An Affective Neuroscience Model of Impaired Approach Motivation in Schizophrenia.

Abstract

Negative symptoms have long been considered a core domain of psychopathology in schizophrenia. There has been increased interest in determining the etiology of negative symptoms given that they are largely resistant to current treatment approaches. Limited progress in the treatment of negative symptoms may be due in part to having conceptualized the construct as a singular dimension with common etiology. However, there is now consistent evidence that negative symptoms can be divided into two dimensions of pathology, one reflecting reduced approach motivation and the other diminished expressivity. Although both dimensions are critically important treatment targets, increased severity of volitional symptoms has generally been associated with poorer outcomes. By gaining a better understanding of the etiology of volitional pathology, the field may be better positioned to develop more precise treatments that directly target the most relevant cognitive and neural mechanisms. In the current document, we review the literature on the etiology of the volitional dimension of negative symptoms through the lens of recent theoretical frameworks developed in the fields of cognitive and affective neuroscience. New evidence is presented indicating that schizophrenia patients display deficits in hedonic experience, but that these only emerge at lower levels of motivational significance. We also summarize evidence indicating that greater severity of volitional pathology is associated with dysfunctional corticostriatal interactions and impairments in several aspects of reward processing (e.g., reinforcement learning, value representation, effort-cost computation, uncertainty-driven exploration, and action selection) and emotion processing (e.g., emotion-attention interactions, emotional memory). A new theoretical model is proposed that builds upon recent models of negative symptoms and incorporates hedonic abnormalities, reward processing deficits, and dysfunctional cognition-emotion interactions into decision-making processes. Several promising directions for future research and treatment are also discussed in relation to this new theoretical formulation.