In developing his mature concept of hebephrenic dementia praecox (DP) in his 4th (1893) through 6th textbook editions (1899), Kraepelin worked from the hebephrenic syndrome first described by Hecker ...(1871) and then carefully studied by his student Daraszkiewicz (1892). Working under Kraepelin's supervision, Daraszkiewicz followed Hecker in emphasizing several key features of hebephrenia (distinctive deteriorative course, importance of silliness and minimal positive psychotic symptoms) but expanded the syndrome to include cases developing severe dementia, rejected the link to prodromal depressive and manic phases, and reduced the emphasis on thought disorder. Daraszkiewicz proposed a soft subtyping of hebephrenia based on level of deterioration, which Kraepelin adopted in his 4th edition with an additional emphasis on severe positive psychotic symptoms. In his 5th edition, Kraepelin created a third subform with even more pronounced and bizarre delusions and hallucinations. In his 6th edition, which contained his first articulation of DP, Kraepelin eliminated his hebephrenia subforms presenting a single syndrome, which, compared to Hecker, included more emphasis on positive psychotic and catatonic symptoms and severe dementia. Kraepelin's paths to hebephrenic and paranoid DP differed in important ways. Paranoid DP was a de novo syndrome created by differentiation from paranoia. Hebephrenia, by contrast, evolved from a disorder created in the Kahlbaum/Hecker paradigm of the iterative study of clinical features, course and outcome. Kraepelin further implemented this approach in substantially reworking, over several drafts, the hebephrenic syndrome to fit into his emerging construct of dementia praecox.
For over a century, psychiatric disorders have been defined by expert opinion and clinical observation. The modern DSM has relied on a consensus of experts to define categorical syndromes based on ...clusters of symptoms and signs, and, to some extent, external validators, such as longitudinal course and response to treatment. In the absence of an established etiology, psychiatry has struggled to validate these descriptive syndromes, and to define the boundaries between disorders and between normal and pathologic variation. Recent advances in genomic research, coupled with large-scale collaborative efforts like the Psychiatric Genomics Consortium, have identified hundreds of common and rare genetic variations that contribute to a range of neuropsychiatric disorders. At the same time, they have begun to address deeper questions about the structure and classification of mental disorders: To what extent do genetic findings support or challenge our clinical nosology? Are there genetic boundaries between psychiatric and neurologic illness? Do the data support a boundary between disorder and normal variation? Is it possible to envision a nosology based on genetically informed disease mechanisms? This review provides an overview of conceptual issues and genetic findings that bear on the relationships among and boundaries between psychiatric disorders and other conditions. We highlight implications for the evolving classification of psychopathology and the challenges for clinical translation.
Edward Spitzka, a prominent New York-based alienist, who spent 3 years in Germany studying psychiatry, published a textbook in 1883-the same year as the first edition of Kraepelin's textbook-that ...contained detailed descriptions of all the seven psychiatric syndromes that formed the basis of Kraepelin's nosologic synthesis: mania, melancholia, katatonia, secondary deteriorations, hebephrenia, circular insanity, and monomania. A study of this text provides us with a "before" picture-a view of the canvas of psychiatric diagnostic categories-from which Kraepelin worked. Studying what Spitzka's diagnostic categories contain and what they are missing highlights the key steps Kraepelin took in the development of his nosologic synthesis. For example, Spitzka does not describe a commonality in symptoms or outcome in katatonia, hebephrenia, and the move severely ill delusional monomaniacs, nor did he link together mania, melancholia, and circular insanity, but instead comments on wide differences in outcome among these three syndromes.
The overall aim of this study is to present descriptive data regarding the treated prevalence of nine common psychiatric and substance use disorders in the first Primary Care Registry (PCR) in ...Sweden: Major Depression (MD), Anxiety Disorders (AD), Obsessive-Compulsive Disorder (OCD), Adjustment Disorder (AdjD), Eating Disorders (ED), Personality Disorder (PD), Attention Deficit Hyperactivity Disorder (ADHD), Alcohol Use Disorder (AUD) and Drug Abuse (DA).
