Does fear reactivity during exposure predict panic symptom reduction?

OBJECTIVE: Fear reactivity during exposure is a commonly used indicator of learning and overall therapy outcome. The objective of this study was to assess the predictive value of fear reactivity during exposure using multimodal indicators and an advanced analytical design. We also investigated the degree to which treatment condition (cognitive training vs. respiratory skill training) moderated fear reactivity and therapeutic outcome. METHOD: Thirty-four patients with panic disorder and agoraphobia completed a total of 123 in-vivo exposure sessions, comprising 3 weekly sessions and a 4th session 2 months following therapy completion. Sessions varied in length and phobic stimuli. Cardiorespiratory physiology (heart rate, carbon dioxide partial pressure [PCO2], respiration rate) and experiential symptoms (panic symptoms and anxiety) were assessed repeatedly throughout exposure sessions, in addition to weekly assessments of panic cognitions, avoidance, and functioning. RESULTS: Panic symptomatology decreased substantially in both treatment conditions during therapy and follow-up. Significant cardiorespiratory and experiential reactivity was observed during all exposures, characterized by activation followed by reduction. Greater within-session activation of anxiety and panic symptoms was inversely related to improvement in panic symptoms severity, but neither physiological activation nor within- or between-session reduction of either physiological or experiential variables was predictive of outcome. No moderating effects of treatment condition were found. CONCLUSIONS: Fear activation and reduction during exposure are weak predictors of corrective learning and fear extinction. Clinical implications for exposure therapy and directions for future research are discussed.

Respiratory and cognitive mediators of treatment change in panic disorder: evidence for intervention specificity.

OBJECTIVE: There are numerous theories of panic disorder, each proposing a unique pathway of change leading to treatment success. However, little is known about whether improvements in proposed mediators are indeed associated with treatment outcomes and whether these mediators are specific to particular treatment modalities. Our purpose in this study was to analyze pathways of change in theoretically distinct interventions using longitudinal, moderated mediation analyses. METHOD: Forty-one patients with panic disorder and agoraphobia were randomly assigned to receive 4 weeks of training aimed at altering either respiration (capnometry-assisted respiratory training) or panic-related cognitions (cognitive training). Changes in respiration (PCO2, respiration rate), symptom appraisal, and a modality-nonspecific mediator (perceived control) were considered as possible mediators. RESULTS: The reductions in panic symptom severity and panic-related cognitions and the improvements in perceived control were significant and comparable in both treatment groups. Capnometry-assisted respiratory training, but not cognitive training, led to corrections from initially hypocapnic to normocapnic levels. Moderated mediation and temporal analyses suggested that in capnometry-assisted respiratory training, PCO2 unidirectionally mediated and preceded changes in symptom appraisal and perceived control and was unidirectionally associated with changes in panic symptom severity. In cognitive training, reductions in symptom appraisal were bidirectionally associated with perceived control and panic symptom severity. In addition, perceived control was bidirectionally related to panic symptom severity in both treatment conditions. CONCLUSION: The findings suggest that reductions in panic symptom severity can be achieved through different pathways, consistent with the underlying models.

[Pareses, myalgias, and massive CK elevation: a severe neurological disorder?]. / Paresen, myalgien und massive CK-erhöhung: eine schwere neurologische erkrankung?

CASE REPORT: The authors report on a 51-year-old patient with transient pareses, myalgias, and a massive creatine kinase elevation which had led to an intensive neurological work-up by the general practitioner. Despite refractory hypertension, primary aldosteronism was not excluded. At the authors' clinic, the patient was diagnosed to have Conn's syndrome. Laparoscopic adrenalectomy revealed a big adenoma of the left adrenal gland. CONCLUSION: Transient pareses, myalgias, and creatine kinase elevation can indicate primary aldosteronism among hypertensive patients. If clinically suspected, the aldosterone-renin ratio should be determined.

Depression and eating pathology: prospective reciprocal relations in adolescents.

The association between disordered eating and depression has been established, but less is known about the temporal relations between these two disturbances. Accordingly, the current study examined the reciprocal relations between depressive and bulimic symptoms over an 8-year period, with longitudinal data from a community sample of 496 female adolescents. Depressive symptoms predicted future increases in bulimic symptoms, and bulimic symptoms likewise predicted increases in depressive symptoms, controlling for earlier levels of symptoms for each outcome. These results provide evidence consistent with the hypothesis that the two disorders contribute reciprocally to each other, and indicate that successful prevention or treatment of one disorder may yield effects for the other. However, the relatively small predictive effect sizes imply that some third variable may contribute to both conditions (e.g., temperamental negative affectivity).

Mediators in the dissonance eating disorder prevention program.

Previous research has supported thin-ideal internalization as a partial mediator of the effects of the dissonance eating disorder prevention program. The current study replicated previous findings and examined an additional mediator, body dissatisfaction, hypothesized to account for partial intervention effects. As a secondary goal, we developed a more rigorous and accurate test of mediation that accounted for the temporal, causal interplay between mediator and outcome, and controlled for "reverse mediation". Results from a sample of 71 high-risk females (M age = 19.8, SD = 1.3) who participated in a four-week dissonance intervention supported thin-ideal internalization as a partial mediator of the effects of the dissonance intervention on bulimic symptoms, even after controlling for body dissatisfaction as a second mediator. Furthermore, results supported body dissatisfaction as a partial mediator for bulimic symptoms after controlling for thin-ideal internalization. Significant "reverse mediation" effects suggested the reciprocal influence of some risk factors for bulimia nervosa and bulimic symptoms. These results contribute to our understanding of the mediators in the dissonance intervention, which can help refine eating disorder prevention programs.

The effects of acute exercise on CO(2) challenge reactivity.

The present study examined the effects of acute exercise on anxiogenic responding to 65% O(2)/35% CO(2) challenge. Participants (N=92) were 51 female and 41 male volunteers ranging in age from 17 to 24 (M=19.43, SD=1.31). Participants had no history of panic attacks and were randomized to moderate treadmill exercise (i.e., 70% of HR(max)) or quiet rest prior to taking a single vital capacity inhalation of 35% CO(2)/65% O(2). Gender and measures of negative affectivity and anxiety sensitivity were included in the design as control variables. Results indicated participants who exercised prior to challenge showed significantly reduced reactivity compared to their counterparts who rested prior to challenge. Importantly, the effect sizes for the advantage of exercise over rest remained in the medium to large range (i.e., partial eta(2)>.07) after controlling for the effects of gender, anxiety sensitivity, and negative affectivity. These findings are the first to demonstrate that the anti-panic effects of exercise are unique from, and cannot be better explained by, established risk factors of CO(2) challenge reactivity.