IQ deficits in each diagnostic category may reflect different functional patterns and temporal vicissitudes of the specific pathogenetic processes involved in different mental disorders.

No abstract

Eugen Bleuler, the founder of the concept of schizophrenia, pointed out that psychotic patients were able to live in two disjoint worlds (namely, the social, intersubjective world and the delusional world). He termed this phenomenon “double bookkeeping,” but did not provide any conceptual elaboration of this phenomenon or its possible mechanisms. Double bookkeeping has been neglected in mainstream psychiatry, but it has been addressed in recent theoretical work, however mainly concerned with the issue of delusion. In this article, we present clinical material that supports the view that double bookkeeping manifests itself across various psychotic phenomena and its antecedent may be observed in premorbid (pre-onset) phases as well as in the schizotypal disorder. We try to conceptualize double bookkeeping to concretize an often atmospheric perception of paradoxicality in the encounter with the patient. A phenomenological analysis of double bookkeeping suggests an instability in the affective (“auto-affection”) articulation of selfhood. We point to four main implications of our presentation: (1) diagnostic, (2) epistemological, (3) therapeutic and (4) pathogenetic research.

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.