Catatonia in the History of Psychiatry: Construction and Deconstruction of a Disease Concept.

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Perspectives in Biology and Medicine, Volume 57, Number 4, Autumn 2014, pp. 524-537 (Article) 3XEOLVKHGE\-RKQV+RSNLQV8QLYHUVLW\3UHVV DOI: 10.1353/pbm.2014.0033

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Catatonia in the History of Psychiatry construction and deconstruction of a disease concept

Victor Mark Tang and Jacalyn Duffin

ABSTRACT Catatonia is a psychomotor disorder that has gone through numer-

ous descriptions since 1874, reflecting the many changes in psychiatric disease conceptualization that have occurred within that time frame. Catatonia has been variously described as a distinct disease entity, as a part of schizophrenia, and as a nonspecific manifestation of many disorders. Because of its association with schizophrenia, the description of catatonia was particularly affected by the psychopharmacological era, beginning in the 1950s, and by the development of the Diagnostic and Statistical Manual of Mental Disorders (DSM). Changing trends in psychiatric research—especially the brain-based disease model, research methods favoured by the evidence-based medicine movement, and the codes and categories of the DSM—also profoundly influenced the evolving concept of catatonia. This paper discusses these important factors that affected recognition, treatment, and study of catatonia in order to reveal the biases and assumptions made when constructing a disease concept.

O

ver the last century, psychiatry has seen many contrasting views on the nature of mental illnesses and how they are to be classified, together with major changes in treatment, both psychological and pharmacological. These advances, combined with recent neuroscience research, have changed the way we understand

School of Medicine, Queen’s University, Kingston, Ontario. Correspondence: Victor Tang, School of Medicine, Queen’s University, 80 Barrie Street, Kingston, ON K7L 3N6, Canada. E-mail: [email protected]. Perspectives in Biology and Medicine, volume 57, number 4 (autumn 2014): 524–537. © 2015 by Johns Hopkins University Press

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Catatonia in the History of Psychiatry

the etiology of all mental illness. Moreover, the Diagnostic and Statistical Manual of Mental Disorders (DSM) has had profound implications for clinical diagnosis and for research methods; it is the predominant classification manual in psychiatry. This article will trace how major changes in psychiatry affected the way physicians understood, identified, treated, and examined catatonia, a syndrome of motor abnormalities associated with psychiatric symptomatology, especially disturbances of thought, perception, and emotion. Motor findings include akinesia, posturing, rigidity, negativism, grimacing, waxy flexibility, immobility, stupor, and repetitive speech and acts. Its diagnosis has been debated since its original conceptualization by German psychiatrist Karl Kahlbaum in 1874. By analyzing the contextual factors that influenced the conceptualization of catatonia through time and exploring how a single diagnostic concept was subtly, subconsciously, or inadvertently transformed, we reveal mechanisms at work in how we conceptualize all disease.

Clinical Approach, Context, and Ideology Catatonia has been formulated in different ways by many significant figures in psychiatry, each working within the context of their own clinical practice, ideological method to disease conceptualization, and interpretation of symptoms. As a result, the syndrome known as catatonia was constructed and reconstructed through time. Understanding the basis for these narratives requires appreciation of the underlying approach and influencing factors for each of these clinicians Late 19th and and Early 20th Centuries

An astute, descriptive psychopathologist, Karl Kahlbaum (1828–1899) believed that close, longitudinal observation, taking into account the patient’s entire history, was the best way to delineate discrete disease entities.Through a series of comprehensive case presentations, he defined catatonia as a distinct, cyclic, progressive disease that alternated through melancholy, mania, stupor, confusion, and dementia (Kahlbaum 1874). Because one or more of these symptoms could be absent, clinicians made the diagnosis “on the basis of their thorough clinical experience” (Neisser 1887, 4). For Kahlbaum, catatonia represented a distinct disease entity. Kahlbaum’s viewpoint was soon challenged and reformulated by Emil Kraepelin (1856–1926). Kraepelin exerted an enduring and decisive influence on psychiatry. His magnum opus, Kompendium der Psychiatrie (first published in 1883), presented a classification of mental disorders, including the landmark idea of two distinct forms of psychosis: manic depression and dementia praecox. In Kraepelin’s view, catatonia formed a subtype of dementia praecox: because they shared a poor prognosis, they constituted variations of the same entity. This emphasis on prognosis characterized his approach to diagnosis (Fink, Shorter, and Taylor 2010). Many have argued that Kraepelin’s categorization by prognosis was simplistic and hampered understanding of complex psychiatric illnesses (Healy 2004); nevertheless, Kraepelin still insisted

