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Richard Noll - One of the best experts on this subject based on the ideXlab platform.

  • Dementia Praecox, 1886: a new turning point?
    History of Psychiatry, 2012
    Co-Authors: Richard Noll
    Abstract:

    Historians of medicine delight in reconstructing the life course – one might say career – of disease concepts. ‘Biographies of disease’ now appear as formal serial offerings by publishers (see, for example, Healy, 2008), granting them a celebrity status equal to that of famous physicians. To borrow the language of historical sociologist Andrew Abbott (2001: 247–9) regarding the study of individual lives, disease histories are framed by ‘trajectories’ (or ‘master narratives’) and ‘turning points’. Trajectories are the ‘smooth befores and afters ... linked by a relatively abrupt “turning point”’(Abbott, 2001: 247). Trajectories are ‘stable regimes’ characterized by their inertial, historicist, causally comprehensible nature. Turning points bracket these deceptively smooth episodes, for they are critical moments when there is a change of trajectory, and they can only be recognized in hindsight. They are ‘causally incomprehensible’ – hence our fascination with them. The life course of an individual – or a disease concept – is the story of a series of chaotic turning points bracketing stable episodes (trajectories). For historians who follow the ‘“who said it first” creed’ (Berrios, Luque and Villagran, 2003: 128), issues of priority are therefore of paramount importance: collapsing a formerly identified turning point into an expanded trajectory, now bounded by a new focal turning point, might, just might, change the way in which we view the entire life course of a disease concept. Or, as is more often the case, not. Heinrich Schule (1840–1916) of the Illenau asylum in Baden, Germany, may now be regarded as the first alienist to use the Latin term Dementia Praecox. He did so in 1886 in the third edition of his textbook, Klinische Psychiatrie: specielle Pathologie und Therapie der Geisteskrankheiten (Schule, 1886: 14, 250, 451–2, 477). His use of this term to describe a psychotic disorder predates its use by the Prague psychiatrist Arnold Pick (1851–1924) in 1891, and by Emil Kraepelin (1856–1926) in Heidelberg in 1893 (see: Pick, 1891; Kraepelin, 1893). Whether Schule was directly influenced by the French alienist Benedict-Augustin Morel (1809–73), who used the term demence precoce in 1852 and 1860 (see: Berrios, Luque and Villagran, 2003: 117–18; Dowbiggin, 1996: 388), now becomes the new problem for historians eager to plum the significance of a potential new turning point in the history of psychiatry.

  • classic text no 72 non Dementia non Praecox note on the advantages to mental hygiene of extirpating a term
    History of Psychiatry, 2007
    Co-Authors: E E Southard, Richard Noll
    Abstract:

    In February 1919 the Harvard neuropathologist Elmer Ernst Southard (1876—1920) presented a paper in which he outlined his reasons for dropping the term `Dementia Praecox' in favour of a competing diagnostic concept and term, `schizophrenia'. Southard's criticisms reflected the opinion of many US psychiatrists at that time, leading to the replacement of Emil Kraepelin's Dementia Praecox by Eugen Bleuler's schizophrenia in US psychiatry by the mid-1920s. The text of Southard's lecture is published here for the first time. Also included are excerpts from letters from US psychiatrists George H. Kirby, Albert M. Barrett, Adolf Meyer and August Hoch to Southard in response to his query as to whether Dementia Praecox or schizophrenia should be adopted in US psychiatric nomenclature.

  • kraepelin s lost biological psychiatry autointoxication organotherapy and surgery for Dementia Praecox
    History of Psychiatry, 2007
    Co-Authors: Richard Noll
    Abstract:

    Kraepelin believed that a chronic metabolic autointoxication, perhaps arising from the sex glands, eventually caused chemical damage to the brain and led to the symptoms of Dementia Praecox. The evolution of Kraepelin's autointoxication theory of Dementia Praecox is traced through the 5th to 8th (1895 to 1913) editions of his textbook, Psychiatrie. The historical context of autointoxication theory in medicine is explored in depth to enable the understanding of Kraepelin's aetiological assumption and his application of a rational treatment based on it — organotherapy. A brief account of the North American reception of Kraepelin's concept of Dementia Praecox, its autotoxic basis, and the preferred American style of rational treatment — surgery — concludes the discussion.

