Memories become labile when recalled. In humans and rodents alike, reactivated fear memories can be attenuated by disrupting reconsolidation with extinction training. Using functional brain imaging, we found that, after a conditioned fear memory was formed, reactivation and reconsolidation left a memory trace in the basolateral amygdala that predicted subsequent fear expression and was tightly coupled to activity in the fear circuit of the brain. In contrast, reactivation followed by disrupted reconsolidation suppressed fear, abolished the memory trace, and attenuated fear-circuit connectivity. Thus, as previously demonstrated in rodents, fear memory suppression resulting from behavioral disruption of reconsolidation is amygdala-dependent also in humans, which supports an evolutionarily conserved memory-update mechanism.

Common sites of action for citalopram and cognitive-behavioral treatment of social anxiety were observed in the amygdala, hippocampus, and neighboring cortical areas, ie, brain regions subserving bodily defense reactions to threat.

Sixty-four individuals with social phobia (social anxiety disorder) were assigned to a multimodal cognitive-behavioral treatment package or to a waiting list control group. Treatment consisted of a 9-week, Internet-delivered, self-help program that was combined with 2 group exposure sessions in real life and minimal therapist contact via e-mail. Results were analyzed on an intention-to-treat basis, including all randomized participants. From pre- to posttest, treated participants in contrast to controls showed significant improvement on most measured dimensions (social anxiety scales, general anxiety and depression levels, quality of life). The overall within- and between-groups effect sizes were Cohen's d = 0.87 and 0.70, respectively. Treatment gains were maintained at 1-year follow-up. The results from this study support the continued use and development of Internet-distributed, self-help programs for people diagnosed with social phobia.

Although the exact diagnostic boundaries for social phobia are difficult to determine, it can be concluded that social anxiety is a distressing problem for a considerable proportion of the general population.

Although there are difficulties in delineating social phobia from subsyndromal social anxiety or shyness, social phobia is even when narrowly defined remarkably common in the general population.

This study provides evidence to support the use of internet-based treatment supplemented by short, weekly telephone calls.

An rCBF pattern of relatively increased cortical rather than subcortical perfusion was observed in the nonphobic subjects, indicating that cortical evaluative processes were taxed by public performance. In contrast, the social phobia symptom profile was associated with increased subcortical activity. Thus, the functional neuroanatomy of social phobia involves the activation of a phylogenetically older danger-recognition system.

No abstract