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Thursday, 23.03.2017


I entered the field of psychiatry in 1954 in Hungary, my native country, about three years before the antidepressant effects of imipramine and iproniazid were discovered (Kuhn, 1957; Loomers, Saunders & Kline, 1957). The presence of serotonin (5-HT) and norepinephrine (NE) in the brain, the monoamine neurotransmitters that were to become the center of interest in depression for several decades, was already demonstrated (Twarog & Page, 1953; Vogt, 1954). The spectrophotofluorometer, the first instrument with the resolution power to study the action of drugs on the monoamine turnover rate in the brain parallel to their clinical effects, was to be introduced within a year (Bowman, Caulfield & Udenfriend, 1955).

I started my apprenticeship in psychiatry at the National Institute of Nervous and Mental Diseases (NINMD) in Budapest. It was at the tail end of the period when spinal tap was routinely carried out in newly admitted patients for ruling out cerebral syphilis, and when insulin coma was the prevailing treatment modality for the schizophrenias. Although electroconvulsive therapy (ECT) was already available for some time, opiate tincture was still the predominant treatment of “depression.” An “opium cure,” was a three-week procedure during which the dose of the substance was raised by daily increments from 3 to 25 minims, then, decreased gradually until discontinued (Ban, 2001).

Management and treatment of “depression” at that time were based almost exclusively on information about the psychopathology of patients. The psychopathological symptom profile of patients allowed assignment to a wide variety of “prototype-based” diagnoses; reasonably accurate predictions about prospective course and outcome of illness, as well as about responsiveness to different pharmacological treatments, e.g., amphetamines, barbiturate-amphetamine combinations, chlorpromazine (that was just introduced as a “major tranquilizer”). Psychopathology in the mid-20th century provided the knowledge base that guided education, clinical practice and research in European psychiatry (Ban, 2004).


The term psychopathology was introduced by Ernst Feuchtersleben (1845) in the mid 19th century and used as a synonym for “psychiatry” for more than 50 years. In the early 20th century the use of the term became restricted to the “science” of psychiatry by Karl Jaspers’ (1910) with a methodology suitable for the study of pathological mental phenomena encountered in the “practice” of psychiatry. The methodology was suitable also for defining the boundaries of psychiatry by separating the psychiatric “disease process” from “personality development.” The signal difference between the two is that “personality development” grows on a predisposition (“Anlage”) in a continuous sequence, with changes brought about by respective age periods, whereas the psychiatric “disease process” follows its own course that interrupts and becomes superimposed on these built-in sequences. It was also recognized that “personality development” could be understood through “meaningful connections” by empathy and introspection, whereas "disease process" could not and had to be explained by a causal factor.

The roots of “Jasperian psychopathology” are in Aristotle’s distinction between “form” and “content” and in the recognition that the “content” of psychopathological symptoms is based on patients' life experiences, whereas the “form” in which the content is experienced is determined by patients’ illness. Jaspers’ recognition that patients with different mental illnesses “process” their sensory-perceptual experiences and ideas differently in their brains, as expressed in the “form” of their psychopathological symptoms, has led to the birth of “phenomenological psychopathology” (“phenomenology”), a discipline that provides a methodology for the detection and monitoring of mental pathology in patients. For the “phenomenological psychopathologist” (“phenomenologist”), it is not the subject matter that the patient talks about, but the form, how the patient talks; and it is not the content of a symptom, such as a “somatic complaint,” but whether the “somatic complaint” is experienced in the form of “bodily hallucinations,” “obsessive ideas,” or “hypochondriacal delusions,” that is relevant to patient’s mental illness and psychiatric diagnosis (Fish, 1967; Hamilton, 1985; Taylor, 1981).


During the years from 1918 to 1933, a group of psychiatrists that included Hans Gruhle and Wilhelm Mayer-Gross in Kurt Wilmanns’ Department of Psychiatry at the University Clinic of Heidelberg spearheaded a “phenomenological analysis,” of psychopathological symptoms. Their work has resulted in a vocabulary that includes distinct words derived from the pathologies of “symbolization,” such as “condensation” (combining diverse ideas into one concept) and “onematopoesis” (building new phrases in which the usual language conventions are not observed), to the pathologies of “psychomotility,” such as “ambitendency” (the presence of opposite tendencies to action) and “parakinesis” (qualitatively abnormal movements). In “phenomenological psychopathology,” “dysphoria,” the negative pole of “vital emotions,” is distinguished from “dysthymia,” the negative pole of mood; “psychomotor retardation,” the experience of a spontaneous slowing down of motor activity, is distinguished from “psychomotor inhibition,” the experience of slowed down or “obstructed“ motor activity, etc.(Fish, 1967; Jaspers, 1913; Nyirö, 1962; Taylor, 1981). Furthermore, by linking the different abnormal forms of experience (“psychopathological symptoms”) to psychiatric diagnoses, the Heidelberg School created a self-contained language of psychiatry that reflected the pathology in mental processing in the brain. In this language, “tangential thinking,” characterized by talking past or around the point (Vorbeireden), was linked with the schizophrenias; “circumstantial thinking,” characterized by overbearing elaboration on insignificant details with the dementias; “rumination,” characterized by endless pondering of unpleasant thoughts, with depressions, etc. (Hamilton, 1985).