  • Kraepelin's 'lost biological psychiatry'? Autointoxication, organotherapy and surgery for Dementia Praecox.
    History of Psychiatry, 2007
    Co-Authors: Richard Noll
    Abstract:

    Kraepelin believed that a chronic metabolic autointoxication, perhaps arising from the sex glands, eventually caused chemical damage to the brain and led to the symptoms of Dementia Praecox. The evolution of Kraepelin's autointoxication theory of Dementia Praecox is traced through the 5th to 8th (1895 to 1913) editions of his textbook, Psychiatrie. The historical context of autointoxication theory in medicine is explored in depth to enable the understanding of Kraepelin's aetiological assumption and his application of a rational treatment based on it — organotherapy. A brief account of the North American reception of Kraepelin's concept of Dementia Praecox, its autotoxic basis, and the preferred American style of rational treatment — surgery — concludes the discussion.

  • Infectious insanities, surgical solutions: Bayard Taylor Holmes, Dementia Praecox and laboratory science in early 20th-century America. Part 2:
    History of Psychiatry, 2006
    Co-Authors: Richard Noll
    Abstract:

    Part I of this article on Bayard Taylor Holmes (1852–1924), a Chicago physician and surgeon, detailed his laboratory research on Dementia Praecox and his presumed discovery in 1915 of evidence in support of a focal infection theory of its aetiology. In May 1916 he began to experiment with a rational therapy based on this theory: abdominal surgery and daily irrigations of the colon. He operated first on his own son, who had been afflicted with Dementia Praecox since 1905, but he died four days later. Part II deals with Holmes' continued surgical treatment of Dementia Praecox patients and the outcomes of the operations. It also describes how Holmes set up the short-lived Psychiatric Research Laboratory of the Psychopathic Hospital at Cook County Hospital in 1917, and discusses the dismissal of a key research colleague, H. M. Jones, whose experimental results directly contradicted those of Holmes.

Kenneth S Kendler - One of the best experts on this subject based on the ideXlab platform.

  • philipp jolly and his 1913 the heredity of psychosis homogeneity versus heterogeneity of familial transmission and an early look at mendelian models for manic depressive illness and Dementia Praecox
    American Journal of Medical Genetics, 2021
    Co-Authors: Kenneth S Kendler, Astrid Klee
    Abstract:

    Philipp Jolly's 1913 extensive monograph "The Heredity of Psychoses" provides, in both his detailed literature review and new pedigree study, an extensive assessment of a key issue in the psychiatric genetics of his day: the degree to which the familial transmission of psychiatric disorders was specific (or homogeneous) versus nonspecific (or heterogeneous). Contrary to a number of earlier observations, Jolly concludes that heterogeneous transmission is rare. Multiple psychiatric disorders can occur in one family because members of a family may have elevated predispositions to more than one disorder rather than one predisposition which increases risk for a wide range of conditions. A notable exception to this, he notes, is within manic-depressive illness (MDI), where different forms of illness run together within families. Jolly is also among the earliest investigators to evaluate simple Mendelian models for MDI and Dementia Praecox (DP). While his methods were primitive and contained only "eye-ball" examinations rather than statistical modeling, Jolly demonstrated considerable conceptual sophistication in the early application of such models. He concludes that DP is likely a recessive disorder. MDI, he states, is either a recessive condition or demonstrates "gender-based dominant heredity" where heterozygote females are affected, and heterozygote males are not.

  • Kraepelin's Final Views on Dementia Praecox.
    Schizophrenia bulletin, 2020
    Co-Authors: Kenneth S Kendler
    Abstract:

    In 1921, at the age of 65, 6 years after completing the final edition of his textbook, 22 years after first proposing the concept of Dementia Praecox (DP), and 1 year before retiring from clinical work, Emil Kraepelin completed the last edition of his "Introduction to Clinical Psychiatry," which contained a mini-textbook for students, 10 pages of which were devoted to DP. This work also included a series of new detailed case histories, 3 of which examined DP. This neglected text represents a distillation of what Kraepelin judged, near the end of his long career, to be the essential features of DP. The relevant text and case histories are translated into English for the first time. Kraepelin did not define DP solely by its chronic course and poor prognosis, acknowledging that remissions and even full recovery might be possible. His clinical description emphasized the frequency of bizarre delusions and passivity symptoms. He recognized the heterogeneity of the clinical presentations, outlining 6 subtypes of DP, including Dementia simplex, depressive and stuporous Dementia, and an agitated and circular DP. Kraepelin's original concept of DP was not impervious to change and expanded somewhat, especially with the inclusion of Diem's concept of simple DP. He also reviews several contributions of Bleuler, including his concept "latent schizophrenia." He writes poignantly of the psychological consequences of DP. His 3 DP cases, for advanced students, included simple DP, "periodic catatonic," and "speech confusion."

