Exposure therapy is an effective approach for treating anxiety disorders, although a substantial number of individuals fail to benefit or experience a return of fear after treatment. Research suggests that anxious individuals show deficits in the mechanisms believed to underlie exposure therapy, such as inhibitory learning. Targeting these processes may help improve the efficacy of exposure-based procedures. Although evidence supports an inhibitory learning model of extinction, there has been little discussion of how to implement this model in clinical practice. The primary aim of this paper is to provide examples to clinicians for how to apply this model to optimize exposure therapy with anxious clients, in ways that distinguish it from a ‘fear habituation’ approach and ‘belief disconfirmation’ approach within standard cognitive-behavior therapy. Exposure optimization strategies include 1) expectancy violation, 2) deepened extinction, 3) occasional reinforced extinction, 4) removal of safety signals, 5) variability, 6) retrieval cues, 7) multiple contexts, and 8) affect labeling. Case studies illustrate methods of applying these techniques with a variety of anxiety disorders, including obsessive-compulsive disorder, posttraumatic stress disorder, social phobia, specific phobia, and panic disorder.

Anhedonia, or loss of interest or pleasure in usual activities, is characteristic of depression, some types of anxiety, as well as substance abuse and schizophrenia. Anhedonia is a predictor of poor long-term outcomes, including suicide, and poor treatment response. Because extant psychological and pharmacological treatments are relatively ineffective for anhedonia, there is an unmet therapeutic need for this high-risk symptom. Current psychological and drug treatments for anxiety and depression focus largely on reducing excesses in negative affect rather than improving deficits in positive affect. Recent advances in affective neuroscience posit that anhedonia is associated with deficits in the appetitive reward system, specifically the anticipation, consumption, and learning of reward. In this paper, we review the evidence for positive affect as a symptom cluster, and its neural underpinnings, and introduce a novel psychological treatment for anxiety and depression that targets appetitive responding. First, we review anhedonia in relation to positive and negative valence systems and current treatment approaches. Second, we discuss the evidence linking anhedonia to biological, experiential, and behavioral deficits in the reward subsystems. Third, we describe the therapeutic approach for Positive Affect Treatment (PAT), an intervention designed to specifically target deficits in reward sensitivity.

Objective: Loss of pleasure or interest in activities (i.e., anhedonia) is a risk factor for suicidality, treatment nonresponse, and relapse. Extant treatments that focus on reducing negative affect have limited effects upon positive affect (a core feature of anhedonia). We investigated whether a novel intervention aimed at increasing reward sensitivity was more efficacious for positive affect than a cognitive–behavior treatment aimed at reducing threat sensitivity, in individuals with clinically severe symptoms of depression or anxiety, and functional impairment. Method: The Treatment for Affective Dimensions trial was offered in a 2-site randomized study at outpatient treatment centers in Los Angeles and Dallas. Ninety-six patients were randomized to 15 weekly, individual sessions of Positive Affect Treatment (PAT) or Negative Affect Treatment (NAT). The primary outcome was improvement in positive affect (Positive and Negative Affect Schedule–Positive) from pretreatment to 6-month follow-up (6MFU). Secondary outcomes were improvements in negative affect (Positive and Negative Affect Schedule–Negative), suicidal ideation, and symptoms (Depression Anxiety Stress Scales). Results: PAT resulted in greater improvements in positive affect, p = .009, d = .52, and higher positive affect at 6MFU, p = .002, d = .67, than NAT. Participants in PAT also reported lower negative affect, p = .033, d = .52, and lower symptoms of depression, p = .035, d = .34, anxiety, p < .018, d = .30, and stress, p = .006, d = .43 at 6MFU. Finally, probability of suicidal ideation at 6MFU was lower in PAT than NAT (1.7% vs. 12.0%), p < .001. Conclusions: Compared to NAT, PAT demonstrated better outcomes (at 6MFU) on positive affect, depression, anxiety, stress, and suicidal ideation, for patients with symptomatic pretreatment levels of these outcomes.

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Recent research suggests that the mere act of retrieving a memory can temporarily make that memory vulnerable to disruption. This process of "reconsolidation" will typically restabilize the neural representation of the memory and foster its long-term storage. However, the process of reconsolidating the memory takes time to complete, and during this limited time window, the original memory may be modified either by the presentation of new information or with pharmacological agents. Such findings have prompted rising interest in using disruption during reconsolidation as a clinical intervention for anxiety, posttraumatic stress, and substance use disorders. However, "boundary conditions" on memory reconsolidation may pose significant obstacles to clinical translation. The aim of this article is to critically examine the nature of these boundary conditions, their neurobiological substrates, and the potential effect they may have on disruption of reconsolidation as a clinical intervention. These boundary conditions also highlight potential constraints on the reconsolidation phenomenon and suggest a limited role for memory updating consistent with evolutionary accounts of associative learning for threat and reward. We conclude with suggestions for future research needed to elucidate the precise conditions under which reconsolidation disruption may be clinically useful.