Mechanisms Underlying Motivational Deficits in Psychopathology: Similarities and Differences in Depression and Schizophrenia

Abstract

Motivational and hedonic impairments are core aspects of a variety of types of psychopathology. These impairments cut across diagnostic categories and may be critical to understanding major aspects of the functional impairments accompanying psychopathology. Given the centrality of motivational and hedonic systems to psychopathology, the Research Domain Criteria (RDoC) initiative includes a "positive valence" systems domain that outlines a number of constructs that may be key to understanding the nature and mechanisms of motivational and hedonic impairments in psychopathology. These component constructs include initial responsiveness to reward, reward anticipation or expectancy, incentive or reinforcement learning, effort valuation, and action selection. Here, we review behavioral and neuroimaging studies providing evidence for impairments in these constructs in individuals with psychosis versus in individuals with depressive pathology. There are important differences in the nature of reward-related and hedonic deficits associated with psychosis versus depression that have major implications for our understanding of etiology and treatment development. In particular, the literature strongly suggests the presence of impairments in in-the-moment hedonics or "liking" in individuals with depressive pathology, particularly among those who experience anhedonia. Such deficits may propagate forward and contribute to impairments in other constructs that are dependent on hedonic responses, such as anticipation, learning, effort, and action selection. Such hedonic impairments could reflect alterations in dopamine and/or opioid signaling in the striatum related to depression or specifically to anhedonia in depressed populations. In contrast, the literature points to relatively intact in-the-moment hedonic processing in psychosis, but provides much evidence for impairments in other components involved in translating reward to action selection. Particularly, individuals with schizophrenia exhibit altered reward prediction and associated striatal and prefrontal activation, impaired reward learning, and impaired reward-modulated action selection.

Translational Assessment of Reward and Motivational Deficits in Psychiatric Disorders

“…These results from human and animal studies suggest that either: a) the sucrose preference test is not a valid assessment of pleasure; or b) psychiatric disorders such as MDD, schizophrenia, and autism are not associated with deficits in pleasure. Notably, several lines of evidence have begun to confirm the latter point, particularly with regard to schizophrenia (Barch et al , 2015; Gard et al , 2007; Heerey and Gold, 2007). …”

“…For example, although deficits in motivation were recognized nearly a century ago in schizophrenia (Kraepelin, 1921), recent evidence suggests that such deficits are dissociable from consummatory pleasure, which is intact in individuals with schizophrenia (Barch et al , 2015; Gard et al , 2007; Heerey et al , 2007). Additionally, autism spectrum disorder is associated with anhedonia relating to social, but not other, stimuli (Chevallier et al , 2012; Damiano et al , 2014), but motivation to complete certain tasks can be greater in autism spectrum disorder compared to healthy controls (Damiano et al , 2012).…”

Working Memory Deficit as a Risk Factor for Severe Apathy in Schizophrenia: A 1-Year Longitudinal Study

“…Disturbance in cognitive flexibility could lead patients incapable of flexibly to modify intentions as a function of environmental stimuli and demands and "in fine" induce schizophrenia patients to drop their current action, leading to an increase of behavioral apathy. 48 The Emotional Involvement dimension (ie, blunting of emotional responses and lack of concern) was associated specifically with working memory. Working memory can influence subjective emotional experience and evaluative response in healthy subjects and is involved in the maintenance of emotions to guide behavior.…”

Frontal-striatum dysfunction during reward processing: Relationships to amotivation in schizophrenia.

“…Based on recent affective neuroscience research, Barch and colleagues (Barch & Dowd, 2010; Barch, Pagliaccio, & Luking, 2015; Kring & Barch, 2014) proposed six major components influencing the ability to translate reward information into goal-directed behavioral responses. One of these components is an important ability for goal-directed behavior, which is to integrate reward values in order to generate action plans, thought to be supported by DLPFC function.…”

“…Here, we will focus on this component as it may be potentially related to the anhedonic phenotype. The “anhedonic phenotype” collectively refers to the constructs of anhedonia and/or amotivation as distinct factors from diminished expression, comprising blunted affect and alogia (Barch & Dowd, 2010; Barch et al, 2015; Kring & Barch, 2014; Strauss, Hong, et al, 2012). Although there is a body of literature on impaired cognitive control function, thought to be due to abnormal DPLFC function in schizophrenia (e.g., Cohen et al,1999), more information is needed on the ability of individuals with schizophrenia to integrate reward information with cognitive control, the neural mechanisms that support such integration, and the ways in which these may relate to anhedonia/amotivation symptoms in schizophrenia.…”