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Schizophrenia: a conceptual history 

Schizophrenia: a conceptual history
Schizophrenia: a conceptual history

Nancy C. Andreasen

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We know that psychotic disorders have been present and publicly recognized at least since classical times because of their portrayals in literature: the madness of Medea, the frenzied behaviour in The Bacchae, or the paranoia of Othello. Perhaps the most ‘valid’ portrayal from a modern clinical perspective is the feigned madness of ‘Poor Tom’ in King Lear. Poor Tom is a ‘bedlam beggar’ who encounters Lear during the great scenes of madness, portrayed while the world itself is also in the midst of a terrible storm. Tom's speech is a classical example of schizophrenic thought disorder, but he also experiences delusions and visual hallucinations:

Who gives anything to poor Tom? Whom the foul fiend hath led through fire and through flame, and through ford and whirlpool, o'er bog and quagmire, that hast laid knives under his pillow, and halters in his pew; set ratsbane by his porridge; made him proud of heart, to ride on a bay trotting-horse over four-inch'd bridges, to course his own shadow for a traitor. Bless thy five wits! Tom's a-cold, –O, do de, do de, do de. Bless thee from whirlwinds, star-blasting, and taking! Do poor Tom some charity, whom the foul fiend vexes. There could I have him now, –and there, –and there again, and there. (King Lear, III. iv. 51–60)

However, the definition and delineation of schizophrenia as a discrete disorder is a relatively recent phenomenon.

The founding fathers of the concept: Kraepelin and Bleuler

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):

If it should be demonstrated that the disease attacks by preference the frontal areas of the brain, the central convolutions and the temporal lobes, this distribution would in a certain measure agree with our present views about the site of the psychic mechanisms which are principally injured by the disease. ([link])

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

…there are apparently two principal groups of disorders which characterise the malady. On the one hand we observe a weakening of those emotional activities which permanently form the mainsprings of volition. In connection with this, mental activity and instinct for occupation become mute. The result of this part of the morbid process is emotional dullness, failure of mental activities, loss of mastery over volition, of endeavor, and of ability for independent action.

The second group of disorders … consists in the loss of the inner unity of the activities of intellect, emotion, and volition in themselves and among one another … the near connection between thinking and feeling, between deliberation and emotional activity on the one hand, and practical work on the other is more or less lost. Emotions do not correspond to ideas. The patients laugh and weep without recognizable cause, without any relation to their circumstances and their experiences, smile while they narrate the tale of their attempts at suicide … ([link][link]).

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.

Certain symptoms of schizophrenia are present in every case and in every period of the illness even though, as with every other disease symptom, they must have attained a certain degree of intensity before they can be recognized with any certainty … Besides the specific permanent or fundamental symptoms, we can find a host of other, more accessory manifestations such as delusions, hallucinations, or catatonic symptoms … As far as we know, the fundamental symptoms are characteristic of schizophrenia, while the accessory symptoms may also appear in other types of illness ([link]).

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).

Schneiderian symptoms, psychosis, and the dominance of diagnostic criteria

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.(3–5)

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.

The development of diagnostic criteria for schizophrenia has also had both advantages and disadvantages. When DSM-III was originally developed, it was intended only as a ‘provisional consensus agreement’ based on clinical judgement. The criteria were created by a small group of individuals who reached a decision about what to include based on a mixture of clinical experience and research data available up to that point. The criteria were chosen to serve as a gatekeeper that would include or exclude individual cases, and they were not intended to be a full description of the illness. Unfortunately, they are now sometimes treated as a textbook of psychiatry. Further, the criteria have become reified and given a power that they originally were never intended to have.

Diagnostic criteria have substantial and undeniable advantages, they improve reliability, provide a basis for cross-centre stand-ardization both nationally and internationally, improve clinical communication, and facilitate research. However, they may also have potential disadvantages and even abuses: they provide an oversimplified and incomplete view of the clinical picture, discourage clinical sensitivity to individual patients and comprehensive history-taking, lead students and even clinicians to believe that ‘knowing the criteria is enough’, reify an agreement that was only intended to be provisional, and discourage creative or innovative thinking about the psychological and neural mechanisms of schizophrenia.

