- Schizophrenia: Recent Concepts
- (See also Schizophrenia: Emergence.)After the Second World War, two contradictory tendencies hallmarked the approach to the psychoses and schizophrenia. One was the growing predominance of psychoanalysis, with its tendency to use the term "schizophrenia" to mean any psychiatric illness not amenable to office-based psychotherapy. The second was the growing thrust of biological research in schizophrenia.Pseudoneurotic schizophrenia (1949). Uneasy about the tendency among psychoanalytically oriented psychiatrists to make a diagnosis of neurosis rather than schizophrenia, in an article in the Psychiatric Quarterly in 1949, Paul Hoch (1902–1964) and Phillip Polatin (1905–1980) of the New York State Psychiatric Institute called attention to a form of schizophrenia without delusions or hallucinations but characterized by what Bleuler had called dereistic (autistic) thinking and by disturbances of personality sufficiently severe to be called "pan-neurosis." This was a bridge between psychodynamic and classical formulations. They considered it possible that these "borderline" patients would evolve into full schizophrenia with deterioration. Hoch, who was born in Budapest and had studied in Göttingen and in Zurich with Manfred Bleuler, was oriented toward Eugen Bleuler’s concepts of schizophrenia.Schizophrenia and psychosis in DSM-"One" (1952). This first volume in the series of diagnostic and statistical manuals of the American Psychiatric Association (APA) accepted the distinction between organic brain disorders ("impairment of brain tissue function") and "psychogenic" disorders. Among the psychogenic variety were involutional psychotic reaction ("involutional" being a Kraepelinian inheritance; see Depression: Emergence: involutional melancholia ), schizophrenic "reactions" (the notion of reaction borrowed from Adolf Meyer rather than Karl Jaspers), and paranoid reactions. In line with the psychoanalytic thinking that dominated American psychiatry in those years, "manic depressive reaction" and "psychotic depressive reaction" were also considered to be "psychogenic."The actual psychopathological symptoms that the APA accepted for schizophrenia reflected the influence of Eugen Bleuler’s definition (see Schizophrenia: Emergence): "The disorders are marked by a strong tendency to retreat from reality, by emotional disharmony, unpredictable disturbances in stream of thought. . . ." Only some deteriorated (p. 26).Schizophrenia and psychosis in DSM-II (1968). The second edition of the DSM series tried to bring American nosology more into line with the European; namely, the World Health Organization’s International Classification of Diseases (ICD, eighth edition), adopted in 1966. "Psychogenic" schizophrenia thus went out the window, and the American Psychiatric Association’s Manual simply distinguished between Organic Brain Syndromes (whether psychotic or not) and "Psychoses not attributed to physical conditions listed previously." Otherwise, there were no big changes from DSM-I, except perhaps to stipulate the psychoanalytic conviction—a movement that by this time predominated in American academic psychiatry—that the delusions and hallucinations "frequently appear psychologically self-protective" (p. 33). In general, both DSM-I and DSM-II used the term "psychosis" as a synonym for "severe" rather than in some specific psychopathological sense.The "St. Louis criteria" of schizophrenia (1972). As part of the diagnostic rethinking leading up to DSM-III, John Feighner and the other members of the St. Louis school published in 1972 in the Archives of General Psychiatry an article on "Diagnostic Criteria for Use in Psychiatric Research." For schizophrenia, they offered a revised set of criteria, including mainly delusions and hallucinations plus some evidence of thought disorder. (There were also several social criteria such as being single and having a poor work history.)Three years later, in 1975, Michael Alan Taylor (1940–) and Richard Abrams (1937–) at the State University of New York at Stony Brook argued in the American Journal of Psychiatry that the St. Louis criteria set the bar too low, proposing more rigorous criteria of their own, including a "formal thought disorder" (not just difficulty in communicating), the presence of "emotional blunting," auditory hallucinations, or sudden, fully formed delusions. In a sample of 89 patients recently hospitalized for "schizophrenia," only 12% satisfied the St. Louis criteria, 11% satisfied the Taylor and Abrams research criteria, and only 5 