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that classification schemes should involve all aspects of the clinical picture, including pathology, etiology, and symptoms, and comprehensive bedside observation. His views eventually enjoyed unprecedented influence on the course of psychiatry, as they became the basis of the DSM (Mayes and Horwitz 2005). Kraepelin’s definition of catatonia as part of dementia praecox entered the DSM I under “schizophrenia” in 1952, where it remained until the DSM-5 (2013). Thus, catatonia within dementia praecox (later schizophrenia) dominated its conceptualization for a century. Kraepelin’s “dementia praecox” is now referred to as “schizophrenia,” a term coined by Paul Eugen Bleuler (1857–1939) in 1911; catatonia remained a subtype. While the framework was unchanged, the root perspective was different. Kraepelin emphasized chronicity and poor prognosis, but Bleuler used schizophrenia to describe a splitting of psychic domains, fragmenting reality perception, thought, and cognition. For the etiology of catatonia he looked to psychological perspectives, suggesting that its presentations were expressions of a psychodynamic complex, based on Freudian psychoanalytic theory (Braunig and Kreuger 2004). For example, in the sign of Schnautzkrampf, a protrusion of the patient’s lips, Bleuler saw a manifestation of feelings of contempt, whereas previously this symptom was viewed neurologically as a tonic contraction of the perioral muscles. Bleuler’s approach paralleled the rise of psychoanalysis and impacted catatonia in three important ways. First, his belief that catatonic symptoms were accessory manifestations of Freudian complexes marginalized their importance in the diagnosis of schizophrenia for generations of psychiatrists (Braunig and Kreuger 2004). Second, the psychoanalytical approach ignored discrete categorizations of all mental illness, as overt symptoms were thought to be symbolic manifestations of interpersonal and subconscious conflicts (Mayes and Horwitz 2005). Clinicians were to look beyond the symptoms to uncover patients’ inability to cope with their environments. For example, leading psychodynamic psychiatrist Karl Menninger (1963) urged clinicians to ask,“what is behind the symptom?” (325).This perspective sidestepped critical analysis of psychiatric nosology and obscured efforts to conceptualize or classify catatonia. Third, Bleuler’s conceptualization eliminated the necessity of poor prognosis and eventual degeneration that had been central to Kraeplin’s linking of dementia praecox and catatonia. Kahlbaum had not supposed that catatonia always signalled poor prognosis; in fact, he proposed that the general tendency was towards recovery (Gelenberg 1976). Indeed, prognosis in catatonia was long a controversial topic. In 1913, the American psychiatrist George Kirby noted that:“Aschaffenburg for instance claims no catatonics completely recover . . . E. Meyer found that from 20–25 per cent of the cases recovered . . .Wilmans, who reviewed Kraepelin’s own Heidelberg cases and found that catatonic symptoms as evidence of a deterioration process had been greatly overrated” (695). Although Kraepelin himself cited a 13% recovery in catatonics, he claimed that these were remissions rather than cures (Kirby 1913). According to Healy (2008), Kraepelin selected his patients and did not trace those

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who never returned. Therefore, self-limiting cases would been underrepresented, a significant omission for a classification system that valued prognosis. One of the greatest challenges in the conceptualization of a psychiatric presentation is to determine what constitutes the primary disturbance and what features are secondary or reactive. Over time, catatonia has confronted this chickenor-egg problem. Kahlbaum saw it as the primary disease, sharing symptoms of dementia praecox/schizophrenia, such as flat affect, delusions, and hallucinations, linked by the unusual motor signs (Lohr and Wisniewski 1987); for him, affective symptoms in catatonia were secondary (Pfuhlmann and Stober 2001). His cases thus would meet DSM IV criteria for bipolar disorder, schizophrenia, major depressive disorder, or delirium (Fink and Taylor 2006); however, controversy over what was “primary” in catatonia arose with reports of catatonic symptoms emerging in patients with manic-depression (bipolar disorder), epilepsy, metabolic disturbances, autism, and other conditions (Fink, Shorter, and Taylor 2010). In contrast to Kahlbaum, Kraepelin and others saw catatonia as a manifestation of a primary dementia praecox/ schizophrenia illness. Some contended that the disorder most commonly associated with catatonia was manic-depressive illness (Kirby 1913). Epidemiological studies have shown that it occurs frequently in affective disorders (Abrams and Taylor 1976). The DSM Era: 1952 to the Present