The concept of positive and negative symptoms

Neither Kraepelin nor Bleuler actually used the terms ‘positive symptoms’ or ‘negative symptoms’, although the concepts are embedded in their writings. While various sources for this term can be cited,(10) one of the earliest and most prominent was Hughlings-Jackson.(11) Although Jackson's work was not published until much later, in the late nineteenth century Jackson speculated about the mechanisms that might underlie psychotic symptoms:

Disease is said to ‘cause’ the symptoms of insanity. I submit that disease only produces negative mental symptoms, answering to the dissolution, and that all elaborate positive mental symptoms (illusions, hallucinations, delusions, and extravagant conduct) are the outcome of activity of nervous elements untouched by any pathological process; that they arise during activity on the lower level of evolution remaining.

Thus Jackson believed that some symptoms represented a relatively pure loss of function (negative symptoms answer to the dissolution), while positive symptoms such as delusions and hallucinations represented an exaggeration of normal function and might represent release phenomena. Jackson presented these ideas at a time when Darwinian evolutionary theories were achieving ascendance, and his concepts concerning the mechanisms that produced the various symptoms were clearly shaped by a Darwinian view that the brain is organized in hierarchical evolutionary layers. Positive symptoms represent aberrations in a primitive (perhaps limbic) substrate that is for some reason no longer monitored by higher cortical functions. Thus Jackson's concept of negative versus positive symptoms rather closely resembles those which are currently discussed. Although today most investigators do not necessarily embrace the specific mechanism that he proposed, they accept his view that they must be understood in terms of brain mechanisms, as well as his basic descriptive psychopathology.

References to positive and negative symptoms occurred sporadically during the 1970s, sometimes making clear references to Jackson's ideas and sometimes simply presenting notions about the clinical meaning of the distinction. Notable examples include the descriptions of Fish,(3) a reference to the terms by Strauss and others,(12) and Iowa work on affective blunting and on thought disorder, classifying it as positive versus negative.(13,14)

In 1980, Crow published an influential paper describing a two syndrome hypothesis of schizophrenia using the terms ‘positive’ and ‘negative’ symptoms.(15) He proposed that schizophrenia could be divided into two different syndromes, which he referred to as Type I and Type II. Type I schizophrenia was characterized by prominent positive symptoms, an acute onset, good premorbid adjustment, a good response to treatment, intact cognition, intact brain structure, and an underlying mechanism that was neurochemical (dopaminergic) and therefore reversible. Type II schizophrenia was characterized by prominent negative symptoms, an insidious onset, poor premorbid adjustment, a poor response to treatment, impaired cognition, structural brain abnormalities (i.e. ventricular enlargement as visualized by Computerized Tomography [CT]), and an underlying mechanism that was characterized by neuronal loss and therefore irreversible. This proposal was highly generative for research in schizophrenia during the 1980s, primarily because it combined speculations about clinical presentation and about underlying neural mechanisms within a single hypothesis.

Two major problems were inherent in Crow's presentation of this hypothesis, however, which initially limited its empirical testing. One problem was its failure to specify a clear method for measuring positive and negative symptoms, and the second was its failure to indicate which of the broad array of variables associated with each of the two syndromes should be considered dependent or independent. Which symptoms of schizophrenia should be considered to be positive and which negative? Which variable—or group of variables—should be used to define the separate syndromes and test whether the hypothesized relationships were present?

Solutions to these problems were proposed by the investigative team at the University of Iowa.(16) Reliable methods for defining and differentiating positive and negative thought disorder and other negative symptoms such as affective blunting had already been developed at Iowa(13,14) and the research group there also had a long tradition of developing diagnostic criteria. Consequently, we developed structured scales for the assessment of both positive and negative symptoms, the Scale for the Assessment of Negative Symptoms (SANS) and the Scale for the Assessment of Positive Symptoms (SAPS).(16–18) These scales were intended to provide a more comprehensive, reliable, and well-anchored set of measurements for the evaluation of psychopathology in schizophrenia than had been provided by standard instruments such as the Brief Psychiatric Rating Scale (BPRS).(19) They were subjected to rigorous assessment of their psychometric properties, including internal consistency, reliability, and validity. They were quickly translated into a variety of languages and widely used throughout the world.

In addition, a solution to the second problem was imple-mented by using a standard strategy in the study of psychopathology: the core clinical syndrome would be treated as the independent variable, while the various associated features would be (somewhat arbitrarily) designated as dependent. To this end, criteria were developed that could be used to classify schizophrenic patients as positive, negative, or mixed. Initial work with these criteria suggested that this strategy could be quite useful.(16,17) As Crow hypothesized, negative patients differed from positive patients in the predicted direction: larger ventricular brain ratio (VBR), poorer premorbid adjustment, lower educational achievement, and poorer cognitive performance. Many subsequent studies continued to explore the two syndrome hypothesis, with the majority confirming at least some aspects of it. However, other problems with this hypothesis also became evident. Perhaps the most vexing for the hypothesis, and for the application of criteria to categorize patients based on clinical presentation, was the large number of patients with a mixture of positive and negative symptoms. The hypothesis had difficulty in explaining how patients who were both positive and negative could have both reversible and irreversible abnormalities, good and poor premorbid adjustment, and other counterintuitive and contradictory findings. For these reasons, most investigators have regretfully abandoned this appealingly simple and heuristic hypothesis during recent years.

