“…[He] was a twenty-five-year-old graduate of the University of Zurich Medical School who had just completed his doctoral thesis on the forebrain of reptiles, had never held formal employment as a clinician or researcher, did not enjoy treating living patients during his medical training, preferred to spend his time studying the brains of the dead, and had little formal training in psychiatry.”
This is a description from Richard Noll’s fascinating book, American Madness: The Rise and Fall of Dementia Praecox, of the man who’d become the most influential psychiatrist in the U.S. in the first few decades of the 20th century — and the one who’d bring dementia praecox to America.
Swiss-born Adolf Meyer didn’t just have little formal training in psychiatry; he essentially knew nothing about it. Fortunately, in 1896, 29-year-old Meyer got the crash course he needed when he set off on a tour of European psychiatric facilities.
At the time he was working as a pathologist at Worcester Lunatic Hospital in Massachusetts; the goal of the trip was to get ideas for potential improvements he could make at his hospital.
His most important stop would be in Heidelberg, the location of a small university psychiatric clinic. There, Meyer met psychiatrist and chief Emil Kraepelin – the man behind dementia praecox. During his visit, Meyer read Kraepelin’s textbook, Psychiatrie, talked with Kraepelin and watched his staff at work.
It was in this book that Kraepelin described dementia praecox, an incurable psychotic disorder. Dementia praecox began after puberty, progressively worsening until it led to irreversible “mental weakness” or “defect.” Individuals with dementia praecox could look very different depending on their combination of symptoms.
In the sixth edition of his textbook, Kraepelin categorized dementia praecox into three subtypes “connected to each other by fluid transitions:” catatonia (abnormal movement; usually started with depression and “nervousness,” and led to hallucinations and delusions); paranoid (fixed delusions of persecution and grandiosity are common with auditory hallucinations) and hebephrenic (disorganized thinking and problems with attention, language and memory).
In the introduction, Noll refers to dementia praecox “as a diagnosis of hopelessness from its creation.” The public along with alienists and other medical authorities viewed dementia praecox as “the terminal cancer of mental diseases.”
In the same edition, Kraepelin also introduced “manic-depressive insanity,” which, according to Noll, “encompassed all the insanities whose primary symptoms were based in mood or affect, characterized by periodic manic states, depressed states, mixed states, or varying combinations thereof, which would wax and wane over the course of a person’s life but leave no or little cognitive defect between episodes.” It had a much better prognosis than dementia praecox.
(This later edition had a major impact. Noll says that “Since the 1970s it has been asserted that neo-Kraepelin clinicians created the structure and diagnostic content of the Diagnostic and Statistical Manual of Mental Disorders, Third Edition” (DSM-III) of 1980, and this bias has continued in successive editions until this day, including both clinical practice and research.”)
Back in America diagnosis was a tricky, murky process. And classification simply didn’t exist. There was no such thing as specificity or discrete diseases.
As Noll writes, most American “alienists” – as they called themselves – believed that there was one form of insanity: “unitary psychosis.” Different presentations were simply different stages of the same underlying disease process. These stages were: melancholia, mania and dementia.
After Meyer returned from his European trip, Worcester became the first hospital in America to use Kraepelin’s theory of insanity. And it was at Worcester that the first person was diagnosed with dementia praecox.
As Noll told the Harvard University Press Blog in this interview, dementia praecox would become the most prevalent diagnosis:
Beginning in 1896, as one American asylum after another slowly introduced dementia praecox as a diagnostic box, it became the most frequently diagnosed condition, labeling a quarter to a half of all patients in each institution. How American psychiatrists were making this diagnosis is anyone’s guess—they were probably just snap decisions based on whether someone was suffering from a “good prognosis madness” (such as manic depression) or a “bad prognosis madness” (dementia praecox). What we do know is that being young and male made it more likely someone would receive this diagnosis.
The public was introduced to dementia praecox by a 1907 piece in the New York Times that recounted the testimony in the murder trial of architect Stanford White. The superintendent of an asylum in Binghamton, N.Y. testified that the murderer, Harry Kendall Thaw, might’ve been suffering with dementia praecox.
In the late 1920s to the 1930s, dementia praecox started making its exit, replaced by Eugen Bleuler’s “schizophrenia.” At first, Noll says, these terms were used interchangeably in both clinical practice and research (which, naturally, made things very confusing). But these disorders had distinct differences.
For instance, the prognosis for “schizophrenia” was more positive. Bleuler, Carl Jung and other staff members at Burgholzli psychiatric hospital – where Bleuler was director – showed that many of the 647 “schizophrenics” were able to get back to work.
Bleuler also viewed some symptoms of schizophrenia as being directly caused by the disease process, while others as “…reactions of the ailing psyche to environmental influences and its own strivings.”
Unlike Kraepelin, Bleuler viewed dementia as “a secondary result of other, more primary symptoms.” Other secondary symptoms included hallucinations, delusions and flat affect.
The symptoms that were directly caused by the disease process were, writes Noll:
The simple functions of thought, feeling and volition that were disturbed were associations (how thoughts are bound together), affectivity (feelings as well as subtle feeling tones), and ambivalence (“the tendency of the schizophrenic psyche to endow the most diverse psychisms with both a positive and a negative indicator at one and the same time”).
Unfortunately, Americans put their own spin on schizophrenia. According to Noll in his interview:
By 1927 schizophrenia became the preferred term for inexplicable madness, but the Americans reframed Bleuler’s disease concept as a primarily functional or psychogenic condition that was caused by mothers or maladjustments to social reality. When Bleuler visited the United States in 1929 he was horrified to see what the Americans were calling schizophrenia. He insisted it was a physical disease with a chronic course characterized by exacerbations and remissions of hallucinations, delusions and bizarre behaviors.
Dementia praecox officially vanished from psychiatry in 1952 when the first edition of the DSM was published – and the disorder was nowhere to be found.
But, while it wasn’t around for long, dementia praecox had a significant impact on the field of psychiatry. According to Noll in American Madness:
Dementia praecox was the vehicle through which American psychiatry reentered general medicine. It descended into American asylums from the Valhalla of superior German medicine and presented American alienists with a divine gift: its first truly specifiable disease concept.
There could have been no modern medical science of American psychiatry in the twentieth century without dementia praecox. There can be no biological psychiatry in the twenty-first century without schizophrenia.
Be sure to check out the excellent book American Madness: The Rise and Fall of Dementia Praecox by Richard Noll, Ph.D, associate professor of psychology at DeSales University.