Previous research has shown that patients with schizophrenia are impaired in reinforcement learning tasks. However, behavioral learning curves in such tasks originate from the interaction of multiple neural processes, including the basal ganglia-and dopaminedependent reinforcement learning (RL) system, but also prefrontal cortex-dependent cognitive strategies involving working memory (WM). Thus, it is unclear which specific system induces impairments in schizophrenia. We recently developed a task and computational model allowing us to separately assess the roles of RL (slow, cumulative learning) mechanisms versus WM (fast but capacity-limited) mechanisms in healthy adult human subjects. Here, we used this task to assess patients' specific sources of impairments in learning. In 15 separate blocks, subjects learned to pick one of three actions for stimuli. The number of stimuli to learn in each block varied from two to six, allowing us to separate influences of capacity-limited WM from the incremental RL system. As expected, both patients (n ϭ 49) and healthy controls (n ϭ 36) showed effects of set size and delay between stimulus repetitions, confirming the presence of working memory effects. Patients performed significantly worse than controls overall, but computational model fits and behavioral analyses indicate that these deficits could be entirely accounted for by changes in WM parameters (capacity and reliability), whereas RL processes were spared. These results suggest that the working memory system contributes strongly to learning impairments in schizophrenia.

The aim of the present study was to examine the contributions to decision making (DM) deficits in schizophrenia (SZ) patients, of expected value (EV) estimation and loss aversion. Patients diagnosed with SZ (n=46) and healthy controls (n=34) completed two gambling tasks. In one task, participants chose between two options with the same EV across two conditions: Loss frames and Keep frames. A second task involved accepting or rejecting gambles, in which gain and loss amounts varied, determining the EV of each trial. SZ patients showed a reduced “framing effect” relative to controls, as they did not show an increased tendency to gamble when faced with a certain loss. SZ patients also showed a reduced tendency to modify behavior as a function of EV. The degree to which choices tracked EV correlated significantly with several cognitive measures in both patients and controls. SZ patients show distinct deviations from normal behavior under risk when their decisions are based on prospective outcomes. These deviations are two-fold: cognitive deficits prevent value-based DM in more-impaired patients, and in less-impaired patients there is a lack of influence from well-established subjective biases found in healthy people. These abnormalities likely affect every-day DM strategies in schizophrenia patients.

Patients with schizophrenia (SZ) show cognitive impairments on a wide range of tasks, with clear deficiencies in tasks reliant on prefrontal cortex function and less consistently observed impairments in tasks recruiting the striatum. This study leverages tasks hypothesized to differentially recruit these neural structures to assess relative deficiencies of each. Forty-eight patients and 38 controls completed two reinforcement learning tasks hypothesized to interrogate pre-frontal and striatal functions and their interaction. In each task, participants learned reward discriminations by trial and error and were tested on novel stimulus combinations to assess learned values. In the task putatively assessing fronto-striatal interaction, participants were (inaccurately) instructed that one of the stimuli was valuable. Consistent with prior reports and a model of confirmation bias, this manipulation resulted in overvaluation of the instructed stimulus after its true value had been experienced. Patients showed less susceptibility to this confirmation bias effect than did controls. In the choice bias task hypothesized to more purely assess striatal function, biases in endogenously and exogenously chosen actions were assessed. No group differences were observed. In the subset of participants who showed learning in both tasks, larger group differences were observed in the confirmation bias task than in the choice bias task. In the confirmation bias task, patients also showed impairment in the task conditions with no prior instruction. This deficit was most readily observed on the most deterministic discriminations. Taken together, these results suggest impairments in fronto-striatal interaction in SZ, rather than in striatal function per se.

Background: Motivational deficits in people with schizophrenia (PSZ) are associated with an inability to integrate the magnitude and probability of previous outcomes. The mechanisms that underlie probability-magnitude integration deficits, however, are poorly understood. We hypothesized that increased reliance on "value-less" stimulus-response associations, in lieu of expected value (EV)-based learning, could drive probability-magnitude integration deficits in PSZ with motivational deficits. Methods: Healthy volunteers (n=38) and PSZ (n=49) completed a learning paradigm consisting of four stimulus pairs. Reward magnitude (3/2/1/0 points) and probability (90%/80%/20%/10%) determined each stimulus' EV. Following a learning phase, new and familiar stimulus pairings were presented. Participants were asked to select stimuli with the highest reward value. Results: PSZ with high motivational deficits made increasingly less optimal choices as the difference in reward value (probability*magnitude) between two competing stimuli increased. Using a previously-validated computational hybrid model, PSZ relied less on EV ("Q-learning") and more on stimulus-response learning ("actor-critic"), which correlated with SANS motivational deficit severity. PSZ specifically failed to represent reward magnitude, consistent with model demonstrations showing that response tendencies in the actor-critic were preferentially driven by reward probability.

Prior research provides evidence for aberrant cognition-emotion interactions in schizophrenia. In the current study, we aimed to extend these findings by administering the “distractor devaluation” task to 40 individuals with schizophrenia and 32 demographically matched healthy controls. The task consisted of a simple visual search task for neutral faces, followed by an evaluative response made for one of the search items (or a novel item) to determine whether prior attentional selection results in a devaluation of a previously unattended stimulus. We also manipulated working memory demands by preceding the search array with a memory array that required subjects to hold 0, 1, or 2 items in working memory while performing the search array and devaluation task, to determine whether the normative process by which attentional states influence evaluative response is limited by working memory capacity. Results indicated that individuals with schizophrenia demonstrated the typical distractor devaluation effect at working memory load 0, suggesting intact evaluative response. However, the devaluation effect was absent at working memory loads of 1 and 2, suggesting that normal evaluative responses can be abolished in people with schizophrenia when working memory capacity is exceeded. Thus, findings provide further evidence for normal evaluative response in schizophrenia, but clarify that these normal experiences may not hold when working memory demands are too high.