We selected 5,397,675 individuals aged ≥18. We examined patterns of comorbidity among these disorders and explored the association between diagnoses in the PCR and diagnoses obtained from Hospital and Specialist care. We explored the proportion of patients with these nine disorders that are only treated in primary health care.
For four of our disorders, 80% or more of the cases were present only in the PCR: AdjD, DA, AD and MD. For two disorders (OCD and ED), 65-70% of cases were only found in the PCR. For three disorders (PD, AUD, and ADHD), 45-55% of the patients were only present in the PCR.
The PCR will, in the future, likely prove to be an important tool for studies in psychiatric epidemiology.
Although the rise of operationalized diagnostic criteria and the creation of DSM-III were influenced in the USA by a neo-Kraepelinian 'revival' of interest in psychiatric nosology, Kraepelin was only ...a distal influence on the specific diagnostic criteria proposed. The historical origins of the DSM-III criteria for mania and major depression (MD) are traceable back to the 1950s and contain no direct link to Kraepelin's writings. George Dreyfus, a student and assistant to Kraepelin, authored in 1907 a monograph on Involutional Melancholia which reviewed cases seen by Kraepelin in Heidelberg. In this monograph, Dreyfus presents the 'characteristic' symptoms for mania and depression 'as described by Kraepelin.' This historical finding provides the unprecedented opportunity to examine the resemblance between the criteria proposed for mania and depression in DSM-III, inspired by Kraepelin's nosologic vision, and those specifically suggested by Kraepelin 73 years earlier. Kraepelin's symptoms and signs for mania paralleled seven of the eight DSM-III criteria (except the decreased need for sleep), with two not included in DSM-III (increased mental activity and short bursts of sadness). Kraepelin's signs and symptoms paralleled six of the nine DSM-III criteria for MD, lacking suicidal ideation and changes in appetite/weight and sleep but including obsessions, reduced expressive movements, and decreased mood responsiveness. Although Kraepelin's overall approach to mania and depression emphasized their close inter-relationship in the cyclic course of manic-depressive illness, it is noteworthy Kraepelin's 'characteristic' symptoms for mania and depression as described by Dreyfus, bear substantial but incomplete resemblance to the criteria proposed in DSM-III.
The development of the modern concept of mania is explored by a review and analysis of 28 psychiatric texts in English, French, and German published in Western Europe and North America from 1780 to ...1900. From 1780 until the 1820s, mania was consistently viewed as a disorder of reasoning/judgment manifest by total insanity and/or the state of undifferentiated fury. For the next 30 years, the consensus shifted, and mania was understood to be largely a disorder of elevated mood. This concurrence of opinion broke down around 1860. For the remaining years of the 19th century, the mood-based model of mania competed for dominance with the view that mania arose primarily from accelerated mental processes and to a lesser degree that mania resulted from psychomotor excitation. While most authors advocated for one of these three positions, a number suggested that two or all three of these processes were central to the etiology of mania. Faculty psychology played an important role in these discussions, providing a framework within which to place the mental disturbance considered foundational to the manic syndrome. When the viewpoints shifted away from mania as a primary disorder of judgment, new approaches were needed to understand the emergence of grandiose delusions. Utilizing the concept of understandability, a number of authors suggested that manic delusions could arise directly from a euphoric mood. The history of mania shares some important similarities and differences with the history of melancholia during this same period. Both histories suggest that our major psychiatric categories evolved through a complex process involving both observations of symptoms, signs and course, and conceptual developments and a priori theories.
While working under Kraepelin in Munich, Ernst Rüdin, a Swiss‐born Psychiatrist, at the age of 26, outlined in a 1911 98‐page article, a detailed plan for a future Mendelian‐informed family research ...program for psychiatry. Rüdin would go on to head the Department of Genealogical and Demographic Studies at Kraepelin's Research Institute which became one of the world's leading programs in psychiatric genetics. I here summarize this article, providing a complete translation online. Rüdin's review outlined a paradigm shift in psychiatric genetics research moving from calculations of aggregate hereditary burden, as they applied to the proband, to examining patterns of transmission within family pedigrees which involved careful individual assessments of relatives. He references widely clinical and statistical genetic studies, many focusing on the newly discovered Mendelian laws. However, Rüdin was no genetic reductionist but recognized the contribution of environmental risk factors to psychiatric illness arguing that they should be studied as part of a comprehensive research program. As a committed eugenicist, Rüdin also explored the implications of such a program for “racial hygiene.” Rüdin's contributions should be viewed in the context of his extensive collaboration from 1933 to 1945 with the National Socialists and his support for their eugenics program, including involuntary sterilizations.
