Electrophysiological evidence of attentional biases in social anxiety disorder.

BACKGROUND: Previous studies investigating attentional biases in social anxiety disorder (SAD) have yielded mixed results. Recent event-related potential (ERP) studies using the dot-probe paradigm in non-anxious participants have shown that the P1 component is sensitive to visuospatial attention towards 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 either sustained hypervigilance or 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 (FG) activation to angry-neutral versus happy-neutral face pairs; (b) decreased P1 amplitudes to probes replacing emotional (angry and happy) versus neutral faces; and (c) higher sensitivity (d') to probes following angry-neutral versus happy-neutral face pairs. SAD participants also showed significantly shorter reaction times (RTs) to probes replacing angry versus happy faces, but no group differences emerged for RT. CONCLUSIONS: The results provide electrophysiological support for early hypervigilance to angry faces in SAD with involvement of the FG, and reduced visual processing of emotionally salient locations at later stages of information processing, which might be a manifestation of attentional avoidance.

Respiratory biofeedback-assisted therapy in panic disorder.

The authors describe a new methodologically improved behavioral treatment for panic patients using respiratory biofeedback from a handheld capnometry device. The treatment rationale is based on the assumption that sustained hypocapnia resulting from hyperventilation is a key mechanism in the production and maintenance of panic. The brief 4-week biofeedback therapy is aimed at voluntarily increasing self-monitored end-tidal partial pressure of carbon dioxide (PCO2) and reducing respiratory rate and instability through breathing exercises in patients' environment. Preliminary results from 4 patients indicate that the therapy was successful in reducing panic symptoms and other psychological characteristics associated with panic disorder. Physiological data obtained from home training, 24-hour ambulatory monitoring pretherapy and posttherapy, and laboratory assessment at follow-up indicate that patients started out with low resting PCO2 levels, increased those levels during therapy, and maintained those levels at posttherapy and/or follow-up. Partial dissociation between PCO2 and respiratory rate questions whether respiratory rate should be the main focus of breathing training in panic disorder.