Seymour S. Kety and the Genetics of Schizophrenia

Holzman, Philip S.

doi:10.1016/s0893-133x(01)00276-7

Cited by 14 publications

(4 citation statements)

References 19 publications

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“…All of these can be observed in schizophrenic patients as well as their relatives (e.g., Crawford et al 1998;Lencer et al 2000;Kojima et al 2001). For smooth pursuit eye movements (SPEM) a genetic linkage to a polymorphism on the short arm of chromosome 6 has recently been shown and replicated (Arolt et al 1996;Holzman 2001). There is evidence that the SPEM-deficit is associated with negative symptoms in schizophrenic patients , as well as with traits for "sensitivity" and "suspiciousness" in relatives (Lencer et al 2003) and in individuals with schizotypal personality (O'Driscoll et al 1998).…”

Section: Natural Selection and Schizophreniamentioning

confidence: 99%

An evolutionary theory of schizophrenia: Cortical connectivity, metarepresentation, and the social brain

2004

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Schizophrenia is a worldwide, prevalent disorder with a multifactorial but highly genetic aetiology. A constant prevalence rate in the face of reduced fecundity has caused some to argue that an evolutionary advantage exists in unaffected relatives. Here, I critique this adaptationist approach, and review – and find wanting – Crow's “speciation” hypothesis. In keeping with available biological and psychological evidence, I propose an alternative theory of the origins of this disorder. Schizophrenia is a disorder of the social brain, and it exists as a costly trade-off in the evolution of complex social cognition. Paleoanthropological and comparative primate research suggests that hominids evolved complex cortical interconnectivity (in particular, frontotemporal and frontoparietal circuits) to regulate social cognition and the intellectual demands of group living. I suggest that the ontogenetic mechanism underlying this cerebral adaptation was sequential hypermorphosis and that it rendered the hominid brain vulnerable to genetic and environmental insults. I argue that changes in genes regulating the timing of neurodevelopment occurred prior to the migration of Homo sapiens out of Africa 100,000–150,000 years ago, giving rise to the schizotypal spectrum. While some individuals within this spectrum may have exhibited unusual creativity and iconoclasm, this phenotype was not necessarily adaptive in reproductive terms. However, because the disorder shared a common genetic basis with the evolving circuitry of the social brain, it persisted. Thus schizophrenia emerged as a costly trade-off in the evolution of complex social cognition.

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Section: Natural Selection and Schizophreniamentioning

confidence: 99%

An evolutionary theory of schizophrenia: Cortical connectivity, metarepresentation, and the social brain

2004

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“…A deficit of pursuit maintenance together with an excess of mainly catch-up saccades has also been observed during predictive pursuit tasks in schizophrenic patients and their healthy relatives (Holzman et al 1974 ;Myles-Worsley et al 1991;Arolt et al a, 1998Lencer et al 1999Lencer et al , 2000Levy et al 2000). There is evidence that this dysfunction is a phenotypic marker for schizophrenia that might be linked to markers on chromosome 6p23-21 (Arolt et al 1996b(Arolt et al , 1999Holzman, 2001 ;Lencer et al 2003). In contrast, latencies and accuracy of saccades elicited by the target step in step-ramp paradigms were normal.…”

Section: Introductionmentioning

confidence: 98%

Smooth pursuit deficits in schizophrenia, affective disorder and obsessive–compulsive disorder

et al. 2004

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Unaltered saccadic parameters indicate intact motion perception in cortical visual area V5. Therefore, the observed deficit of pursuit maintenance implies a dysfunction of frontal networks in all patient groups including the pursuit region of the frontal eye field (FEF). In patients with schizophrenia and affective disorder reduced post-saccadic pursuit initiation may indicate an impaired interaction between the pursuit and the saccadic system.

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“…The DSM-III Seymour S. Kety, with his studies of the genetics of schizophrenia (Holzman, 2001), resurrected in the United States the concept of schizophrenia proposed by Kraepelin. In a 1978 book chapter, Klerman called Eli Robins and Samuel Guze "neo-Kraepelinians" because they followed Kraepelin's model, but in his chapter baptizing them with this name, Klerman explained that Robins and Guze simply read Mayer-Gross' textbook (Klerman, 1978).…”

Section: The Psychopharmacology Revolution In the United Statesmentioning

confidence: 99%

Reflections on US Psychiatry

León

2021

J Nerv Ment Dis

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The medical model in psychiatry and descriptive psychopathology were established in Germany by Krapelin's textbook and Jaspers' General Psychopathology. In the United Kingdom, Mayer-Gross' textbook synthesized both books, influencing US psychiatry. US psychiatrists from the World War II generation defeated the US academic psychoanalytic establishment by building three pillars: biological psychiatry (brought by Wortis), the psychopharmacology revolution, and the Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition (DSM-III). The psychopharmacology revolution included immigrants (e.g., Gershon), Cole's marketing, and textbooks by Klein and Fink. The "neo-Kraepelinians" introduced the medical model in US psychiatry and defined 15 valid psychiatric disorders. Spitzer supervised DSM-III's development. Its 1980 publication started the world dominance of US psychiatry and the multiplication of diagnoses. Major contributions by US psychiatrists include a) McHugh's update of the Jaspersian approach, b) Fink's inclusion of catatonia as a syndrome in DSM-5 (following Abrams and Taylor's studies), and c) DSM-III's departure from the Jaspersian hierarchy of schizophrenia and affective symptoms.

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Seymour S. Kety and the Genetics of Schizophrenia

Cited by 14 publications

References 19 publications

An evolutionary theory of schizophrenia: Cortical connectivity, metarepresentation, and the social brain

An evolutionary theory of schizophrenia: Cortical connectivity, metarepresentation, and the social brain

Smooth pursuit deficits in schizophrenia, affective disorder and obsessive–compulsive disorder

Reflections on US Psychiatry

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