The Copenhagen High-risk Project, 1962-86

Mednick, Sarnoff A.; Parnas, Josef; Schulsinger, Fini

doi:10.1093/schbul/13.3.485

Cited by 156 publications

(78 citation statements)

References 43 publications

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“…longitudinal follow-up studies of offspring of patients with schizophrenia [83,86,87] . The high-risk studies have decisively challenged the picture of schizophrenia as a temporally well-demarcated disorder with datable onset.…”

Section: Biological Considerationsmentioning

confidence: 99%

Core of Schizophrenia: Estrangement, Dementia or Neurocognitive Disorder?

Urfer-Parnas¹,

Mortensen²,

Parnas³

2010

Psychopathology

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Background: The recent literature frequently represents schizophrenia as a deteriorating neurocognitive process similar to organic degenerative dementia. Methods: This study addresses the following questions: (1) Did the classic authors equate degenerative dementia with schizophrenia? (2) Is there empirical evidence pointing to a close similarity between schizophrenia and organic dementia? (3) Does empirical evidence support the view that intellectual impairment and/or more specific neuropsychological dysfunctions are core features of schizophrenia? The classic authors agreed that the intellectual dysfunctions were most likely a consequence rather than a primary, causal factor in the manifestation of schizophrenia despite their consensus on the assumption of its neurobiological origins. Rather, they considered impairments of intelligence and neurocognition as an expression of pseudodementia, i.e. a dementia-like clinical picture caused by a weakening of motivation. Results: The empirical data from the draft, high-risk birth cohort and clinical samples show a low IQ and a variety of neurocognitive dysfunctions in schizophrenia. These findings are far from universal since substantial proportions of patients do not show deficits. In addition, the empirical morphological and neuropathological evidence does not support any close analogy of schizophrenia with neurodegenerative dementia. Moreover, neurocognitive dysfunctions cannot be considered a core feature of schizophrenia if core is understood as ‘essential’, i.e. constitutive of a diagnosis, or as ‘generative’, i.e. symptom producing. In the phenomenological psychopathological tradition, schizophrenia is seen as a progressive condition marked by autism, which is a profound alteration in the structures (frameworks) of subjectivity (consciousness), manifest in self-relation (self-disorders) and in the relation to the world (lack of natural evidence) and to others (eccentricity, solipsism and isolation). Conclusion: It is suggested that the neurodevelopmental model should integrate interactions between emerging psychological structures and genetic and environmental factors.

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Section: Biological Considerationsmentioning

confidence: 99%

Core of Schizophrenia: Estrangement, Dementia or Neurocognitive Disorder?

Urfer-Parnas¹,

Mortensen²,

Parnas³

2010

Psychopathology

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“…These strategies do often, though not always, implicate each other. In our view, the pervasive estrangement from the communal world and the difficulties that these patients often experience in the social domain are not primarily a product of fluctuating psychotic symptoms [89,90] but linked to their self-disorders [32] . As described earlier, self-disorders may impede the process of group identification, which is a necessary condition for "we-intentionality."…”

Section: Complicated "We" and Self-disordersmentioning

confidence: 99%

Intersubjectivity and Psychopathology in the Schizophrenia Spectrum: Complicated We, Compensatory Strategies, and Self-Disorders

Henriksen

Nilsson

2017

Psychopathology

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Recent studies in phenomenological psychopathology emphasize the importance of intersubjectivity for our understanding of schizophrenia. Yet, the central role of the “we” in social experience and engagement is largely absent from this literature. Our study explores the relation between psychopathology and intersubjectivity in the schizophrenia spectrum through the prism of the “we.” First, we explore the role of intersubjectivity in the current schizophrenia spectrum definitions and discuss the main contemporary research trends. Second, we recollect some of the classical accounts of schizophrenia, which offer a different perspective on the pervasive and often persistent intersubjective difficulties in these conditions. Third, capitalizing on recent advances in collective intentionality studies, we present and discuss a conceptual framework of the “we” and of how the “we” may be disrupted in schizophrenia. Through this framework and with the use of clinical vignettes, we elicit 3 compensatory strategies, which, we suggest, reflect a fragile sense of “we” in the schizophrenia spectrum, i.e. (i) positive withdrawal, (ii) imposing a goal-oriented, spatiotemporal structure on intersubjective engagement, and (iii) preferring social activities with a clear attribution of social roles and rules. Finally, we discuss the relation between anomalous self-experiences (i.e. self-disorders) and the complicated “we.”

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“…Brains of schizophrenics were reported to show alterations in the cell arrangement in the hippocampus (Scheibel and Kovelman, 1981;Kovelman and Scheibel, 1984; but see Altshuler et al, 1987), and it has been suggested that this is due to a disturbed process of cell migration as a result of maternal viral infection during the second trimester Mednick et al, 1987). In addition to the hippocampus, structural abnormalities in the entorhinal cortex might indicate a disturbance of neuronal migration in month 4 or 5 of gestation (Jacob and Beckman, 1986; see also Falkai et al, 1988).…”

Section: Morphological Changes In Hippocampus and Related Areas Are Pmentioning

confidence: 99%

Hippocampal dysfunction in schizophrenia

Schmajuk

2001

Hippocampus

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Although not necessarily primary to the disease, hippocampal dysfunction in schizophrenia is suggested by morphological changes in the hippocampal formation reported in schizophrenic patients. This notion receives additional support from studies showing that 1) similar behavioral deficits are exhibited by both schizophrenics and animals with hippocampal lesions, and 2) some of these behavioral deficits are reversed by neuroleptics in both schizophrenics and lesioned animals. A brain-mapped neural network model is used to explain how some impairments in attention can be caused by hippocampal dysfunction and ameliorated by dopaminergic blockers.

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The Copenhagen High-risk Project, 1962-86

Cited by 156 publications

References 43 publications

Core of Schizophrenia: Estrangement, Dementia or Neurocognitive Disorder?

Core of Schizophrenia: Estrangement, Dementia or Neurocognitive Disorder?

Intersubjectivity and Psychopathology in the Schizophrenia Spectrum: Complicated We, Compensatory Strategies, and Self-Disorders

Hippocampal dysfunction in schizophrenia

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