Any of a group of severe mental disorders that have in common symptoms such as hallucinations, delusions, blunted emotions, disorganized thinking, and withdrawal from reality. Five main types are recognized: the paranoid, characterized by delusions of persecution or grandeur combined with unrealistic, illogical thinking and frequent auditory hallucinations; the disorganized (hebephrenic), characterized by disordered speech and behaviour and shallow or inappropriate emotional responses; the catatonic, characterized by motor inflexibility or stupor along with mutism, echolalia, or other speech abnormalities; the simple or undifferentiated type, which conforms to basic definitions of schizophrenia but does not exhibit particular behaviours in the aforementioned types; and the residual type, which is a chronic stage indicating advancement toward later-stage schizophrenia. Schizophrenia seems to occur in 0.5–1percnt of the general population, and more than half of those so diagnosed will eventually recover. There is strong evidence that genetic inheritance plays a role, but no single cause of schizophrenia has been identified. Stressful life experiences may help trigger its onset. Treatment consists of drug therapy and counseling.

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Dementia praecox ("premature dementia") is a term first used in 1891 in this Latin form by Arnold Pick (1851-1924), a professor of psychiatry at the German branch of Charles University in Prague. His brief clinical report described the case of a person with a psychotic disorder resembling hebephrenia (see below). It was popularized by German psychiatrist Emil Kraepelin (1856-1926) in 1896 in his first detailed description of a condition that would eventually be reframed and relabeled as schizophrenia. It refers to a chronic, deteriorating psychotic disorder characterized by rapid cognitive disintegration, usually beginning in the late teens or early adulthood.

The primary disturbance in dementia praecox is not one of mood (as is the case in manic-depressive illness), but of thinking or cognition. Cognitive disintegration refers to a disruption in cognitive or mental functioning such as in attention, memory, and goal-directed behavior.

From the outset, dementia praecox was viewed by Kraepelin as a progressively degenerating disease from which no one recovered. However, by 1913, and more explicitly by 1920, Kraepelin admitted that although there seemed to be a residual cognitive defect in most cases, the prognosis was not as uniformly dire as he had stated in the 1890s.

History

First use of the term

The term demence precoce was used to describe a psychotic disorder by the French physician Benedict-Augustin Morel in 1853, and later used in his 1860 textbook, Traité des maladies mentales. Morel used the term to define a disorder that first struck men in their teenage or young adult years, after which their intellectual functioning rapidly deteriorated. Morel saw this mental disorder as being within the larger context of his theory of degeneration. These young men were beginning a rapid intellectual deterioration that would result in total disability and possible death.

Morel described an entire category of psychotic disorders that ended in dementia, and as a result he may be regarded as the first alienist or psychiatrist to develop a diagnostic system based on presumed outcome rather than on the current presentation of signs and symptoms. Morel, however, did not conduct any long-term or quantitative research on the course and outcome of dementia praecox (Kraepelin would be the first in history to do that) so this prognosis was based on speculation. It is impossible to discern whether the brief description of the disorder described by Morel was equivalent to the disorder later called dementia praecox by Pick and Kraepelin. Nor is there any reason to conclude that either of these men used Morel as a source of inspiration for their concepts.

The time component

In 1863, Karl Kahlbaum (1828-1899) of Danzig, Prussia published Die Gruppierung der psychischen Krankheiten (The Classification of Psychiatric Diseases). In this book, Kahlbaum described a class of progressively degenerating psychotic disorders that he grouped under the term "Vesania typical" (typical insanity). In 1866 Kahlbaum became the director of a private psychiatric clinic in Görlitz, Prussia, a small town near Dresden. He was accompanied by his younger assistant, Ewald Hecker (1843-1909), and together they conducted a series of research studies on young psychotic patients that would become a major influence on the development of modern psychiatry.

Together Kahlbaum and Hecker were the first to describe and name such syndromes as dysthymia, cyclothymia, paranoia, catatonia, and hebephrenia. Perhaps their most lasting contribution to psychiatry was the introduction of the "clinical method" from medicine to the study of mental diseases, a method which is now known as psychopathology.