  • The Development of Kraepelin's Concept of Dementia Praecox: A Close Reading of Relevant Texts.
    JAMA psychiatry, 2020
    Co-Authors: Kenneth S Kendler
    Abstract:

    In 1893 and 1896, in his fourth and fifth textbook editions, Emil Kraepelin brought together 3 syndromes to form the first and second of his 2 prequels to Dementia Praecox (DP), a definitive version of which he would propose in his 1899 sixth textbook edition. These syndromes, which would become hebephrenic DP, catatonic DP, and paranoid DP, each had distinct histories. Hebephrenic DP was derived from syndromes first proposed by Hecker, and catatonic DP was derived from syndromes first proposed by Kahlbaum, and then both were substantially revised. Kraepelin created paranoid DP de novo from a division of his early broad delusional syndrome Verrucktheit, distinguishing it from paranoia. Two of these syndromes (catatonic DP and paranoid DP) were present in different forms in his earlier textbook editions, and 1 syndrome (hebephrenic DP) was not. In his 2 prequels, the 3 syndromes were listed together with a brief preface. In the sixth textbook edition, they became “clinical forms” of DP with a lengthy integrative introduction. Much more than in his prequels, in his sixth edition, Kraepelin stitched these 3 syndromes together, emphasizing their shared signs, symptoms, and course. Hebephrenia was the core of Kraepelin’s DP concept, while the paranoid subtype fitted least comfortably within his framework. His termDementiawas meant in a broad sense consistent with both short-term and rare long-term recoveries. Kraepelin was a pragmatist, not a purist, in his nosologic work and focused both on clinical features and course and outcome. He experimented with various nosologic categories, willing to revise earlier formulations in the light of new data. He was more tentative about his conclusions than many who followed him.

  • Tracing the Roots of Dementia Praecox: The Emergence of Verrücktheit as a Primary Delusional-Hallucinatory Psychosis in German Psychiatry From 1860 to 1880.
    Schizophrenia bulletin, 2020
    Co-Authors: Kenneth S Kendler
    Abstract:

    While the roots of mania and melancholia can be traced to the 18th century and earlier, we have no such long historical narrative for Dementia Praecox (DP). I, here, provide part of that history, beginning with Kraepelin's chapter on Verrucktheit for his 1883 first edition textbook, which, over the ensuing 5 editions, evolved into Kraepelin's mature concepts of paranoia and paranoid DP. That chapter had 5 references published from 1865 to 1879 when delusional-hallucinatory syndromes in Germany were largely understood as secondary syndromes arising from prior episodes of melancholia and mania in the course of a unitary psychosis. Each paper challenged that view supporting a primary Verrucktheit as a disorder that should exist alongside mania and melancholia. The later authors utilized faculty psychology, noting that primary Verrucktheit resulted from a fundamental disorder of thought or cognition. In particular, they argued that, while delusions in mania and melancholia were secondary, arising from primary mood changes, in Verrucktheit, delusions were primary with observed changes in mood resulting from, and not causing, the delusions. In addition to faculty psychology, these nosologic changes were based on the common-sense concept of understandability that permitted clinicians to distinguish individuals in which delusions emerged from mood changes and mood changes from delusions. The rise of primary Verrucktheit in German psychiatry in the 1860-1870s created a nosologic space for primary psychotic illness. From 1883 to 1899, Kraepelin moved into this space filling it with his mature diagnoses of paranoia and paranoid DP, our modern-day paranoid schizophrenia.

  • the development of kraepelin s mature diagnostic concept of catatonic Dementia Praecox a close reading of relevant texts
    Schizophrenia Bulletin, 2020
    Co-Authors: Kenneth S Kendler
    Abstract:

    Through a close reading of texts, this essay traces the development of catatonia from its origination in Kahlbaum's 1874 monograph to Kraepelin's catatonic subtype of his new category of Dementia Praecox (DP) in 1899. In addition to Kraepelin's second to sixth textbook editions, I examine the six articles referenced by Kraepelin: Kahlbaum 1874, Brosius 1877, Neisser 1887, Behr 1891, Schule 1897, and Aschaffenburg 1897 (Behr and Aschaffenburg worked under Kraepelin). While Brosius and Neisser confirmed Kahlbaum's descriptions, Behr, Schule, and Aschaffenburg concluded that his catatonic syndrome was nonspecific and only more narrowly defined forms, especially those with deteriorating course, might be diagnostically valid. Catatonia is first described by Kraepelin as a subform of Verrucktheit (chronic nonaffective delusional insanity) in his second to fourth editions. In his third edition, he adds a catatonic form of Wahnsinn (acute delusional-affective insanity). His fourth and fifth editions contain, respectively, catatonic forms of his two proto-DP concepts: Psychischen Entartungsprocesse and Die Verblodungsprocesse. Kahlbaum's catatonia required a sequential phasic course. Positive psychotic symptoms were rarely noted, and outcome was frequently good. While agreeing on the importance of key catatonic signs (stupor, muteness, posturing, verbigeration, and excitement), Kraepelin narrowed Kahlbaum's concept, dropping the phasic course, emphasizing positive psychotic symptoms and poor outcome. In his fourth to sixth editions, as he tried to integrate his three DP subtypes, he stressed, as suggested by Aschaffenburg and Schule, the close clinical relationship between catatonia and hebephrenia and emphasized the bizarre and passivity delusions seen in catatonia, typical of paranoid DP.

Jean-luc Martinot - One of the best experts on this subject based on the ideXlab platform.

  • 1910s' brains revisited. Cortical complexity in early 20th century patients with intellectual disability or with Dementia Praecox.
    Acta psychiatrica Scandinavica, 2014
    Co-Authors: Anca-larisa Sandu, M.-l. Paillère Martinot, Eric Artiges, Jean-luc Martinot
    Abstract:

    Objective The idea of cortical surface anomalies in subjects with intellectual disability (mental retardation) and schizophrenia can be traced back to early 20th century qualitative observations. Since it is unknown whether modern quantitative measures of cortical complexity and folding would retrieve those early empirical observations, we measured fractal dimension and sulcal span index in photographs of human brains taken in the 1910's. Method Brain photographs were compared between 36 patients with mental retardation and 21 patients with Dementia Praecox for the fractal dimension and sulcal span index. Also, a mental retardation subgroup with no-or-non-understandable speech (n = 12) was compared with a subgroup with comprehensible speech (n = 23). Results Mental retardation group had a lower whole-brain fractal dimension than Dementia Praecox, and a higher sulcal span index in left posterior cortex. The mental retardation subgroup with comprehensible speech had a lower fractal dimension in left hemisphere than the subgroup with no-or-non-understandable speech and a lower sulcal index in left posterior cortex. Conclusion Measures of cortical complexity and folding suggest differences between mental retardation and Dementia Praecox, and regional variations according to language abilities in mental retardation. The findings provide a unique picture of cortical surface changes in their original untreated form, one century ago.

R F Zec - One of the best experts on this subject based on the ideXlab platform.

William C Miller - One of the best experts on this subject based on the ideXlab platform.

  • treatment of Dementia Praecox by intra venous injections of sodium chlorid
    2015
    Co-Authors: William C Miller
    Abstract:

    WARREN, PA. Kraepelin1 noted that sodium chlorid infusions caused an increased appetite and thirst, and improvement of the general health of cases of confusion and restlessness. Ishida2 administered a 0.9 per cent. common salt solution intravenously, as far as circumstances permitted, in ten cases of Dementia Praecox. In five untreated cases of catatonia the quantity of chlorin in the blood was tabulated. The amount varied from 0.199 to 0.220 per cent. (Estimations made by Professor Horinchi by the Volhard-Salkowski method.) Ishida calls attention to this low chlorin content of the blood and says, "I am led to infer that common salt in the blood in catatonic patients as well as those with other clinical forms of Dementia Praecox might be deficient, and that the infusion of physiologic salt solution would meet this deficiency, though the results might be but transitory." As the result of treatment of the ten cases he concludes that "in nearly 50 per cent. of all cases I have observed the awakening of interest in work directly following treatment. Remissions have been observed in four cases; the longest duration being four months." Fever occurred in some instances after the infusion was given. Ishida suggests that this might be due to impurities of the solution as a result of defective sterilizing methods. Guthrie,3 in a paper read at the fiftieth annual meeting of the West Virginia Medical Association, stated that he followed Ishida's suggestions and gave normal salt solution intravenously. He reported the results of treatment of fifteen cases based on chemical analysis of the blood. These analyses showed a deficiency of sodium chlorid. Of the fifteen cases, ten, "very unclean before treatment, were improved in this respect. In eight cases, there was an awakening in interest in work directly following the treatment, and in seven of these cases this