Mobile Virtual Positive Experiences for Anhedonia

Anhedonia is a symptoms dimension that characterizes many individuals suffering from depression, as well as some types of anxiety, psychosis, and substance use. Anhedonia refers to deficits in positive affect as observed through 1) loss of enjoyment in pleasurable activities and/or 2) loss of desire to engage in pleasurable activities. Within depression, anhedonia is more strongly associated with the core disturbance of depressions (e.g. lassitude) than with the nonspecific symptoms that are shared without emotion disorders (e.g. insomnia). Approximately one¬-third of depressed individuals have clinically significant anhedonia symptoms, as defined by cutoffs on scales that measure enjoyment of social and physical pleasure. Anhedonia extends beyond major depression to social anxiety disorder and generalized anxiety disorder, although with a smaller magnitude of effect than depression. Anhedonia is also relevant to schizophrenia and substance use disorder. Thus, anhedonia represents a dimension of psychopathology that crosses diagnostic boundaries.

Anhedonia is associated with several indices of psychopathology. First, self¬-reported anhedonia (lower levels of positive emotion) is a robust predictor of poorer longitudinal course of symptoms of major depression across a number of prospective studies. Relatedly, the trait variance component of low positive affect prospectively predicts the onset of not only major depression, but also social anxiety disorder and generalized anxiety disorder, albeit through correlates with neuroticism. Second, anhedonia within major depression is a major predictor of suicide, and the predictive effects upon suicidal ideation persist even when controlling for other cognitive and affective symptoms of depression. Third, anhedonia is a predictor of poorer response to pharmacological treatments for depression. Some preliminary data from our laboratory replicate this relationship in terms of psychological treatments, at least for social anxiety disorder: in a sample of 75, the investigators found that low positive affect again significantly predicted poorer outcomes (b = ¬-.70, B = -¬.25, p < .05).

Approach Motivation: Dopaminergic signaling is related to the motivation for reward. In humans, neural regions most strongly linked to the approach motivation for reward include the ventral tegmental area, amygdala, and striatum, all of which are innervated by or project to dopaminergic nuclei. Phasic bursts in dopaminergic neurons in the ventral tegmental area have been shown to co¬-occur in response to violations in reward expectancy. Dopamine signaling in the nucleus accumbens (which has dense dopaminergic projections from the ventral tegmental area) is also associated with reward motivation in rodents. Increased mPFC activation may function to reduce striatal response and behavioral drive for rewarding dopaminergic stimulation. Approach motivation is also tied to reward learning, which involves Pavlovian or instrumental associations and predictions about future rewards based on past experiences. As with the approach motivation for reward, learning of reward is associated with dopaminergic signaling. Various areas of the prefrontal cortex have been implicated in decision making and reward learning, and animal research highlights areas such as the ACC, orbitofrontal cortex, vmPFC and dlPFC. Not only do depressed individuals show reduced activation in reward circuitries in anticipation of reward but reduced ventral striatum responsivity to incentive stimuli is particularly related to anhedonic symptoms. Further evidence is derived from behavioral indices in which trait anhedonia among healthy individuals correlates with choosing easy tasks for a small reward over harder tasks for larger rewards, indicative of less motivation (i.e., expenditure of effort) to gain reward. Also, depressed individuals make fewer higher reward/high effort choices than healthy controls, and importantly, the motivational effort they expend to obtain rewards correlates negatively with anhedonia. In self-¬report measures, dysphoric individuals expect to feel less positive emotion in future positive events and report less positive emotion in anticipation of a monetary reward compared to healthy controls, although the evidence is not entirely robust.

Responsiveness to Reward Attainment: Responsiveness to reward attainment (or hedonic capacity) is more strongly related to opioid and endocannabinoid pathways. Neural regions most strongly linked with liking of reward include the ventral striatum (representing overlap with the approach motivation component) and orbitofrontal cortex. Depressed individuals show ventral striatum hypo-activity to positive stimuli, and the hypo-activity is particularly strongly associated with symptoms of anhedonia. Furthermore, Wacker et al. (2009) established that the effects were specific to anhedonia above and beyond negative symptoms of anxiety and depression. Further evidence for deficits in initial responsiveness to attainment derives from cognitive measures, with depressed individuals showing less attention to positive stimuli than controls as measured by response latency times in dot probe tasks and eye tracking. Moreover, attention to positive information is associated with positive affect. The evidence for deficits in self-¬rated liking of reward in depressed individuals is mixed. Importantly, lower levels of self¬-reported positive emotions to positive stimuli (e.g. sweet taste test) are more strong related to anhedonia than depression.

Targeted Treatment for Anhedonia: In light of the evidence summarized above, a treatment that specifically targets reward approach motivation and learning, and responsiveness to reward attainment may be particularly potent for anhedonia. As noted, existing psychological treatments mostly target negative affect, and while behavioral activation is designed to increase engagement in pleasant activities, little attention has been given to date to how to optimize positive emotions during the planning and conduct of such activities. Drawing from affective neuroscience and experimental psychopathology, the investigators have developed a treatment that specifically targets these components of the reward system. The treatment is comprised of therapeutic techniques that directly target one or more of these subdomains. The first phase of treatment (sessions 1-7) involves modified behavioral activation (called behavioral training), which combines planning for engagement in pleasurable activities (reward approach and motivation) and reinforcement via positive mood inducing effects (reward learning) with 'in¬-the-¬moment' recounting designed to savor pleasurable moments and enhance hedonic impact (responsiveness). The second phase of treatment (sessions 8¬-13) adds two additional components to ongoing behavioral training: cognitive training designed to shift attention towards positive stimuli in the environment (reward approach motivation), reinforce associations between responses and positive outcomes (reward learning) and train motivation for positive events and emotions through imagery (reward approach motivation); and compassion training that focuses on motivating toward (reward approach motivation) and savoring positive experiences (responsiveness). The investigators found that this treatment is effective in both reducing negative affect (depression and anxiety) and improving positive affect, especially for individuals who are most anhedonic at baseline. Specifically, patients who meet entry criteria of elevated levels of depression, anxiety (somatic), or stress (worry) on the Depression, Anxiety and Stress Scale (DASS-21), and who are at least moderately impaired according to the Sheehan Disability Scale (SDS), are randomly assigned to receive treatments aimed at increasing reward sensitivity (Positive Affect Treatment, PAT) or at reducing threat sensitivity (Negative Affect Treatment, NAT). Here the investigators present data from the first 61 enrolled patients (N=20 PAT and N=41 NAT) who began the 15 ¬treatment session protocol. Self-¬reported symptoms of depression (DASS-¬D) and stress (DASS-¬S) decreased from a severe range at pre-¬treatment to a normal range at post-¬treatment in PAT and NAT (DASS¬-D: Cohen's d=1.89 and 1.41, respectively; DASS¬-S: d=1.35 and d=1.65, respectively). Self¬-reported anxiety (DASS¬-A) decreased from extremely severe to normal for PAT and from moderate to mild for NAT (d=1.02 and 1.47). The investigators found significant improvements for our anhedonia outcome measure, Positive and Negative Affect Schedule Positive Scale (PANAS-¬P). Positive affect improved linearly in both treatment, but significantly greater changes occurred with PAT (d=1.40) versus NAT (d=.59) (Group x Time; p=.001). Only PAT significantly and satisfactorily normalized deficits in positive affect (changes from 20th to 46th percentile on the scale developed by Crawford Henry, 2004. In NAT treatment, levels of PANAS-¬P remained lower than the population average (change from 18th to 32nd percentile).