Abstract
In 1917, Eugen Bleuler published an article (Mendelismus bei Psychosen, speziell bei der Schizophrenie Mendelism in the Psychoses, especially Schizophrenia) in response to the recently ...published first systematic family study of dementia praecox (DP) by Ernst Rüdin, then working under Kraepelin in Munich. Although briefly commented upon by David Rosenthal in 1978, this article has never been thoroughly reviewed or translated. Of the many themes addressed, four are especially noteworthy. First, Bleuler argues that understanding the transmission patterns of schizophrenia in families requires definitive knowledge about the boundaries of the phenotype which he argues are unknown. Rüdin’s choice—Kraepelin’s concept of DP—is, he asserts, too narrow. Clarifying the genetics of schizophrenia is inextricably bound up with the problem of defining the phenotype. Second, Bleuler argues for the importance of “erbschizose” (literally “inherited schizoidia”) wondering whether his “4 As” or other “brain-anatomical, chemical, or neurological characteristics” might underlie the genetic transmission of schizophrenia. Third, Bleuler was deeply interested in the nature of the onset of schizophrenia, suggesting that environmental adversity could provoke “latent illness to become manifest.” It was important, he argued, to identify such risk factors and incorporate them into genetic models. Fourth, although not optimistic that current knowledge would permit a resolution of the transmission model for schizophrenia, he finds single-locus models implausible and at several points wonders whether polygenic models might better apply. A complete translation of the article is provided.
The world learned of the heated dispute about the methodology of the early works by Davenport and Rosanoff claiming Mendelian transmission patterns for mental handicap and psychiatric illness in a ...bold headline in the New York Times on Sunday, November 9, 1913: ENGLISH EXPERT ATTACKS AMERICAN EUGENIC WORK. I here focus on the debate surrounding Rosanoff's 1911 study where he presented evidence that the neuropathic constitution, including, among its manifestations, dementia praecox, and manic‐depressive illness, was an autosomal recessive trait. The “English expert,” David Heron, a student of Pearson's, launched the debate in his 1913 paper which argued that Rosanoff's field work methods were biased, his clinical assessments sloppy, his phenotype far too broad, and his statistical approach flawed. Both Davenport, Rosanoff's mentor, and Rosanoff vigorously defended their methods. Behind this sometimes personal debate was the long simmering controversy about the relative validity of Biometrical genetic (represented by Heron and Pearson) and Mendelian genetic (represented by Rosanoff and Davenport) models for genetic transmission in plants, animals and, especially, humans. A review suggests that most of Heron's criticisms were valid. This episode presages later controversies within psychiatric genetics, for example between twin and linkage researchers in the 1980s and 1990s.
In 1911, Aaron Rosanoff published among the first pedigree studies of psychiatric illness, and the first ever in the United States, claiming that the neuropathic constitution was transmitted in as a ...Mendelian recessive disorder. In 1917, Abraham Myerson harshly critiqued that study, focusing on the very wide phenotypic definition of neuropathic constitution. Here, I describe Rosanoff and Myerson's backgrounds, the details of Rosanoff's study, and Myerson's critique and put this controversy in the context of the history of psychiatric genetics, emphasizing four themes: a) the close interrelationship between psychiatric diagnosis and models of genetic transmission, b) the strong attraction of Mendelian models to psychiatric geneticists after their 1900 rediscovery, c) the controversy about whether familial transmission of psychiatric illness is largely homogeneous or heterogeneous, and d) the methods taken by researchers to the problems of psychiatric genetics that typically emerged as part of their broader approach to the nature of psychiatric illness.
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