Differential aversive Pavlovian conditioning with a foul odor as unconditioned stimulus (US) and neutral faces as conditioned stimuli (CS) was compared between 9 noncriminal psychopaths as defined by the Hare Psychopathy Checklist Revised and 12 healthy controls. Event-related potentials (ERP), heart rate, skin conductance response, corrugator EMG, and startle response potentiation as well as valence, arousal, and contingency of the CS were assessed. Whereas the healthy controls (HC) showed significant CS +/CS- differentiation, the psychopaths (PP) failed to exhibit a conditioned response although unconditioned responses were comparable between the groups. N100, P200, and P300 to the CSs revealed that psychopaths were not deficient in information processing and showed even better anticipatory responding than the HC group indicated by the terminal contingent negative variation (tCNV), that lacked, however, CS+ and CS- differentiation. These data indicate a deficit in association formation in psychopaths that may be related to deficient interaction of limbic-subcortical and cortical structures.

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Aversive pavlovian delay conditioning was investigated in a sample of 11 criminal psychopaths as identified by using the Psychopathy Checklist-Revised and 11 matched healthy controls. A painful electric stimulus served as unconditioned stimulus and neutral faces as conditioned stimuli. Event-related potentials, startle response potentiation, skin conductance response, corrugator activity, and heart rate were assessed, along with valence, arousal, and contingency ratings of the CS and US. Compared to healthy controls, psychopathic subjects failed to differentiate between the CS+/CS- as shown by an absence of a conditioned response in startle potentiation and skin conductance measures. Through use of a fear-eliciting US, these data confirm previous findings of a deficient capacity to form associations between neutral and aversive events in psychopathy that appears unrelated to cognitive deficits and is consistent with hypothesized frontolimbic deficits in the disorder.