I want to make a point that matters for my book. It has nothing to do with Bleuler himself, but rather with the way he is sometimes spoken of today.

In popular accounts of the history of psychiatry, including some online sources, one may encounter claims that Bleuler supposedly had some sort of “biochemical theory of schizophrenia,” that he isolated “toxic substances,” “thyroxine,” or something similar from the brains or blood of patients, and that he allegedly concealed the failure of this theory for the sake of his reputation. While these claims circulate, none of them are supported by historical sources. Neither Bleuler’s own works nor scientific biographies written by psychiatrists contain any such facts.

Bleuler was a rigorous clinical phenomenologist. He described what he observed without venturing into biochemical explanations, as the tools of biochemistry at the beginning of the 20th century did not permit such insights. He left theoretical conjectures to his biologically oriented contemporaries, focusing instead on understanding the lived experiences of his patients.

Why is it important to state this directly? Because in our book, which examines myths in psychiatry, we don’t want to commit the same mistake. Criticizing 20th-century psychiatric practices is not only possible but necessary. However, such criticism must be grounded in documented evidence. Inventing “Bleuler’s biochemical crimes” is just as dishonest as believing in “Hellinger’s constellations”—both are fantasies presented as facts.

Thus, by the beginning of the 20th century, psychiatry had been gifted both the term and the concept by Kraepelin and Bleuler. Schizophrenia ceased to be a random collection of symptoms and became a clinical entity. It was this entity that the next generations would have to grapple with.

And this is where the true tragedy began.

Because there was a concept, but no treatment.

This was the state of psychiatry—armed with a diagnosis but devoid of answers. The word alone was enough. It meant a sentence. There were no treatments to speak of. And into this yawning void—like water flooding a breached hull—poured theories. One after another. Hypotheses. “Methods.” Each new decade proclaimed itself a breakthrough. Each left a graveyard in its wake. Malaria. The patient was injected with the malaria parasite. The idea was monstrously simple: fever would burn away psychosis. Sometimes it did. Along with the patient. Along with the person. Insulin comas. Patients were plunged into severe hypoglycemia—right to the edge beyond which there is no return. To the brink. And then—pulled back. Sometimes—not pulled back. Sometimes—not in time. Sulfazin. Lobotomy. Electroshock. The list grew. So did the list of victims. Only by the mid-20th century did the first antipsychotics emerge. Those that truly helped millions. Though they, too, opened their own complex chapter of problems.

Yet until that moment—from Kraepelin in 1899 to chlorpromazine in 1952—psychiatry would grope its way forward. And it would not find the path right away. And it would pay a colossal price for the search, in human lives.

The following chapters tell of some of those quests—and what they cost.