Kraepelin’s situating catatonia within schizophrenia was adopted into the first edition of the DSM, published in 1952, and it remained unchanged through the 4th edition (DSM-IV) in 1994 to the text revision (DSM-IV-TR) in 2000 (Healy 2004). Despite the longstanding adherence of the DSM to this concept of catatonia, many dissenters have argued against this primary association between catatonia and schizophrenia (Abrams and Taylor 1976; Fink and Taylor 2006; Fink, Shorter, and Taylor 2010; Kirby 1913). While the first two editions of DSM were not widely adopted by practitioners, the third edition (1980) pushed the DSM to the forefront of psychiatric diagnosis, promoting Kraepelin’s nosology as a way of thinking (Feighner et al. 1972). Kraepelin’s conceptualization of catatonia as a subtype under the umbrella of dementia praecox was a school of thought some consider far simpler than others being described at the time (Healy 2004). The nosological system that Kraepelin’s eventually eclipsed was the WernickeKleist-Leonard (WKL) school of psychiatry (Ungvari 1993). Karl Leonhard (1904– 1988), along with Carl Wernicke (1848–1905) and Karl Kleist (1879–1960), wrote extensively on the varied presentations of catatonia. Wernicke delineated several subtypes of catatonia—hyperkinetic, hypokinetic, akinetic, cyclic, complete, and compound (Braunig and Kruger 2004)—and he associated some with mania or melancholia. Later, Kleist distinguished chronic schizophrenic catatonia from what he called “cycloid motility psychoses,” characterized by a mix of affective bipolarity and psychosis. Leonhard (1957) joined Kleist to describe opposite-pair subtypes in chronic schizophrenic catatonia: parakinetic or manneristic catatonia, speech-


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prompt or speech-retarded catatonia, proskinetic or negativistic catatonia. Together, Wernicke, Kleist, and Leonhard were first to describe a pathophysiological concept of catatonia. For example, Kleist elaborated a hypothesis about how the speechprompt subtype came from frontal lobe malfunction in dampening brainstem activity, resulting in symptoms such as impoverished thought and echo responses (Ungvari and Rankin 1990). This highly differentiated, WKL nosological system contrasted with Kraepelin’s much simpler form, which, many argue, failed to provide homogenous disease groups required for fruitful investigation into genetics, biology, or pathology (Beckmann 1995; Ungvari 1993). Why did the Kraepelinian perspective prevail? Some suggest it was because of Wernicke’s early accidental death (Heckers 2011). Another important factor was that the DSM-III, while based on Kraepelin’s ideas, formed what became known as the “Neo-Kraepelinian” movement: operationally defined criteria would designate disease entities and the origins would eventually be uncovered through neurobiological research (Mayes and Horwitz 2005). Research based on a consistent and reliable classification of mental illness was now envisioned; it would correct previous inconsistencies in diagnostic practices (Feighner et al. 1972; Pope and Lipinski 1978). DSM-III catered to this previously unmet need, and it soon became widely adopted. As American psychiatrist Gerald Klerman (1987) wrote, the “DSM-III is an advancement towards the fulfillment of the scientific aspirations of the profession” (3). And Paul Mullen (2007) has described how the DSM came to dictate all dialogue and discovery in psychiatry: “To even contribute to the professional debates on nosology you are constrained within the premises which sustain the manuals. To be a researcher or even a mainstream clinician plunges you into the very core of the self-justifying and self-sustaining hermeneutic world of today’s manuals of mental disorders” (114). As a result of the DSM’s increasing hegemony, earlier theories of psychiatric disorders, including catatonia, were overlooked, and thus catatonia as a subtype of schizophrenia was reinforced as the undisputed starting point for practice and research. Although the terminology is not commonly used now, pathophysiological research can be undertaken through either the “contrast” or “kinetic” method (Stokes 1939). The contrast method compares data taken from groups of patients and healthy controls, seeking significant differences, and it is easily amenable to the DSM-III classification system and to the bulk of the scientific literature from the past 30 years. The kinetic method, on the other hand, is longitudinal, involving comprehensive study of selected cases (Crammer 1976). In the mid-20th century, the kinetic method was applied to catatonia by German psychiatrist Rolv Gjessing (1976), who published exhaustive reports on roughly 40 patients, with meticulous measures, such as basal metabolic rate, autonomic function, nitrogen excretion, and temperature. For each individual, he devised individualized treatment based on the physiological abnormality found. For example, nitrogen retention during catatonic episodes was effectively treated with thyroxine or thyrotrophic hormone,