Other than Morel’s description of his degeneration theory, the element of time had largely been missing from definitions of mental disorders. Psychiatrists made assumptions about prognosis that were not based on careful observation of the changing symptoms of patients over time. Psychiatrists and other physicians who wrote about the insane arbitrarily invented names for insanities and described their characteristic signs and symptoms based on a short-term, cross-sectional observation period of their lunatic patients.

When the element of time was added to the concept of diagnosis, a diagnosis became more than just a description of a collection of symptoms: diagnosis now also defined prognosis (course and outcome). An additional feature of the clinical method was that the characteristic symptoms that define syndromes should be described without any prior assumption of brain pathology (although such links would be made later as scientific knowledge progressed). Karl Kahlbaum first made his appeal for the adoption of the clinical method in psychiatry in his 1874 book on catatonia. Without Kahlbaum and Hecker there would be no dementia praecox.

The quantitative component

In 1891 Emil Kraepelin left his position at the university in Dorpat (now Tartu, Estonia) to become a professor and director of the psychiatric clinic at the University in Heidelberg, Germany. Convinced of the value of Kahlbaum’s suggestions for a more exact qualitative clinical method in psychiatry, Kraeplin realized that by adding a quantitative component to such a research program he could place psychiatry on a more scientific foundation.

Quantification helped to eliminate any subjective biases on the part of the researcher. He began the first such research program of this nature in the history of psychiatry at Heidelberg in 1891, collecting data about every new patient that was admitted to the clinic (not just interesting cases, as had been the case in the past) and summarizing them on specially prepared index cards, his famous Zahlkarten. He had been keeping data on such cards since 1887. In his posthumously published Memoirs (first published in German 61 years after his death) Kraepelin described his method:

. . . after the first thorough examination of a new patient, each of us had to throw in a note [in a "diagnosis box"] with his diagnosis written on it. After a while, the notes were taken out of the box, the diagnoses were listed, and the case was closed, the final interpretation of the disease was added to the original diagnosis. In this way, we were able to see what kind of mistakes had been made and were able to follow-up the reasons for the wrong original diagnosis (p. 61).

Kraepelin was obsessed with finding patterns in the data on these cards, at times taking them home with him or on vacation. In 1893, two years after starting his more rigorous research program in Heidelberg, the 4th edition of Kraepelin’s textbook, Psychiatrie, reflected some preliminary impressions derived from the analysis of his cards. Clinical syndromes involved not only a diagnosis according to signs and symptoms, but also included course and outcome. In that edition he introduced a class of psychotic disorders he called "psychic degenerative processes." Three of these came directly from the work of Kahlbaum and Hecker: dementia paranoides (a sudden-onset, degenerative form of Kahlbaum’s paranoia; catatonia (directly from Kahlbaum’s 1874 monograph on the subject); and dementia praecox, which was essentially Hecker’s hebephrenia (as described in 1871). Dementia precox was hebephrenia and would remain so in Kraepelin’s thinking for 6 more years.

In March 1896 the 5th edition of Kraepelin’s textbook appeared. In it, Kraepelin stated that he was confident of the value of his clinical method of using qualitative and quantitative data collected over a long period of observation of patients as a way of developing a diagnosis that included prognosis (course and outcome):

What convinced me of the superiority of the clinical method of diagnosis (followed here) over the traditional one, was the certainty with which we could predict (in conjunction with our new concept of disease) the future course of events. Thanks to it the student can now find his way more easily in the difficult subject of psychiatry.

In the 1896 5th edition, dementia praecox (still essentially hebephrenia), dementia paranoides, and catatonia are separate psychotic disorders included among "metabolic disorders leading to dementia."

Kraepelin's influence on the next century

In the 6th edition of Psychiatrie of 1899, Kraepelin reordered the psychiatric universe for the next century by grouping most of the insanities into two large categories, dementia praecox and manic-depressive illness. They were distinguished by the following characteristics: (1) dementia praecox was primarily a disorder of intellectual functioning, manic-depressive illness was primarily a disorder of affects or mood; (2) dementia praecox had a uniformly deteriorating course and a poor prognosis, manic-depressive insanity had a course of acute exacerbations followed by complete remissions with no lasting deterioration of intellectual functioning; and (3) there were no recoveries from dementia praecox, whereas in manic-depressive illness there were many complete recoveries. In 1899 dementia praecox took its now-familiar form as a heterogeneous class of psychotic disorders comprising hebephrenic, catatonic, and paranoid forms. These forms have persisted until today through Eugen Bleuler’s schizophrenia of 1908 (to which he added a fourth form, dementia simplex, or simple schizophrenia], and the main types of schizophrenia in DSM-IV-TR (the paranoid, catatonic and disorganized types, with the latter retaining its historical designation as the hebephrenic type in ICD-10 [1992]).

