[The role of premorbid personality in the genesis of psychopathological symptomatology in patients with organic anxiety-depressive disorder, schizophrenia and endogenous depression].

OBJECTIVE

The current study has been performed in order to find the influence of premorbid personality traits on psychopathological symptomatology in patients with endogenous depression (ED), schizophrenia and organic anxiety-depressive disorder (OADD).

MATERIAL AND

METHODS

191 patients (57 with OADD,93 with schizophrenia and 41 with ED) were included into study. The Munich personality test (MPT) and Toronto alexithymia scale (TAS) were used for the evaluation of premorbid personality; the SCL-90 - for the assessment of psychopathological structure. The multiple regression analysis has been used for the assessment of relationships between premorbid personality constructs and psychopathological status separately in each diagnostic group.

RESULTS

The SCL-90 scores were maximal in ED and schizophrenia patients and minimal in OADD patients (p<0.047). Comparison of premorbid personality constructs revealed the maximal values of neuroticism and motivation in ED (p=0.005), rigidity, extraversion and esoteric tendencies in schizophrenia (p<0.007) and frustration tolerance, tendency to isolation and alexithymia in OADD (p<0.02). Regression analysis revealed the positive dependence of anxiety and depression on alexithymia score (TAS-26) (p<0.002) and negative dependence on frustration tolerance in ED and schizophrenia patients (p<0.016). The negative dependence of anxiety Zung scale score on frustration tolerance in OADD patients also has been observed (p=0.003). The rigidity construct has not stochastically significant relationships neither with anxiety, nor with depression in none diagnostic group.

CONCLUSION

The analysis revealed the predominance of certain personality constructs in each of the diseases, with a universal negative effect of alexithymia and a positive effect of frustration tolerance in anxiety-depressive disorders of any etiology.