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DOI: 10.1055/s-0038-1628372
Neurobiologische Korrelate der Verarbeitung von Feedback bei antisozialer Persönlichkeitsstörung
Neurobiological correlates of feedback processing in antisocial personality disorderPublication History
Eingegangen am:
01 September 2010
angenommen am:
14 September 2010
Publication Date:
22 January 2018 (online)
Zusammenfassung
Gegenstand und Ziel: Wir untersuchten die neuronalen Mechanismen der Verarbeitung von Belohnungssignalen bei Personen mit antisozialer Persönlichkeitsstörung (APS) mithilfe der funktionellen Magnetresonanztomografie (fMRT) und die Modulation dieser Aktivierungsmuster durch eine serotonerge Substanz, mCPP. Material und Methoden: Studie 1: Acht Personen mit Cluster B (antisoziale oder Borderline)-Persönlichkeitsstörung und 14 Kontrollpersonen. Studie 2: 23 Probanden mit APS und 25 Kontrollprobanden. In beiden Studien kam eine Belohnungsaufgabe zum Einsatz, in Studie 1 wurde zusätzlich ein Verlustparadigma eingesetzt. In Studie 2 erhielt ein Teil der Teilnehmer mCPP vor der Belohnungsaufgabe. Ergebnisse: In Studie 1 zeigte sich eine verminderte Aktivierung vorwiegend präfrontaler Strukturen in der Patientenim Vergleich zur Kontrollgruppe. In Studie 2 konnte eine vermehrte Ansprechbarkeit des Belohnungssystems nach mCPP-Gabe, vor allem in der APSGruppe, gezeigt werden. Schlussfolgerungen: Die Studien bestätigten die Rolle präfrontaler Strukturen in der Entstehung der APS. Serotonin scheint nicht nur in impulsivem Verhalten, sondern auch in der Verarbeitung von Belohnungen eine Rolle zu spielen. Klinische Relevanz: Serotonerge Substanzen führen möglicherweise zu einer Normalisierung von neuronalen Aktivierungsmustern bei antisozialen Patienten.
Summary
Objective: To investigate the neuronal mechanisms of reward in individuals with antisocial personality disorder (ASPD) using functional magnetic resonance imaging (fMRI) and their modulation following a serotonergic intervention with mCPP. Material and methods: Study 1: Eight individuals with Cluster B (antisocial or borderline) PD and 14 control subjects. Study 2: 23 participants with ASPD and 25 control subjects. In both studies a block design reward task was used, in study 1 a loss task was also employed. Study 2 used mCPP to explore modulation of brain activations in both groups. Results: In study 1 we found decreased activations particularly in prefrontal brain structures in the patient compared to the control group. In study 2 increased neuronal activations were observed following mCPP compared to placebo, particularly in the patient group. Conclusions: Our studies confirmed that altered brain function, particularly in prefrontal structures, may underpin antisocial personality disorders. Serotonin appears to play a role not only in impulsivity but also in reward processing. Clinical relevance: Serotonergic substances might normalise neuronal activations in antisocial individuals.
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