Change in prognosis

In the 7th edition of 1904 there was little change in the description of dementia praecox, but Kraepelin does admit for the first time that in a small number of cases that recovery from dementia praecox might occur.

The 8th edition of Kraepelin’s Psychiatrie was a four-volume opus, each of which appeared in different years between 1909 and 1915. In this edition dememtia praecox became one of the "endogenous dementias." It is in the 1913 third volume (second part) of this edition that Kraepelin adjusts his concept of prognosis to admit that a partial remission of symptoms occurred in approximately 26 percent of his patients.

This brought dementia praecox in line with Eugen Bleuler’s claims about schizophrenia, which he had insisted from the start (in 1908) that (a) in many cases there was no fateful progressive deterioration, that (b) in some cases the symptoms did indeed remit for periods of time, and (c) that there were cases of complete recovery.

The 8th edition of 1913 is also notable for the fact that Kraepelin increased the number of forms of dementia to 11. However, the three classical original subtypes would remain as the most influential description of this disorder for the century that followed. The 8th edition of Psychiatrie was that last Kraepelin would produce in his lifetime. He was working on a 9th edition with Johannes Lange (1891-1938) but died in 1926 before it could be completed. Lange finished the bulk of it and published it in 1927.

Addition of etiology

Kraepelin realized that the state of scientific knowledge was such that definitive claims about the cause of dementia praecox could not be made. Heredity clearly played a role, as Kraepelin and his research associates had demonstrated this in their quantitative research. As a result of following the clinical method suggested by Kahlbaum, Kraepelin set aside claims about underlying brain disease or specific neuropathology in diagnostic descriptions of mental disorders. However, from the 5th edition of 1896 to the third volume of the 8th edition of 1913 it was clear that Kraepelin believed that dementia praecox was caused by a poisoning of the brain, and “autointoxication,” probably arising from the sex glands after puberty.

Universality of the disease

Kraepelin believed that dementia praecox was not a culture-bound syndrome and that it represented a disease process that could be found all over the world. Kraepelin himself loved to travel, and in Asia he observed that dementia praecox was similar to the European form of the illness in Chinese, Japanese, Tamil and Malay patients, leading him to suggest in the 8th edition of Psychiatrie that, "we must therefore seek the real cause of dementia praecox in conditions which are spread all over the world, which thus do not lie in race or in climate, in food or in any other general circumstance of life . . . ."

Treatment

Without knowing the cause of dementia praecox or manic-depressive illness, Kraepelin repeatedly stated that there could be no treatments specific to these conditions. Treatment for these insanities was the same for any institutionalized patient with any diagnosis: the occasional use of drugs (opiates, barbiturates, and so on) to alleviate acute episodes of distress, prolonged baths (greatly admired by Kraepelin as a humane method of calming patients), and occupational activities (if possible). Kraepelin himself had experimented with hypnosis early in his career and found it lacking. Psychotherapy as such was not part of the medical cognition of Kraepelin. In fact, Kraepelin detested both Freud and Jung for introducing diagnostic terms and forms of treatment that had no empirical basis. Kraepelin did, however experiment for a while with organotherapy -- the injection of glandular extract from the thyroid, gonads and other organs -- but without success. This experimental therapy was a rational treatment based on his presumed cause of dementia praecox -- an autointoxication arising from the sex glands.

Use of term spreads

By 1899 Kraepelin himself had counted almost 20 German-language publications which made reference to his new diagnostic term, dementia praecox. In the decade after 1899 the number of German-language publications using Kraepelin’s categories of dementia praecox and manic-depressive illness as a basis for clinical speculation and experimental research exploded. German-language psychiatric concepts were always introduced much faster in America (than, say, Britain) where émigré German, Swiss and Austrian physicians essentially created American psychiatry. Swiss-emigree Adolf Meyer (1866-1950), arguably the most influential psychiatrist in America for the first half of the 20th century, published the first critique of dementia praecox in an 1896 book review of the 5th edition of Kraepelin’s textbook. But it was not until 1900 that the first three American publications regarding dementia praecox appeared, one of which was a translation of a few sections of Kraepelin’s 6th edition of 1899 on dementia praecox.

