The earliest academic formulations of the concept of schizophrenia occurred in the mid-nineteenth century in the work of Bénédict-Auguste Morel and Karl Kahlbaum.⁽¹⁾ Morel coined the term ‘démence precoce’ to refer to a disorder that he observed in young people that was characterized by cognitive impairments and progressive degeneration. He did not develop the concept fully, however. Instead, under the influence of Darwinian thinking, he became preoccupied with the general concept of hereditary
degeneration, which he described in disorders ranging from intellectual disability to alcoholism. This general concept was highly influential throughout the nineteenth and early twentieth century, which led to some of the earliest studies of the familiality of mental illnesses, and laid early foundations for later efforts to examine the role of genetic factors in schizophrenia. Kahlbaum’s seminal contribution was an emphasis on using course of illness (as opposed to symptoms) to define discrete disorders. He objected to the concept that there was only one form of severe mental illness (‘unitary psychosis’ or ‘einheitspsychose’) and argued that various kinds of psychotic disorders could be differentiated from one another based on changing patterns of symptoms and long-term outcome. Kahlbaum identified one type as ‘hebephrenia’.

Our modern concept of schizophrenia primarily derives, however, from the interaction between two great clinicians early in the twentieth century: Emil Kraepelin and Eugen Bleuler.

Although his ideas were presaged by Morel and Kahlbaum, Emil Kraepelin was clearly the first to give a detailed description of this syndrome and a compelling justification for its delineation. Kraepelin highlighted his concept of the key features of the disorder in the name that he chose for it: It was an illness that tended to begin at an early age (‘praecox’) and to have a relatively chronic course characterized by significant cognitive and social impairment (‘dementia’). Alois Alzheimer was a member of Kraepelin’s department in Munich and used the tools of neuropathology to study a similar dementia that began at a later age; examination of the brains of these individuals at post-mortem revealed a characteristic neural signature—plaques and tangles. Kraepelin began to call this disorder Alzheimer’s disease and thus gave it its current name, as well as its differentiation from dementia praecox. A similar neuropathological signature was sought for dementia praecox, but it was never found, although Kraepelin hypothesized that it must be a disease involving prefrontal and temporal regions⁽²⁾:

Kraepelin did not select any specific clinical feature as pathognomic, but he did stress the importance of several symptoms as characteristic:

Thus, for Kraepelin, what we now refer to as negative symptoms and fragmenting of thought were two key features of the disorder.

Bleuler was a near contemporary of Kraepelin. During their two long careers they maintained a dialogue between their native countries of Germany and Switzerland. Kraepelin was a thoroughgoing empiricist with a keen eye for detail, while Bleuler was primarily a high-level conceptualizer, although he clearly also had vast clinical experience. Bleuler chose to highlight fragmenting of thinking as the most fundamental feature of schizophrenia and designated it as the pathognomonic symptom. That is, he explicitly stated that this particular symptom (‘loosening of associations’) was present in all patients with schizophrenia and did not occur in other disorders. Because of the importance that he gave to this particular symptom, he renamed the illness after it (schizophrenia = fragmenting of mind). To this symptom, he added several others that he also considered to be of high importance. These included loss of volition, impairment in attention, ambivalence, autism, and affective blunting. He regarded these symptoms as basic or fundamental and the other symptoms observed in the disorder, such as delusions or hallucinations, as secondary or accessory. He pointed out that these accessory symptoms tended to occur in a variety of other conditions, such as manic-depressive illness, delirium, or dementia.

Bleuler’s conceptualization of the disorder captured the imagination of clinicians and investigators throughout the world, and the name he chose for the disorder eventually became the one that is now universally used. The prophecy of Kraepelin’s tombstone came true: ‘though his name will be forgotten, his work will live on’. During the much of the twentieth century, Bleuler’s conceptualization and terminology prevailed. Although he drew on Kraepelinian concepts, very few people were aware of the magnitude of Kraepelin’s contributions. Students of schizophrenia used Bleuler’s name for the disorder and defined it in terms of ‘the four A’s’ (associations, autism, affect, and ambivalence).

The Bleulerian emphasis slowly began to change, however, beginning in the late 1960s and 1970s. This change in emphasis arose primarily from an interest in improving diagnostic precision and reliability. Because they are essentially ‘all or none’ phenomena, which are relatively easy to recognize and define, florid psychotic symptoms such as delusions and hallucinations were steadily given greater prominence and indeed even placed at the forefront of the definition of schizophrenia. Bleuler’s secondary or accessory symptoms began to be treated as the pathognomonic symptoms.

The emphasis on florid psychotic symptoms arose because of the influence of Kurt Schneider and the interpretation of his thinking
by influential British psychiatrists. Schneider was greatly influenced by the work of Karl Jaspers, who explored phenomenology and created a bridge between psychiatry and philosophy. Jaspers believed that the essence of psychosis was the experience of phenomena that were ‘nonunderstandable’—i.e. symptoms that a ‘normal’ person could not readily imagine experiencing. Schneider, like Bleuler, wished to identify symptoms that were fundamental. He concluded that one critical component was an inability to find the boundaries between self and not-self and a loss of the sense of personal autonomy. This led him to discuss various ‘first-rank’ symptoms that were characterized by this loss of autonomy, such as thought insertion or delusions of being controlled by outside forces.^{(3, 4 and 5)}

Schneiderian ideas were introduced to the English-speaking world by British investigators and began to exert a powerful influence on the concept of schizophrenia. An emphasis on Schneiderian first-rank symptoms satisfied the fundamental need to find an anchor in the perplexing flux of the phenomenology of schizophrenia. Schneiderian symptoms were incorporated into the first major structured interview developed for use in the International Pilot Study of Schizophrenia, the Present State Examination (PSE).⁽⁶⁾ From this major base, they were thereafter introduced into other standard diagnostic instruments such as the Schedule for Affective Disorders and Schizophrenia (SADS),⁽⁷⁾ Research Diagnostic Criteria (RDC),⁽⁸⁾ and the Diagnostic and Statistical Manual (DSM-III).⁽⁹⁾

The emphasis on positive symptoms, and especially Schneiderian symptoms, derived from several concerns. The first was that Bleulerian symptoms were difficult to define and rate reliably. They are often continuous with normality, while positive psychotic symptoms were clearly abnormal. In addition to concerns about reliability, work with the IPSS and the US/UK study also had indicated that in the United States the concept of schizophrenia had broadened to an excessive degree, particularly in the Northeastern parts of the United States. Thus, in the United States, there was clearly a need to narrow the concept of schizophrenia. Stressing florid psychotic symptoms, particularly Schneiderian symptoms, was a useful way to achieve this end, since it appeared that schizophrenia was often being diagnosed on the basis of mild Bleulerian symptoms. When diagnostic criteria such as the RDC and later DSM-III were written, these placed a substantial emphasis on positive symptoms and minimized negative symptoms.

While there have been many good consequences of this progression and of the interest in Schneider’s work, there have also been problems.

From a Schneiderian perspective, Schneider’s work and point of view has been oversimplified and even misunderstood. As a Jasperian phenomenologist, Schneider was in fact deeply interested in the subjective experience of schizophrenia—in understanding the internal psychological processes that troubled his patients. For him, the fundamental core of the illness was not the specific first-rank symptoms themselves, but rather the internal cognitive and emotional state that they reflected. It is somewhat ironic that he has become the symbol of objective quantification and reductionism. He himself was a complex thinker who was concerned about individual patients.