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This paper reports on an attempt to investigate empirically whether the common personality dimensions S or Insensitivity, E or Extraversion, N or Neuroticism, and G or Orderliness, as postulated in Van Kampen's modification of Eysenck's PEN model, would in principle give rise to the same level of predictive accuracy as a set of personal traits obtained in each of a series of assessments of separate individuals. Using a special methodology to ‘convert’ the nomothetic dimensions into factors that are of idiographic relevance, (within-person) correlations and multiple correlations between the idiographic traits and the nomothetic dimensions S, E, N, and G (predictors) were computed in a sample of 83 subjects. Results showed that the idiographic traits could be expressed in most cases as linear combinations of the four idiographically converted nomothetic factors, and that the degree to which an individual's idiographic data could be explained nomothetically was unrelated to this individual's conformity to the nomothetic zero-correlational structure of the four dimensions. Copyright © 2000 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Postulating that the predisposition to illness in Claridge's disease model of schizophrenia can be equated with the personality dimensions S or Insensitivity, (low) E or Extraversion, and N or Neuroticism, as measured by Van Kampen's 3DPT, and assuming that the mode of transmission of schizophrenia is basically polygenic, the genetic and environmental etiology of S, E, and N was assessed in a sample of 52 MZ and 76 DZ twin pairs and their parents by means of LISREL. Besides, in a sample of 2118 subjects MAXCOV–HITMAX analyses were conducted for these factors as well as for the personality dimension G or Orderliness, but now assessed by the 4DPT, in order to find out whether a discrete or quasi-discrete variable might also underlie these dimensions, giving support to the possibility of dominance or epistasis. The results obtained in these investigations favoured a model for all three dimensions, allowing for both additive and non-additive genetic effects in combination with non-shared environmental influences. It was not possible to choose between a model involving dominance and a model involving epistatic genetic effects. With the use of scores corrected for sex and age, which were converted to normal scores, the proportion of variance explained by additive genetic factors was 20% for S, 40–41% for E, and 26–29% for N. Dominance or multiple-gene epistasis accounted for 37–38% (S), 19–20% (E), and 30–31% (N), and unshared environmental influences for 42–43% (S), 41% (E), and 42–43% (N) respectively. Copyright © 1999 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]