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which promote nitrogen excretion in the urine. Using this kinetic method, others proposed similar treatments based on individual abnormalities (Gornall et al. 1953). This intellectual approach and research method seems to have been lost, a method that John Crammer (1976) described as the following: “Don’t study large numbers of patients or worry about conventional diagnoses… but know one or two patients really well over many years… Pay attention to a wide variety of bodily processes, watch their fluctuations with time, try to understand how they interact physiologically and psychologically” (761–62). The findings of Gjessing and others would be difficult to replicate in the contrast method, since individual differences are less likely to be detected or recognized (Gornall et al. 1953). But “contrast-type” research is now favored, not only because of the DSM or industrial influence, but also because of reverence for the controlled clinical trial, the currency of the evidence-based medicine. Controlled clinical trials are “contrast” style, comparing groups given either treatment or placebo, on quantifiable outcome scores. This type of evidence is valued over all other forms of study, and clinical training in psychiatry is now defined by it: for example, guidelines rank treatments supported by randomized controlled clinical trials as level 1, and anecdotal reports or expert opinion as level 4 (Yatham et al. 2013). While this state of affairs does not speak to the conceptualization of a single diagnosis per se, it shows an emphasis on discrete disease categories and a theoretical shift away from the individualized approach pioneered by those using the “kinetic” method and “the notion that clinical trials provide a higher form of knowledge than knowledge born in a clinical encounter—the realm of the experiential and the singular” (Healy, Mangin, and Applbaum 2014, 520–21). Furthermore, the tradition of descriptive psychopathology and phenomenology is disappearing from approaches to disease conceptualization (Andreasen 2007; Mullen 2007). In 1994, the DSM-IV created a category of “catatonia secondary to a medical disorder” and a “catatonia specifier” embedded in mood disorder (Fink 2013). DSM specifiers indicate features that can present within a diagnosis but are not diagnostic categories themselves. As a specifier and without a unique coding number to incentivize use in diagnosis or research, catatonia within mood disorders enjoyed no increase in attention, demonstrating this rigidity of thinking with DSM categories. Catatonia remained a subtype of schizophrenia in DSM-IV, and arguments for dissociation continued (Fink, Shorter, and Taylor 2010). Less concerned with etiology, these critics argued that clinicians’ indoctrination of “catatonia = schizophrenia” harms patients through under-recognition and under-treatment. The classification also favors antipsychotic medications that are less effective and possibly damaging, compared to electroconvulsive therapy (ECT) and benzodiazepines, neither of which are indicated in schizophrenia (Taylor and Fink 2003). Finally, changes appeared with the DSM-5 (APA 2013). While some had hoped that catatonia would have its own category, the DSM-5 authors adopted a more cumbersome, diffuse approach: catatonia was now a “specifier” for 10 different


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psychiatric diagnoses (including schizophrenia); “catatonia secondary to medical disorder” remained; and the new diagnosis “catatonia not elsewhere classified” was created. Importantly, catatonia as a subtype of schizophrenia was deleted. These changes accommodated the intended practical implications on treatment, but catatonia was still secondary, not primary as Kahlbaum had envisaged.

