Understanding the interplay between motivation and social cognition performance in schizophrenia

To the Editor

Motivational deficits account for 6–16% of the variance in general neurocognition in schizophrenia (Fervaha et al., 2014). This is a reminder that motivation assessments should accompany cognitive testing in schizophrenia and performance should be interpreted in this light. However, schizophrenia patients also experience deficits in social cognition (SC). While SC performance depends substantially on neurocognitive ability, how motivation influences this relationship is not well studied.

Here we examine this relationship from our data on 170 schizophrenia patients (Mehta et al., 2014) who underwent assessments of SC (theory of mind, emotion processing, social perception and attributional styles), neurocognition (processing speed, verbal/visual learning and memory, planning, and cognitive flexibility), symptoms (Positive and Negative Syndrome Scale), and motivation (motivation item, Quality of Life Scale). Global SC and neurocognitive scores were computed as averages of the z-scores corresponding to each subdomain. We observed significant direct correlations between motivation, and global SC (r=0.448, p<0.001) and neurocognition (r=0.348, p<0.001). Motivation also correlated with each SC subdomain (correlation range=0.21–0.33; p<0.01). Global SC and neurocognitive scores were highly correlated (r=0.587, p<0.001). Age (r=0.16, p=0.03), education (r=0.437, p<0.001) and negative symptoms (r=−0.21, p<0.01) also correlated with global SC. Linear regression with global SC as the outcome, and motivation, global neurocognition, age, education and negative symptoms as predictor variables revealed a model comprising global neurocognition (β=0.491, p<0.001) and motivation (β=0.278, p<0.001) that together accounted for 41% of the variance in global SC (Figure 1).

Figure 1.

Scatter plot with regression fit-line demonstrating the relationship between social cognition, neurocognition and motivation. Note: higher scores indicate better cognitive performance and motivation.

Our results suggest that motivation is not only related to neurocognitive performance, but also SC performance, even after controlling for the influence of potential confounders. In future SC remediation trials, identifying individuals in whom SC deficits are attributable to poor motivation may have a critical impact on interpreting treatment outcomes.

In addition, SC may also be under the influence of social-motivation – a central drive to enhance our suitability for collaborative/interpersonal environments (Chevallier et al., 2012). It is likely that at least part of the SC deficits observed in schizophrenia actually reflect deficits in both intrinsic- and social-motivation. This highlights the need to develop instruments that diligently tap social-motivation. Further, expanding our biological models from aberrant frontostriatal dopaminergic signaling essential to intrinsic-motivation and cognition (Fervaha et al., 2014) to the dynamic interplay between the oxytocin–dopaminergic pathways in the orbitofrontal–striatum–amygdala network that support social-motivation and social cognition (Chevallier et al., 2012), may add to our understanding of schizophrenia. Our inferences are limited by the cross-sectional nature of assessments.