What might be responsible for what appears to have been an epidemic of both dementia praecox and manic depression beginning in 1913? Richard Noll’s American Madness: The Rise and Fall of Dementia Praecox provides important context here, particularly the influence of such key European figures as Emil Kraepelin and Adolf Meyer on American psychiatry from the 1890s well into the 20th century. According to Noll, as late as the 1890s American psychiatry was an “intellectual wasteland.” (Noll, p. 47) Asylum doctors still relied upon the same theories of madness that were in place when Dix opened in the 1850s: essentially that there was but one general form of insanity, which varied according to its symptomatic expression along a continuum from melancholy to mania. Kraepelin proposed the division of insanity into two major categories: dementia praecox and manic depression. To make a very simplistic and ahistorical distinction: the former was an untreatable set of “peculiar debilities” that led to progressive deterioration; the latter was a chronic affective disorder that did not result in cognitive deterioration.
Meyer would wrestle with Kraepelin’s nomenclature and nosology for decades, overlaying his own theories, terminology and diagnostic process, but the basic binary would persist well into the 20th century and influence the Diagnostic and Statistical Manual of Mental Disorders. Through his position at Johns Hopkins University, Meyer became, according to Noll, the most influential psychiatrist in America in the early 20th century. He trained or recommended the appointment of asylum superintendents across the country. (Noll, p. 36) The first patient to be diagnosed with dementia praecox in the U.S. was at the Worcester asylum in Massachusetts in 1896. By 1916 asylums were dealing with thousands of what were believed to be uncurable, untreatable, and ultimately doomed patients, many of whom had been so diagnosed in early adulthood.
We can see how this nosological revolution plays out at Dix. The superintendent with the longest tenure between 1889 and 1913 was James McKee (1901-1912), whose university studies were interrupted by the Civil War and whose medical degree was conferred in 1869. The superintendent from 1913 to 1932 was Albert Anderson, who trained at several hospitals in the late 1890s. In her history of the hospital, Marjorie O’Rorke notes that Anderson was influenced by Meyer in several respects, including his emphasis on recording patient histories, “which enabled him to identify hereditary and environmental causes of mental illness.” (O’Rorke, p. 45)
Anderson’s assumption of the post of superintendent at Dix corresponds with the striking rise in the number of cases of both dementia praecox and manic depression after 1912. Noll argues that when superintendents “converted” to some version of the Kraepelian schema, medical staff had little choice but to follow. (Noll, p. 106). Anderson was superintendent at the time of Mrs. Jones’s admission and treatment at Dix and led the “examination” (medical staff interview) of her on March 24, 1917.
The nomenclature/nosological category dementia praecox received much more attention from the medical and psychiatric community in North America and Europe than did manic depression. The latter was introduced by Kraepelin in 1899 in the 6th edition of his textbook on psychiatry as an umbrella category for various types of chronic mental illness associated with moods and affect. It was characterized by periodic episodes of mania, depression, or a mixed state. These states might recur over a lifetime, but the prognosis for the condition was believed to differ from that of dementia praecox in two key respects: there were no lasting effects of an episode of manic depression, which meant that an individual retained cognitive functions (attention, memory, language, etc.), and, as a result, there was no associated progressive deterioration of the individual’s mental state. Some historians regard it as a convenient nosological foil for dementia praecox. Noll argues that it became a common and uncontroversial diagnosis in the early 20th century, and remained unchallenged–and largely unresearched–for one hundred years. (Noll, pp. 94-95).
For Kraepelin, Meyer, and other leading psychiatrists of the era the etiology of dementia praecox remained a mystery. Kraepelin suggests an as yet undiscovered biological cause. Might there be a hereditary component? Given the dire prognosis associated with dementia praecox and the early life stage at which symptoms appear, it becomes all the more important to determine if life circumstances might contribute to the development of the disease, and/or if there is a personality type most susceptible. Noll argues that by 1911, dementia praecox is “promoted by prominent members of the psychiatric elite as a fundamentally psychogenic condition that sprouted from a ‘pre-dementia praecox’ personality defined by ‘habit disorganization’ or an essential cluster of maladaptive psychological ‘reactions’ to biological, social, and emotional or psychological ‘events’.” (Noll, p. 186)
The redefinition of dementia praecox as a psychogenic condition fundamentally changes the initial relationship of patient to psychiatrist and elevates the role of the case history in diagnosis in general. As Noll puts it, “the case history method located the roots of insanity in the unique life circumstances of the individual, each individual being a ‘type’ of one, not an example within a category of mental disease.” (Noll, p. 168) Reconstruction of a life narrative might uncover tale-tell signs of “habit deterioration” or of a “shut-in personality” as early as adolescence. How patients understand their own conditions and how they narrate the history of their selves become diagnostic evidence. The social relationships and lived experience of each patient become relevant to the circumstances under which they were brought to the asylum. Although the examination transcripts uncover a process much more interrogative than therapeutic, this historical turn and the role of the individual patient account in it opens the door to psychoanalysis (Noll, p. 169).
What does not appear in the typescripts of the examination is a discussion of treatment. An initial treatment plan might have been formulated at the time of admission, proposed as a part of the case history, or discussed in the medical staff meeting after the examination was concluded. Particularly in the case of dementia praecox, however, Noll suggests another reason for this lacuna in surviving asylum records. Despite robust and sustained debates among the leading psychiatrists of the era over causes, types, and prognosis of dementia praecox, the question of a specific treatment was largely ignored. Kraepelin recommended water therapy, physical activity, and a regular diet—common treatment options for asylum patients regardless of diagnosis. Sedatives were used at some overcrowded facilities as “chemical restraints.” In short, as Noll puts it, “No one really knew what to do to treat insanity.” (Noll, p. 194)
Although there was considerable debate regarding the long-term prognosis for dementia praecox patients, many psychiatrists in the early 20th century defined it in relation to the probability of the inexorable downward trajectory of the disease, which would play out over years or decades. Diagnosis with the condition could be the psychiatric equivalent of a life sentence. The increase in the frequency of dementia praecox diagnoses in the early 20th century had the long-term effect of making asylums custodial facilities for a persistent population of incurable, untreatable individuals. The second patient admitted to Dix diagnosed with dementia praecox (1896) died there in 1916. Some dementia praecox patients at Dix admitted after 1912 were discharged as “cured” or “improved” after a year or more of confinement, but it is impossible to know what these terms meant or how these outcomes were related to the therapies administered. Most of them show nothing in the columns for the disposition of the patient in the admissions ledger spreadsheet, which probably means they were there after 1918 (one hundred years prior to the date of transcription).
Proceed to next chapter