Influence of Treatment and Research on Categorization Psychiatry has always looked to effective treatments to inform its understanding of etiology. When Kahlbaum and Kraepelin wrote of catatonia, there were no antipsychotics, but the recent psychopharmacological revolution has impacted the conceptualization not just of catatonia, but of all psychiatric disease. Early biologic treatments for catatonia included convulsive therapy with chemicals or electricity and psychosurgery, both of which were more invasive and controversial than psychotherapy. But treatment strategies were redirected in 1953, with the introduction of chlorpromazine. Simple and effective, the drug changed the outlook for intractable psychoses. Finally, treatment could address the debilitating symptoms of delusions, hallucinations, and mental disorganization that had previously necessitated chronic hospitalization. Biochemical and clinical research proliferated in following years, resulting in the discovery of the putative, therapeutic mechanism: antagonism of dopamine transmission. The availability of antipsychotics soon contributed to the large-scale deinstitutionalization movement (Meyer and Simpson 1997). Whereas in 1955, 559,000 individuals lived in American state-run mental institutions; in 1965, this number had declined by 15% to 475,000; and 1980 saw a 60% decrease to 138,000 (Mayes and Horwitz 2005). Moreover, the duration of stay fell from years to just days or short weeks. Deinstitutionalization affected the conceptualization of catatonia in two ways. First, it was less frequently seen, dampening interest, debate, and inquiry. Catatonia has always been identified by physical examination, which was much more common in a hospital than in an outpatient setting (Gelenberg 1976; Patterson 1978). Inpatient settings also provided opportunities for observing patients over time for mannerisms, stereotypy, or odd sounds, as well as for even more obvious, classic catatonic signs, such as stupor, mutism, or excitement, which last for only short periods and which might not be reported by patients. The second effect of deinstitutionalization was the assumption that catatonia was no longer developing, because the new antipsychotics were treating schizophrenia well. Catatonia became a historical artefact of the days of intractable schizophrenia. If clinicians do not expect to find something, they will not look for it; consequently, that thing is much less likely to be recognized even when it is present. Pharmacotherapy further entrenched the idea of catatonia as schizophrenia. In the late 20th century, practice ignored the unsettled controversies surrounding

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etiology and classification and instead focused on diagnosis in order to select the indicated drug. As Fink and Taylor (2006) explain: “clinical interest shifted from the detailed descriptions of behaviour that had been the staple of psychiatric practice to the goal of labelling the most prominent signs in order to select a medicine for its relief. Illnesses were described as depression or psychosis, and the treatments labelled antidepressant or antipsychotic” (10). Antipsychotics were the treatment for schizophrenia and all it encompassed. With a few broad strokes, the complexities of enigmatic diseases were simplified into monolithic targets for their respective drugs. Driving this movement, pharmaceutical companies quickly realized that in order to sell drugs, they first had to sell disease concepts. DSM-III did not include treatment guidelines, but the new categories of specific, symptom-based diseases provided a framework for industry to direct drug development and promotion. Marketing campaigns educated physicians to recognize conditions as singular entities resistant to deconstruction (Healy 2004). Since catatonia was embedded within schizophrenia, it was out of sight: with no specific drug for catatonia, the pharmaceutical industry had no incentive for education about it, and psychiatrists came to adopt a limited concept of it. At the same time, however, the prevalence of antipsychotic medications introduced an array of new symptoms from side effects. Some of these revolve around the extrapyramidal system of the brain, involved in the regulation, planning, and coordination of movements; its disruption provokes reactions such as akathisia (inner restlessness), tremor, rigidity, and bradykinesia (slowed movements) (Meyer and Simpson 1997). Since these symptoms overlap with catatonia, motor disorders in medicated patients were seen as side effects, not disease (Rogers 1992). And in an ironic twist, antipsychotics, the very drugs intended to treat schizophrenia, were found to provoke catatonic reactions, such as the sometimes fatal neuroleptic malignant syndrome (NMS) (Fink 2013). From as early as the 1960s, the influential marketing campaigns had spoken louder than the sporadic reports of NMS (Delay, Pichot, and Lempérière 1960). However, the coining of the term NMS in 1978 brought renewed interest in catatonia, and now literature describing catatonia must also delineate it from NMS (Caroff 1980; Fink 1996). As the side effects of psychotropic drugs are often neurological or psychological, they are confusingly intertwined with the underlying psychiatric illness. Research into antipsychotic medications has demonstrated their effects on brain structure, brain function, hormones, and metabolism (Boyda et al. 2010; Scherk and Falkai 2006). Initial neuropathology in catatonia patients came before the pharmacotherapy era; yet present-day research would be challenged to find untreated patients. Consequently, the study population now may differ neurobiologically from those studied in the past. Furthermore, some early studies of schizophrenic catatonia found changes in brain regions now known to be altered by neuroleptic drugs, such as the basal ganglia (Scherk and Falkai 2006).