patients were considered schizophrenic by both criteria.Finding metabolic abnormalities in schizophrenia: frontal lobes (1974). Although previous researchers had discovered numerous scattered brain abnormalities in schizophrenia, none had been reliably reproducible. In 1974, David Henschen Ingvar (1924–2000), professor of clinical neurophysiology at Lund University in Sweden, and Göran Anders Franzén (1929–), on-staff in the psychiatry department, discovered with the aid of radiolabeled xenon gas that blood flow was reduced in the frontal lobes of schizophrenia patients, especially older ones, compared to controls. This pointed to lower metabolic activity in the frontal lobes, meaning less activity in the neurons. In their article in Acta Psychiatrica Scandinavica they commented, "The finding of a significantly low resting blood flow in the frontal lobes (the ‘hypofrontal’ rCBF [regional cerebral blood flow] pattern) . . . warrants discussion of similarities between the symptoms in frontal lobe lesions and in chronic schizophrenia" (p. 457). They went on to point out numerous similarities between schizophrenia and organic frontal lobe lesions and helped direct attention of psychosis researchers to this area of the brain.First computerized tomography finding of brain abnormalities in schizophrenia (1976). A group of researchers led by Eve C. Johnstone (1944–), who had just received her M.D. from the University of Glasgow (see Women in Psychiatry), and Timothy J. Crow in the Divisions of Psychiatry and Radiology of the Clinical Research Centre in Harrow, Middlesex, England, found that, compared to controls, 17 institutionalized patients with schizophrenia had larger cerebral ventricles, and that increased ventricular size was "associated with poor performance on cognitive testing." This was the first finding of structural change in schizophrenia involving controls. It was published in the Lancet. (Gerd Huber’s [1921–] earlier finding in 1964 at Heidelberg University of organic defects in schizophrenia employed pneumoencephalography (see his article in Gruhle, ed., Psychiatrie der Gegenwart, vol. 1). (See Neuroimaging.)Much "schizophrenia" turns out to be manic-depressive illness (1978). In the Archives of General Psychiatry, Harrison G. Pope, Jr. (1947–) and Joseph F. Lipinski, Jr. (1940–), both of the Harvard University department of psychiatry, found in a review of studies that "schizophrenia" had been greatly overdiagnosed in United States psychiatry; manic-depressive illness (MDI) was similarly underdiagnosed. They also concluded that "‘Schizophrenic’ symptoms [as then understood] have virtually no demonstrated value in predicting outcome in psychoses" (p. 826). Furthermore: "Given that a patient, once misdiagnosed, is often misdiagnosed again and again, it is possible that there are upwards of 100,000 patients in this country carrying a diagnosis of schizophrenia who in fact suffer from MDI" (p. 825). This article helped shift the emphasis in psychosis from schizophrenia to affective disorder. Type I vs. Type II syndromes of schizophrenia (1980).Schizophrenia and psychosis in DSM-III (1980). Based on preliminary work by the St. Louis school, Taylor and Abrams, and the "RDC" criteria (see above), in DSMIII the psychoanalytic and Meyerian traditions were cast aside, and the classical German interpretations of psychopathology were given a new lease on life. The DSM drafters drew upon Emil Kraepelin in insisting that "deterioration from a previous level of functioning" be present before the diagnosis was granted. They drew upon Kurt Schneider’s first-rank symptoms in asserting that a certain "content of thought" was often present, involving such symptoms as thought insertion, thought withdrawal, and the delusion of thoughts being controlled by some outside power. And they drew upon Bleuler’s "basic symptoms" in saying that schizophrenics often had a certain "form of thought" involving the loosening of associations: "When loosening of associations is severe, incoherence may occur, that is, speech may become incomprehensible" (p. 182). (The points in this section are referenced at Schizophrenia: Emergence.)One can see virtually the entire European tradition of psychopathology culminating in the symptoms that the DSM drafters were willing to accept: disorders of perception involving, in particular, auditory hallucinations, the blunting of affect, the diminution of drive. Dereism, catatonia, and other symptoms from the classic tradition also received their toll.Yet, the actual checklist of symptoms for which—in the