Adolf Meyer was the first to apply the new diagnostic term in America. He used it at the Worcester Lunatic Hospital in Massachusetts in the fall of 1896.

Both dementia praecox (in its three classic forms) and ‘manic-depressive psychosis’ gained wider popularity in the larger institutions in the eastern United States after being included in the official nomenclature of diseases and conditions for record-keeping at Bellevue Hospital in New York City in 1903. The term lived on due to its promotion in the publications of the National Committee on Mental Hygiene (founded in 1909) and the Eugenics Records Office (1910). But perhaps the most important reason for the longevity of Kraepelin’s term was its inclusion in 1918 as an official diagnostic category in the uniform system adopted for comparative statistical record-keeping in all American mental institutions, The Statistical Manual for the Use of Institutions for the Insane. Its many revisions served as the official diagnostic classification scheme in America until 1952 when the first edition of the Diagnostic and Statistical Manual of Mental Disorders, or DSM-I, appeared. Dementia praecox disappeared from official psychiatry with the publication of DSM-I, replaced by the Bleuler/Meyer hybridization ‘schizophrenic reaction.’

The reception of dementia praecox as an accepted diagnosis in British psychiatry came much slower, perhaps only taking hold around the time of the First World War. There was substantial opposition to the use of the term "dementia" as misleading, partly due to findings of remission and recovery. Some argued that existing diagnoses such as "delusional insanity" or "adolescent insanity" were better or more clearly defined. In France an older psychiatric tradition regarding the psychotic disorders predated Kraepelin, and the French never fully adopted Kraepelin’s classification system. Instead the French maintained an independent classification system throughout the 20th century. After 1980, when DSM-III totally reshaped psychiatric diagnosis, French psychiatry began to finally alter its views of diagnosis to converge with the North American system. Kraepelin thus finally conquered France via America.

From dementia praecox to schizophrenia

Because so many influential American physicians began to take psychoanalysis seriously after Freud and Jung attended a conference at Clark University in 1909, psychogenic theories of dementia praecox and, by 1920, Bleuler’s schizophrenia were openly accepted. Until 1910 Bleuler had been peripherally connected through Jung to Freud’s psychoanalytic movement, and this eased the adoption of his broader version of dementia praecox (schizophrenia) in America over Kraepelin’s more narrow and prognostically more negative one.

The term "schizophrenia" was first applied by American alienists and neurologists in clinical settings around the year 1918. It is first mentioned in The New York Times in 1925. Until 1952 the terms dementia praecox and schizophrenia were used interchangeably in American psychiatry, with occasional use of the hybrid terms "dementia praecox (schizophrenia)" or "schizophrenia (dementia praecox)."

Diagnostic manuals

Editions of the Diagnostic and Statistic Manual of Mental Disorders since the first in 1952 had reflected views of schizophrenia as "reactions" or "psychogenic" (DSM-I), or as manifesting Freudian notions of "defense mechanisms" (as in DSM-II of 1968 in which the symptoms of schizophrenia were interpreted as "psychologically self-protected"). The diagnostic criteria were wide, including either concepts that no longer exist or that are now labeled as personality disorders (for example, schizotypal personality disorder) There was also no mention of the dire prognosis Kraepelin had made. Schizophrenia seemed to be more prevalent and more treatable than either Kraepelin or Bleuler would have allowed.

Conclusions

As a direct result of the effort to construct Research Diagnostic Criteria (RDC) in the 1970s that were independent of any clinical diagnostic manual, Kraepelin’s ideas began to return to prominence. For research purposes, the definition of schizophrenia returned to the narrow range allowed by Kraepelin’s dementia praecox. Furthermore, the disorder was a progressively deteriorating one once again, with the notion that recovery, if it happened at all, was rare. This revision of schizophrenia became the basis of the diagnostic criteria in DSM-III. Some of the psychiatrists who worked to bring about this revision referred to themselves as the "neo-Krapelinians."