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Just as a schizophrenia diagnosis led to an antipsychotic, so it followed that clinicians envisaged an underlying mechanism of abnormal dopamine neurotransmission (Fink 2013). Notwithstanding the influence of pharmaceutical marketing, this etiological explanation owed as much to modern neuroscience. Soon after chlorpromazine in 1953, the monoamine neurotransmitters—serotonin, dopamine, norepinephrine, and epinephrine—were described in the context of brain physiology (Carlsson 1959). These neurotransmitters have since become pivotal foundations to neurobiological models of psychiatric illness. Virtually all psychiatry textbooks explaining pathophysiology display a figure of a neuronal synapse—one neuron releasing of monoamine neurotransmitters to bind with a second—and explain the influence of increased or decreased neurotransmitter activity and how drugs can ameliorate the change.Yet while many psychiatric disorders fit this line of thinking, catatonia did not. Successful therapy for catatonia predated chlorpromazine and included thyroxin extracts, ECT, and barbiturates (Healy 2004). However, none fit the abnormal-neurotransmitter-level-in-synapse model, nor were they considered profitable. Consequently they received little attention. Nevertheless, these theories of the brain and psychiatric disease stimulated research, especially with new innovations in neuroimaging technology (Filler 2009). CT studies, available in the 1970s, showed diffuse cortical enlargement (Northoff et al. 1999a). Single photon emission computerized tomography (SPECT), starting from the 1980s, demonstrated lower gamma-Aminobutyric acid (GABA) binding (Northoff et al. 1999b). From the 1990s, functional magnetic resonance imaging (fMRI) revealed abnormalities in the medial orbitofrontal cortex associated with the affective symptoms of catatonia (Northoff et al. 2004).With the clues offered by the NMS-catatonia connection, dopamine abnormalities were identified. Excitement from the rise of neuroscience pushed “brain disorder” as the preferred lens through which to view most psychiatric disorders, including catatonia (Andreasen 1984). The National Institutes of Mental Health stated that psychiatric disorders are essentially disorders of brain circuits and networks, and that psychiatry should be rebranded as “clinical neuroscience”: “The recognition that mental disorders are brain disorders suggests that the psychiatrist of the future will need to be educated as brain scientists” (Insel and Quirion 2005, 2223). We now favor a more limited focus on brain-based pathophysiology, but in the past, psychiatric illnesses were often described as whole-body, multi-system disorders. Researchers would consider brain pathology as a component of psychiatric illnesses. For example, studies of autoimmune dysfunction and tissue oxygenation attempted careful correlations with brain functioning through EEG, which acknowledged the brain as the pathway for the expression of psychopathology (Bonkalo, Doust, and Stokes 1955; Heath and Krupp 1967). These conceptions proposed a cause for psychopathology that did not necessarily start or perpetuate solely within the brain. Similarly, catatonia’s pathophysiology was previously thought of more holistically. Several studies highlighted hormonal imbalance in the form of altered

