Impulsivity, the orbitofrontal cortex and borderline personality disorder
Damage to the orbitofrontal cortex (OFC) has been associated with disinhibited or socially inappropriate behaviour and emotional irregularities in both humans and monkeys. Prominent characteristics of several personality disorder syndromes, in particular Borderline Personality Disorder (BPD), are impulsivity and affective instability. This investigation aimed to determine if certain aspects of the Borderline Personality syndrome, in particular impulsivity, are associated with OFC dysfunction. Basic questionnaires of personality, emotion, and impulsivity together with tasks sensitive to frontal lobe dysfunction that assess possible factors related to impulsivity, including time perception, sensitivity to reinforcers, and spatial working memory (SWM), were administered to OFC lesion, BPD, non-OFC prefrontal cortex lesion control, and normal control participants. OFC and BPD patients performed similarly, in that they were more impulsive, reported more inappropriate behaviours, BPD traits, anger, and less happiness than both control groups. They were also less open to experience and had a faster perception of time (in terms of time production) than normal controls. They performed differently on other tasks: BPD patients were less extraverted and conscientious and more neurotic and emotional than all other groups. OFC patients had more severe deficits in reversing stimulus-reinforcer associations compared to all other groups and had a faster perception of time (in terms of time estimation) than normal controls. Both OFC and non-OFC lesion patients had mixed lesions that included dorsolateral prefrontal cortex (DLFC) damage. Accordingly, they both had SWM deficits, a task used to control for DLFC damage, compared to normal and BPD participants. Since BPD participants were not impaired on this task and non-OFC patients did not perform poorly on the same tests that OFC patients did, the neuropsychological deficits of BPD and OFC patients could not be attributed to SWM deficits or DLFC dysfunction. The findings suggest that some of the cognitive/behavioural deficits commonly found in BPD patients are related to OFC dysfunction while others are unrelated and are perhaps related to other brain systems. The possibility of amygdala dysfunction is discussed. The similarities and dissociations found between BPD and OFC patients on certain tasks may lead to a better understanding of the aetiology of BPD and the functions of the OFC. Theoretical and therapeutic implications of the findings are discussed.