[Oxytocin in schizophrenia : Evidence for an etiological and therapeutic relevance of the social neuromodulator].

Neurobiological results from animal models as well as biochemical and genetic findings in patients indicate that the oxytocin (OT) system may be dysfunctional in schizophrenia. On this pathogenetic basis transnasally administered OT (tnOT) could be an innovative treatment option for schizophrenia. Experimental data from animal studies are also suggestive of a particular effectiveness in treatment-resistant schizophrenia. To date, clinical data on tnOT treatment of schizophrenia patients does not unequivocally support a general therapeutic effect on the psychopathology but suggests positive effects on higher integrated social cognitive performance, such as empathy and mentalization. In particular, tnOT augmentation of a social cognitive skills training resulted in a marked and lasting treatment effect; however, numerous person- and context-dependent variables can potentially moderate individual effects of OT and may even reverse effects in certain constellations. Most clinical studies so far have not systematically accounted and controlled for these factors with the probable result of larger variance of recorded treatment effects and lower likelihood of ascertaining positive effectiveness. Furthermore, there is still a gap of knowledge on dose response relations and central nervous system (CNS) permeation in man following tnOT administration. This review aims to give a concise overview on the evidence for the etiological relevance of the neurohormone OT and its treatment potential in schizophrenia.