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levels of androgenic-type or corticosteroid-type hormones linked to adrenal cortex pathology (Gornall et al. 1953). Catatonic psychomotor symptoms were also linked to inefficient oxygen metabolism in tissues (Bonkalo, Doust, and Stokes 1955). Additionally, catatonic and psychotic symptoms could be induced by antibodies that bind to areas of the basal forebrain, suggesting that schizophrenia could be an immune disorder (Heath and Krupp 1967). Today, a finding of autoimmune antibodies that provoke schizophrenic symptoms would not be diagnosed as schizophrenia. Indeed, a recently discovered syndrome that presents with symptoms of catatonia and psychosis is caused by an antibody against N-methyl-D-aspartic acid (NMDA) receptors in the brain has been named “anti-NMDA receptor encephalitis”; it would exclude a diagnosis of schizophrenia or catatonia (Wandinger et al. 2011). But if catatonia and psychosis presented with underlying neurotransmitter-receptor-gene polymorphisms or decreased functional connectivity in frontal-striatal circuits, it would be considered as “true” schizophrenia or catatonia because the findings fit with the present standard of psychiatric disorders being brain disorders. Thus, brain-based research has changed conceptualizations of psychiatric diagnoses: they are “true” psychiatric disorders when nothing but presumed neurobiological abnormalities underlie them. Consequently, current etiological reviews of catatonia focus primarily on neurobiology, ignoring metabolic, hormonal, or immune findings (Fink and Taylor 2006; Francis 2010). Ironically, no neurobiological biomarker exists to guide diagnosis or treatment for this or any other disease. The fact that they are sought betrays a preconviction about etiology. One reason for this situation is the possible lack of validity in the current classification scheme, which is still based on Kraepelin. As Karl Leonhard wrote in 1957: Lack of success in clinical etiological research in my opinion is the result of the fact that endogenous psychoses have been roughly divided into only two forms. In this way a majority or even a multitude of disorders have been lumped together and therefore no uniform etiology could of course be found . . . as if underlying the so colorful and even extremely different clinical pictures there was only one disease with only one uniform heredity. (1)

Opposing the Kraepelinian approach, the WKL school maintained that psychiatric dysfunction should be conceptualized as the dynamic interplay between different neural systems, rather than as discrete natural disease units having one-to-one alignment of function with morphological substrate (Ungvari 1993). Had the WKL nosological system prevailed, psychiatric research might have followed a different trajectory.


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Conclusion A disease concept evolves in many ways, although only a few are ever recognized or discussed in full. Furthermore, the recent insistence on medicine as a strict scientific and evidence-based enterprise has led to the expectation that disease concepts will progress uniformly in clarity and precision. Our examination of the history of catatonia shows that this linear evolution is decidedly not the case. Ignorance of the contexts influencing disease concepts leads us to miss the biases inherent in our clinical practice and research. Beginning with Kahlbaum, catatonia shifted as it was passed through the lenses of various ideologies. Depending on which ideology was applied, it was either a singular or a multifaceted disease, a disorder of psychosis or otherwise, and one that led to either recovery or irreversible dementia. Although the biggest change in the concept of catatonia occurred when Kraepelin subsumed it under the dementia praecox entity, two large contextual shifts perpetuated this change: the rise of psychopharmacology and of the DSM. Each concept had wide-ranging implications for classification and treatment. Ideological bias still influences our conceptualizations of psychiatric disease: a neo-Kraepelinian ideology that defines the DSM classification; neurotransmitter and pharmacology based disease models; and clinical trials research as the arbiter of truth for clinical practice. Since DSM-III, psychiatry has distanced itself from the ideological dissent that was so prominent in the past. leading to the assumption that theoretical biases and disputes no longer exist, which is of course not the case. The concept of catatonia did not follow a unitary approach.This examination of the major influences and trends throughout its evolution not only gives us a deeper understanding of this particular disease’s history, but it also invites us to consider the conceptualization and classification of any disease, a process that ultimately dictates diagnosis, research, and the way patients are treated within the health-care system.

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The concept of disease and its implications for psychiatry.

Organic chemistry. Construction and deconstruction of aldehydes by transfer hydroformylation.

Phenomenology and the history of psychiatry.

Stability in intensive psychiatry: a concept analysis.

Psychiatry and natural history.

Liaison psychiatry: a brief history.

The construction of anosognosia: history and implications.

Psychiatry and religion: A variable history.

History of the Concept of Addiction.

Recurrent Catatonia in Parkinson Disease.

[Anti-NMDA encephalitis in psychiatry; malignant catatonia, atypical psychosis and ECT].

Post-traumatic stress disorder: the history of a recent concept.

Catatonia: an unusual manifestation of Wilson's disease.

Further comment on the history of general hospital psychiatry.

[The concept of racial democracy in Brazilian intellectual history].

The concept of disease.

The concept of disease.

The concept of disease.

The concept of disease.

Research on the history of psychiatry * : Dissertation Abstracts, 2011 (continued).

[Reimbursement in psychiatry and psychosomatics: proof of concept for a system based on daily costs].

Catatonia in the ICU.

Reviving a ghost in the history of technology: the social construction of the recumbent bicycle.

Andre G. Ombredane and the psychiatry of multiple sclerosis: a conceptual and statistical history.