The pilot data provide preliminary support for the use of short-term dosing of d-cycloserine as an adjunctive intervention to exposure therapy for SAD.
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.
Background Previous studies investigating attentional biases in social anxiety disorder (SAD) have yielded mixed results. Recent event-related potential (ERP) studies employing the dot-probe paradigm in non-anxious participants have shown that the P1 component is sensitive to visuospatial attention toward emotional faces. We used a dot-probe task in conjunction with high-density ERPs and source localization to investigate attentional biases in SAD. Method Twelve SAD and 15 control participants performed a modified dot-probe task using angry-neutral and happy-neutral face-pairs. The P1 component elicited by face-pairs was analyzed to test the hypothesis that SAD participants would display early hypervigilance to threat-related cues. The P1 component to probes replacing angry, happy or neutral faces was used to evaluate whether SAD participants show sustained hypervigilance or rather decreased visual processing of threat-related cues at later processing stages. Results Compared to controls, SAD participants showed relatively (a) potentiated P1 amplitudes and fusiform gyrus activation to angry-neutral vs. happy-neutral face-pairs; (b) decreased P1 amplitudes to probes replacing emotional (angry and happy) vs. neutral faces; and (c) higher sensitivity (d′) to probes following angry-neutral vs. happy-neutral face-pairs. SAD participants also showed significantly shorter reaction times to probes replacing angry vs. happy faces, but no group differences emerged for reaction time. Conclusions The results provide electrophysiological support for early hypervigilance to angry faces in SAD with involvement of the fusiform gyrus, and reduced visual processing of emotionally salient locations at later stages of information processing, which might be a manifestation of attentional avoidance.
Background-Given growing evidence that respiratory dysregulation is a central feature of panic disorder (PD) interventions for panic that specifically target respiratory functions could prove clinically useful and scientifically informative. We tested the effectiveness of a new, brief, capnometry-assisted breathing therapy (BRT) on clinical and respiratory measures in PD.Methods-Thirty-seven participants with PD with or without agoraphobia were randomly assigned to BRT or to a delayed-treatment control group. Clinical status, respiration rate, and end-tidal pCO 2 were assessed at baseline, posttreatment, 2-month and 12-month follow-up. Respiratory measures were also assessed during homework exercises using a portable capnometer as a feedback device.Results-Significant improvements (in PD severity, agoraphobic avoidance, anxiety sensitivity, disability, and respiratory measures) were seen in treated but not untreated patients, with moderate to large effect sizes. Improvements were maintained at follow-up. Treatment compliance was high for session attendance and homework exercises; dropouts were few.Conclusions-The data provide preliminary evidence that raising end-tidal pCO 2 by means of capnometry feedback is therapeutically beneficial for panic patients. Replication and extension will be needed to verify this new treatment's efficacy and determine its mechanisms.
The present study investigated the phenomenon of sudden gains in 107 participants with social phobia (social anxiety disorder) who received either cognitive-behavioral group therapy or exposure group therapy without explicit cognitive interventions, which primarily used public speaking situations as exposure tasks. Twenty-two out of 967 session-to-session intervals met criteria for sudden gains, which most frequently occurred in Session 5. Individuals with sudden gains showed similar improvements in the 2 treatment groups. Although cognitive-behavioral therapy was associated with more cognitive changes than exposure therapy, cognitive changes did not precede sudden gains. In general, the results of this study question the clinical significance of sudden gains in social phobia treatment.Keywords sudden gains; social anxiety disorder; social phobia; cognitive-behavioral therapy; exposure therapyIn recent years, psychotherapy researchers have investigated the phenomenon of large, rapid, and stable decreases in symptomatology during treatment, which has been referred to as sudden gains (Tang & DeRubeis, 1999b). Sudden gains are typically defined by a set of three quantitative criteria: (a) the sudden gain must be large in absolute terms, (b) the sudden gain must represent at least a 25% reduction from the level of symptomatology before the gain occurred, and (c) the mean level of symptomatology in the three therapy sessions preceding the gain must be significantly higher than the mean level of symptomatology in the three postgain sessions. Most studies of sudden gains have examined treatment changes in depression with the Beck Depression Inventory (BDI; Beck, Ward, Mendelson, Mock, & Erbaugh, 1961; but see also Stiles et al., 2003;Vittengl, Clark, & Jarrett, 2005).When applying these criteria, Tang and DeRubeis (1999b) found that sudden gains occurred in more than 50% of individuals who responded to cognitive-behavioral therapy for depression and that these gains accounted for more than 50% of these individuals' total improvement in depression. Compared with participants who did not experience sudden gains at posttreatment, individuals with sudden gains showed better outcome at posttreatment and at 6-month and 18-month follow-ups.The initial study by Tang and DeRubeis (1999b) was followed by a number of other studies examining sudden gains (Gaynor et al., 2003;Hardy et al., 2005;Kelly, Roberts, & Ciesla, 2005;Tang, DeRubeis, Beberman, & Pham, 2005;Tang, Luborsky, & Andrusyna, 2002;Vittengl, Clark, & Jarrett, 2005). Interventions in these studies ranged from traditional cognitive therapy to supportive expressive therapy or pharmacotherapy. Although sudden gains were primarily assessed in efficacy trials of time-limited individual treatments (e.g., Tang NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript DeRubeis, 1999b;Vittengl et al., 2005), their incidence was also assessed in group therapy for depression (Kelly et al., 2005) and individuals with mixed psychiatric diagnoses who were g...
OBJECTIVE To test whether d-cycloserine, a partial agonist at the glutamatergic N-methyl-D-aspartate receptor, augments and accelerates a full course of comprehensive cognitive behavioral therapy (CBT) in medication-free adults with generalized social anxiety disorder. METHOD A randomized placebo-controlled efficacy-study conducted at Boston University, Massachusetts General Hospital, and Southern Methodist University between 9/2007 and 12/2011 of 169 medication-free adults with generalized social anxiety disorder; 144 completed treatment, and 131 completed the follow-up assessments. Patients were randomized to receive 50 mg of d-cycloserine or placebo 1 hour before each of 5 exposure sessions that were part of a 12-session cognitive behavioral group treatment. Response and remission status was determined at baseline, throughout treatment, post-treatment, and at 1, 3, and 6-month follow-up assessments rated by assessors who were blind to treatment condition. RESULTS D-cycloserine-augmented and placebo-augmented CBT were associated with similar completion rates (87% and 82%), response rates (79.3% and 73.3%), and remission rates (34.5% and 24.4%) at post-treatment that were largely maintained at follow-up. Although d-cycloserine was associated with a 24–33% faster rate of improvement in symptom severity and remission rates relative to placebo during the 12-week treatment phase, the groups did not differ in response and remission rates. CONCLUSIONS D-cycloserine did not augment a full course of comprehensive CBT for social anxiety disorder. TRIAL REGISTRATION http://www.ClinicalTrials.gov, ID# NCT00633984, http://www.clinicaltrials.gov/ct2/show/NCT00633984
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