familiar DSM-III style—the patient would have to qualify in order to receive the diagnosis was heavily weighted toward Kraepelinian "positive" symptoms (Kraepelin did not use the phrase "positive"). Of the six "class A" diagnostic criteria, five involved hallucinations and delusions. (Class B involved deterioration; class C stipulated a minimum 6 months’ duration.) Thus, the American DSM-III shifted the balance away from the generous Bleulerian view with its optimistic prognoses and back to the restrictive Kraepelinian with its florid psychoses and dim prognosis. It was partly for this reason (and partly because DSM-III represented a revival of "disease-thinking" in general) that Gerald Klerman referred to it in 1990 as "neo-Kraepelinian." DSM-III granted independent status to schizoid personality. As well, in DSM-III several other diagnoses once grouped under the schizophrenia umbrella became independent. "Paranoia," "schizophreniform disorder," and "brief reactive psychosis" all acquired statuses of their own. Psychotic depression became firmly arrayed under affective disorders, and "schizoaffective disorder" and "atypical psychosis" also struggled free.When the definitions conventionally used in U.S. psychiatry in the 1960s were applied to a group of patients, 163 qualified for the diagnosis of schizophrenia. When the DSM-III criteria were applied to the same group, only 19 did so. As English psychiatrist Ian Brockington noted in European Psychiatry in 1992, "There must be something profoundly wrong with a concept which has proved so unstable in its usage" (p. 203). (See also Wernicke–Kleist–Leonhard Pathway.)First quantitative magnetic-resonance study of schizophrenia (1986). Nancy Andreasen at the University of Iowa led a team using the neuroimaging technique of magnetic resonance imaging (MRI) to establish that schizophrenic patients had smaller frontal lobe size and also smaller intracranial and cerebral volume. This led the group, publishing in the Archives of General Psychiatry in 1986, to reinforce the hypothesis that schizophrenia was a "neurodevelopmental" disorder. In this work, they also pioneered a technique for making quantitative measurements of MRI images that eventuated in "voxel-based morphimetry."Weinberger launches the "DLPFC" hypothesis (1986). Although researchers had long known there was some kind of frontal lobe problem in schizophrenia, in 1986 Daniel Weinberger (1947–), of the Section on Clinical Neuropsychiatry of the National Institute of Mental Health at St. Elizabeths Hospital in Washington, D.C., suggested that some of the symptoms of schizophrenia—both positive and negative— were owing to a lesion in the dorsolateral prefrontal cortex (DLPFC). The researchers had looked at regional blood flood in schizophrenics as compared to controls as they inhaled radiolabeled xenon gas (Xe 133): While doing a card-sorting test, the controls experienced a clear rise in blood flow in that area, whereas that of the schizophrenics underwent no change, suggesting lowered responsiveness (lesion) in that area of the brain. "The changes were regionally specific, involving only DLPFC" (p. 114). This research in the Archives of General Psychiatry promised to "shed light on one of the most physiologically mysterious aspects of schizophrenia—its tendency to appear in late adolescence." Weinberger analogized to other kinds of central nervous system lesions "the clinical manifestations of which appear or change with maturation as the affected neural system comes ‘on line’ " (p. 123).Location of a possible single-gene locus for schizophrenia (1988). In work led by Robin Sherrington in the psychiatry department of the former Middlesex School of Medicine of the University of London, a group of nine co-authors reported in an article in Nature that two DNA "polymorphisms" (variant forms) on the long arm of Chromosome 5 were reliably linked to seven families in Britain and Iceland with histories of schizophrenia. The finding remained tentative because other groups at the time were not able to reproduce it. (See also PSYCHIATRIC GENETICS .)Late onset schizophrenia (1997). In 1997 in the American Journal of Geriatric Psychiatry, Dilip V. Jeste (1944–) and co-workers at the University of California at San Diego proposed the concept of "late onset schizophrenia" (LOS). Three years later, in 2000, at a consensus conference led by Robert Howard (1961–) of the Institute of Psychiatry in London, late onset schizophrenia replaced such older concepts as "paraphrenia in the elderly."(See Paraphrenia).
Edward Shorter. 2014.