The goal of the this study was to test the hypotheses that (a) BPD patients are characterized by abnormal reward processing even during a euthymic state; and (b) the presence of residual anhedonic symptoms would exacerbate this dysfunction. Using a probabilistic reward task, which assesses how behavior is modulated by reinforcement history, we found that both euthymic and symptomatic BPD patients showed reduced and delayed acquisition of response bias toward the more frequently rewarded stimulus, even after controlling for residual depressive or anhedonic symptoms. In addition, BPD patients reporting anhedonic symptoms in their daily life (e.g., loss of pleasure) showed the most impaired reward learning. Highlighting the specificity of this finding, a relationship between anhedonic symptoms and reduced response bias remained after controlling for subjects’ residual manic and anxious symptoms as well as general distress, replicating recent findings from two non-clinical samples (15
) and a medication-free sample with major depressive disorder (Pizzagalli, Iosifescu, Hallett, Ratner, Fava, unpublished). Unlike our recent findings in major depression, BPD patients exhibited cumulative learning over the course of the three blocks; however, the blunted nature of the response bias and its delayed acquisition point to a dysfunctional integration of reward information in early phases of the experiment.
Of note, additional analyses indicated that reduced response bias in BPD patients was not due to general task deficits, as evident from the lack of group differences in discriminability or reaction time. Rather, the performance of BPD participants was characterized by their increased tendency to misclassify the more frequently rewarded (rich) stimulus, whereas they showed no differences from comparison subjects in classifying the lean stimulus. Interestingly, elevated miss rates for the rich stimulus emerged only when it was immediately preceded by either a non-rewarded rich stimulus, or by a rewarded lean stimulus, indicating that BPD subjects were impaired in developing a response bias toward the more frequently rewarded stimulus in the absence of a proximal rich reward or after receiving a reward for the less advantageous response.
The finding of increased misclassification of the rich stimulus immediately after a rewarded lean stimulus is intriguing, particularly in light of theoretical accounts linking BPD to dysregulation of the behavioral approach system (BAS; 39–41), a system assumed to regulate appetitive motivation and goal-directed behavior in response to signals of reward (42
). Notably, in BPD, increased
BAS sensitivity and experiences of goal-striving and -attainment events predicted future manic symptoms (43
) and behavioral activation scores distinguished euthymic BPD patients from healthy controls (46
). The current finding that reduced response bias toward the more frequently rewarded stimulus was partially explained by increased sensitivity and behavioral switching following rewards of the less advantageous (lean) stimulus is consistent with the general hypothesis of heightened responsivity to minimal environmental incentives in BPD (39
) . Our results also extend a recent report of maladaptive BAS hypersensitivity in subjects with bipolar spectrum disorder (47
). In the current study, an increased sensitivity to the infrequently occurring lean reward might, in turn, have led to impaired cumulative reward learning in BPD subjects.
Overall, the present findings of impaired integration of reward feedback are in line with recent reports showing that medicated euthymic and acutely manic BPD patients displayed an increased tendency to select the less favorable of two possible response options in a gambling task (14
) and exhibited deficits in learning fluctuating stimulus-reward contingencies (12
). Moreover, since omission of reward could be interpreted by the participants as reflecting a potential erroneous response, the increased miss rate observed in trials immediately following a non-rewarded rich trial is consistent with a prior finding of increased behavioral switches after error feedback in mania (14
). Unlike prior studies however, the current findings provide direct evidence that BPD, even during euthymic states, is characterized by reduced and delayed integration of reinforcements over time, and thus provide novel insights about the potential source of dysfunctional reward processing in this disorder.3
The limitations of the present study should be acknowledged. First, the sample of BPD, particularly euthymic, patients was relatively small, and all patients were medicated. We note that all prior studies investigating reward processing in BPD have also assessed medicated subjects (6
), highlighting the practical and ethical difficulties of investigating medication-free BPD subjects. Second, no patient was in a manic state, and the range of clinical symptomatology was limited. Thus, it is unclear whether acutely manic BPD patients might show potentiated
, rather than blunted, reward learning. Third, patients with a history of substance use dependence were excluded to avoid potential confounds deriving from possible dopaminergic abnormalities that characterize these disorders (21
). Thus, it is unclear whether our findings will generalize to other BPD samples. Fourth, only reward feedbacks were included, so future studies will be needed to evaluate whether BPD patients might show deficits in other types of incentive learning (e.g., punishment feedback).
In sum, BPD patients, particularly those with residual anhedonic symptoms, showed reduced behavioral bias toward a more frequently rewarded stimulus. Future studies will be required to evaluate whether this abnormality is associated with dysfunction in brain regions coding the representation of reward values (e.g., orbitofrontal cortex; 48, 49) and/or the down-regulation of dopaminergic synaptic mechanisms, which have been hypothesized to follow the hyperdopaminergic state observed in mania (4