However, the clinical distinction between positive and negative symptoms has remained relatively robust. The tendency to distinguish between these two classes of symptoms has become widespread, and the terms have passed into standard clinical usage. The alacrity with which the terms have been adopted suggests that they fill a useful linguistic and conceptual niche. Negative symptoms are an important component of schizophrenia, and the use of the ‘positive’ and ‘negative’ terminology gives them recognition and even equal weight. As the Bleulerian symptoms received de-emphasis because of concerns about reliability, they left a void in the descriptive lexicon. Patients were designated as having ‘recovered’ when their delusions and hallucinations were no longer present or prominent; yet many remained unemployed, unable to return to school, or socially isolated. What might explain this outcome if their symptoms were genuinely absent? Upon reflection, it became evident that only some of their symptoms were absent, and that a group of ‘no name’ symptoms were the likely explanation. If these symptoms could be named ‘negative’, grouped together, measured objectively and reliably, and related to outcome and treatment, an important mechanism for clinical description and communication was restored. Although the oversimplified distinction between positive and negative implied in the two syndrome hypothesis might be misleading, it was useful to recognize that some symptoms tend to get patients hospitalized and to call these ‘positive’ and that other symptoms tend to lead to psychosocial morbidity and to call these ‘negative’. Thus the distinction at the level of symptoms (as opposed to syndromes or disease categories) is helpful descriptively.

The distinction has also persisted because standardized and reliable methods have been developed for assessing these symptoms and placing them in broad general classes. Instruments such as the SANS and SAPS have facilitated the persistence of the terminology because they have provided the tools for rating and measuring. Although tools were at hand for most positive symptoms, no scale was available at all for negative symptoms prior to the SANS. The extensive and repeated documentation of its reliability has quieted concerns that negative symptoms are too ‘soft’ to be assessed precisely, accurately, and objectively. Furthermore, other simpler scales, targeted primarily for use in clinical drug trials, have also been developed.(20) By the time that DSM-IV(21) and ICD-10(22) were written, the concept of positive and negative symptoms was so widely accepted that negative symptoms were included in their diagnostic criteria for the first time.

Beyond diagnostic criteria and the search for fundamental mechanisms

As the present moves towards the future, corrective readjustments are continuing to occur. Paradoxically, these often occur by returning to the past and coming back full circle to the work of Kraepelin, Bleuler, Jackson, and Schneider.

Clinically, the emphasis on negative as well as psychotic symptoms is leading to increased interest in the full range of symptoms of schizophrenia and in developing methods for treating that full range. In particular, there has been a growing interest in developing improved treatments for negative symptoms. The interest in negative symptoms has been complemented by a return to an interest in cognitive aspects of schizophrenia. Many negative symptoms are cognitive in nature—alogia (poverty of thought and speech), avolition (inability to formulate plans and pursue them), and attentional impairment. While their assessment may emphasize objective aspects of behaviour in order to achieve reliability, their underlying essence is in the domains of thought and emotion. Increasingly, therefore, investigators are returning to the original insights of Kraepelin and Bleuler that the core symptoms of schizophrenia represent a fundamental deficit in cognition and emotion.

Several prominent investigators have turned from a focus on explaining and ‘localizing’ the specific symptoms of schizophrenia to a search for more fundamental underlying cognitive mechanisms.(23) Examples include Frith's hypotheses concerning an inability to think in ‘metarepresentations’,(24) Goldman-Rakic's studies of working memory,(25) our descriptions of cognitive dysmetria Andreasen,(26) or the work of Holzman,(27) Braff,(28) Swerdlow and Geyer,(29) and Freedman(30) on information processing and attention. These cognitive models provide a general theory of the disease that is consistent with its diversity of symptoms, permit testing in human beings with a variety of convergent techniques (e.g. imaging, neurophysiology), and even permit modelling in animals. This efficient and parsimonious approach offers consider hope for the future because it facilitates the search both for improved treatments and for molecular mechanisms.

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