Page:Jung - The psychology of dementia praecox.djvu/58

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THE PSYCHOLOGY OF DEMENTIA PRÆCOX.

destined to regulate our relations to our environments and to direct our adaptation to the same, which are a protection to the organism and represent the motive powers of self-preservation, are alienated from their natural destiny. Owing to the organically strong feeling tone of the delusional stream of thought, no matter what the emotional state may be, this and this only is always reproduced. These fixations of the affects destroy the ability of feeling joy or compassion and lead to an emotional isolation of the patient which runs parallel with the intellectual alienation."

Neisser describes here the familiar picture of apperceptive dementia. Lack of new acquisition, paralysis of purposeful progress (adapted to reality), disintegration of personality and autonomy of complexes. Finally, he adds the "Fixierung der Affecte" (fixation of affects), that is, the fixation of the emotionally accentuated complexes (for affects have always regularly an intellectual content, though it is not always known). From this he explains the emotional dementia (Masselon invented for this the fitting expression "clotting"). Following Freud, fixation of affects means that the repressed complexes (the carriers of affects) can no more be disconnected from the contents of consciousness, they remain and so prevent the further development of personality.

To avoid misconceptions I must here add that the continued persistence of a strong complex in normal psychic life can lead only to hysteria. Yet the consequent manifestations of the hysterogenic affect are different from the symptom-complex of dementia præcox. For the origin of dementia præcox we must demand a totally different disposition than we do for hysteria. If a purely hypothetical supposition be permitted one could perhaps venture the following train of thought: The resultant manifestations of the hysterogenic complex are reparable, while the affect of dementia præcox gives opportunity for the appearance of an anomalous metabolism (toxine?), which injures the brain in a more or less irreparable manner, so that in consequence of this defect the highest psychic functions become paralyzed. It is for this reason that the acquisition of new complexes becomes difficult or ceases altogether. The pathogenic or rather the inciting complex remains to the last, and the further development of