Bibliography

• G. E. Berrios, Luque, Rogelio, and Villagran, Jose M. Schizophrenia: a conceptual history. International Journal of Psychology and Psychological Therapy, 2003, 3: 111-140.
• Burgmair, Wolfgang & Eric J. Engstrom & Matthias Weber, et al., eds. Emil Kraepelin. 7 vols. Munich: Belleville, 2000-2008.

Vol. VII: Kraepelin in Munich, Teil II: 1914-1926 (2008, forthcoming)
Vol. VI: Kraepelin in Munich, Teil I: 1903-1914 (2006), ISBN 3-933510-95-3
Vol. V: Kraepelin in Heidelberg, 1891-1903 (2005), ISBN 3-933510-94-5
Vol. IV: Kraepelin in Dorpat, 1886-1891 (2003), ISBN 3-933510-93-7
Vol. III: Briefe I, 1868-1886 (2002), ISBN 3-933510-92-9
Vol. II: Kriminologische und forensische Schriften: Werke und Briefe (2001), ISBN 3-933510-91-0
Vol. I: Persönliches, Selbstzeugnisse (2000), ISBN 3-933510-90-2

• Hippius, Hanns, and Muller, Norbert (2008). The work of Emil Kraepelin and his research group in Munchen. European Archives of Psychiatry and Clinical Neuropsychiatry, 258 (Suppl. 2), 3-11.
• Ion, R.M. and Beer, M.D. (2002a) The British reaction to dementia praecox 1893-1913. Part 1. History of Psychiatry, 13, 285-304.
• Ion, R.M., and Beer, M.D. (2002b) The British reaction to dementia praecox 1893-1913. Part 2. History of Psychiatry, 13, 419-431.
• Emil Kraepelin. Psychiatrie: Ein Lehrbuch fur Studirende und Aerzte. Sechste, vollstandig umgearbeitete Auflage. Leipzig: Verlag von Johann Ambrosius Barth, 1899.
• Kraepelin, E. Psychiatry: A Textbook for Students and Physicians. 2 volumes. Edited by Jacques Quen. Translated by Helga Metoui and Sabine Ayed. Canton, Massachusetts: Science History Publications, 1990 [translation of the 1899 sixth edition].
• Kraepelin, Emil. Memoirs. Berlin: Springer-Verlag, 1987.
• Richard Noll. Kraepelin's 'lost biological psychiatry"? Autointoxication, organotherapy and surgery for dementia praecox. History of Psychiatry, 2007, 18 (3): 301-319.
• Noll, Richard. Introduction: From dementia praecox to schizophrenia. Classic Text 72: “Non-Dementia Non-Praecox: Note on the Advantages to Mental Hygiene of Extripating a Term,” by E.E. Southard (1919). History of Psychiatry, 2007, 18(4): 483-502.
• Noll, Richard. Infectious insanities, surgical solutions: Bayard Taylor Holmes, dementia praecox and laboratory science in early twentieth-century America. Part 1 and Part 2. History of Psychiatry, 2006, 17 (2): 183-204; 17 (3): 299-311.
• Noll, Richard. The blood of the insane. History of Psychiatry, 2006, 17 (4): 395-418.
• Noll, Richard. Chicago’s Dr. Bayard Taylor Holmes: A forgotten pioneer in the history of biological psychiatry. Chicago Medicine, 2006 (Spring), 109: 28-32.
• Noll, Richard. Historical Review: Autointoxication and focal infection theories of dementia praecox. World Journal of Biological Psychiatry, 2004, 5: 66-72.
• Noll, Richard. Dementia Praecox Studies [letter to the editor and historical note]. Schizophrenia Research, 2004, 68:103-104.
• Noll, Richard. The American reaction to dementia praecox, 1900. History of Psychiatry, 2004, 15: 127-128.
• Noll, Richard. Styles of psychiatric practice: Clinical evaluations of the same patient by James Jackson Putnam, Adolf Meyer, August Hoch, Emil Kraepelin and Smith Ely Jelliffe. History of Psychiatry, 1999, 10: 145-189.
• Pick, Arnold. Ueber primare chronische Demenz (so. Dementia praecox) im jugendlichen Alter. Prager medicinische Wochenschrift, 1891, 16: 312-315.

Additional Resources

• Bibliography of scholarly histories on schizophrenia and dementia praecox, part 1 (2000-mid 2007).

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