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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.
University Department of Psychiatry, Psychiatric Center Hvidovre, Copenhagen, Denmark.
This article was published in the following journal.
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Diagnoses of DEMENTIA and AMNESTIC DISORDER are subsumed here. (DSM-5)
Disturbances in registering an impression, in the retention of an acquired impression, or in the recall of an impression. Memory impairments are associated with DEMENTIA; CRANIOCEREBRAL TRAUMA; ENCEPHALITIS; ALCOHOLISM (see also ALCOHOL AMNESTIC DISORDER); SCHIZOPHRENIA; and other conditions.
A dibenzothiazepine and ANTIPSYCHOTIC AGENT that targets the SEROTONIN 5-HT2 RECEPTOR; HISTAMINE H1 RECEPTOR, adrenergic alpha1 and alpha2 receptors, as well as the DOPAMINE D1 RECEPTOR and DOPAMINE D2 RECEPTOR. It is used in the treatment of SCHIZOPHRENIA; BIPOLAR DISORDER and DEPRESSIVE DISORDER.
A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia.
A chronic form of schizophrenia characterized primarily by the presence of persecutory or grandiose delusions, often associated with hallucination.
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