With the employment of "phenomenology” in a period of less than two decades, the Heidelberg group turned psychiatry into an experimental discipline with the potential to separate one mental illness from another. They also separated “abnormal behavior,” the subject matter of “abnormal psychology,” in which behavioural anomalies are perceived as deviation from instrumental means which are accepted as normal for a subject with a particular social background, from “psychopathology, the subject matter of “psychiatry,” in which abnormal mental phenomena are perceived within the frame of reference of mental illness (Juhász & Pethö, 1983; Schneider, 1950).

The "golden years" in the development of "phenomenology” came to an end in 1933 with the removal of Wilmanns from his position by the Nazi regime, partly because of his reference in his lectures, to the “hysterical blindness” of Adolf Schicklgruber (alias Adolf Hitler), towards the end of the first World War. He was replaced by Carl Schneider, who was to authorize the murder and sterilization of many mental patients. Hans Walter Gruhle, who was the intellectual leader of the group, left the university to take a position at a provincial psychiatric hospital; Wilhelm Mayer-Gross moved to England, and before long the team that was instrumental in developing “phenomenological psychopathology” as a foundation of psychiatric research at the Heidelberg psychiatric clinic disintegrated (Shorter, 2005).

Although the "golden years" had ended, the tradition of Heidelberg continued even during the tenure of Carl Schneider, who contributed to the classification of “acute schizophrenia.” When Kurt Schneider took the helm in 1946 at the Heidelberg University Psychiatric Clinic, all the different areas of research Jaspers subsumed under “general psychopathology” had evolved into a discipline of its own. Thus, by the mid-1950s, “general psychopathology” has included in addition to “phenomenological psychopathology,” “performance psychology” that deals with “objective,” observable or measurable performances of mental life such as perception and memory; “somatopsychology” that is focused on somatic symptoms accompanying mental pathology; “understanding psychology” that is concerned with meaningful connections and comprehensible relations, i.e., how one mental event emerges from another; “explanatory psychology” that studies cause–effect relationships in mental life; and “nosology” that provides the methodology for synthesizing psychiatric disease from “psychopathological symptoms” and classifying the diseases synthesized. Kurt Schneider (1957) himself suggested that disturbance of ego (self)-integrity was central to the psychopathology of the schizophrenias and referred to symptoms which reflect this pathology, as “thought broadcasting,” “thought withdrawal,” etc., as “first rank symptoms” of schizophrenia. With the application of Jaspers’ (1910) distinction between ”personality development” and “psychiatric disease process,” Schneider was first in 1920 to separate “vital depression,” an illness, from “depressive psychopathy” and “reactive depression.” During Kurt Schneider’s nine-year tenure, “phenomenological psychopathology” flourished once again at the Heidelberg clinic. His retirement in 1955, followed shortly by the introduction of several new “psychotropic drugs,” ended an era in psychiatry with the last attempt to render mental pathology accessible to research directly, in statu nascendi, as the pathology in mental processing emerges in the brain before it becomes translated into social behavior.

Kurt Schneider’s (1920) “vital depression” with so called “vital feelings,” (experienced by patients as if their whole body was affected by their illness), “corporization,” (experienced as if they were more ill than in any physical illness they ever had), somatic symptoms and disturbance of vital balance (experienced by feeling tired in the morning), was one of the frequently encountered forms of depression we saw in our service in the mid-1950s. But clearly, it was only one of the many forms of disease we saw that were diagnosed as “depression.” It was different from the “depression” described by Emil Kraepelin (1899) and characterized by retarded thinking and decreased motor activity that in some cases was so severe that “stupor” ensued that could only be relieved transiently with small doses of intravenously administered, short-acting barbiturates. It was also different from the many other prototypes of depression: one dominated by “anhedonia,” another by “depressive evaluations,” a third by “micromania,” etc. (Nyirö, 1962). Each of these forms differed distinctly from one another by “elementary” psychopathological symptoms that dominated the clinical picture (Krahl, 2000; Wernicke, 1892). They also differed in responsiveness to ECT, verbal interaction and life events, to the extent that in some forms of the illness, e.g., “vital depression,” ECT, the most reliable treatment of depression at the time, had a negative effect (Shorter, 2013).

By the time I left Hungary in 1956 I learned that even if almost all the different forms of depressive illness follow an episodic course with full remission between episodes, and even if almost all patients with depressive illness regardless of which prototype they fit suffer severely during their episode, the responsiveness of each patient to physical, behavioral or psychological approaches to treatment is dependent on patients psychopathological symptom-profile.

Since the time I left Hungary, more than half a century has passed and during these years I have participated in the clinical development of numerous drugs for the treatment of depression, from desipramine to reboxetine, with trazodone and viloxazine in between (Ban and Lehmann, 1962; Ban et al, 1974, 1998; Petrie et al, 1982). Working with patients while studying these drugs, I became keenly aware that each of these drugs can give life if given to the right patient, but can add to the hell of a patient if given to the wrong one. I also learned that, as far as treatment with antidepressants is concerned, the chances are that by prescribing any one of these drugs without identifying the form of depression each patient has, one could potentially harm, by inducing side effects, at least as many patients than one would potentially help.

By the dawn of the 21st century, “phenomenological psychopathology” had become the forgotten language of psychiatry; neuropsychopharmacologists had become involved studying epigenetic mechanisms to develop treatment for depression; and psychiatrists were treating patients with ”major depression” using a wide variety of “antidepressant” drugs with limited success (American Psychiatric Association, 1980). Yet, as “major depression” provides the only clinical end-point for both treatment and research in “depressive illness” is a consensus-based diagnostic concept that covers up psychopathology-based diagnoses, in this monograph a methodology is proposed for deconstructing “major depression” to open the path for the study of the biology and genetics of the different forms of depression.