Individuals suffering from social anxiety disorder (SAD), classified as ‘social phobia’ in DSM-IV-TR , show exaggerated fear responses in social or performance situations. In particular, patients are excessively concerned about being evaluated negatively by others. In search of the neural basis of SAD, different brain areas have been identified that seem to be involved in SAD. By means of functional brain imaging, heightened activation of the amygdala has been found during the processing of disorder-related stimuli (for example, [2–9]) as well as during symptom provocation in SAD patients (for example, [10–14]), supporting the assumed role of the amygdala in threat processing [15, 16]. Furthermore, several other regions have been associated with increased activation in SAD, including medial prefrontal areas, for example, dorsal anterior cingulate cortex (ACC) and dorsomedial prefrontal cortex (dmPFC), and the insular cortex (for example, [3, 5, 8, 10, 17–20]). Medial prefrontal cortex areas have been proposed to be linked to explicit emotional evaluation, emotional-cognitive interactions, self-referential processing, and emotion-regulation [21–26]. The insula seems to be involved in interoception and representation of bodily states [27–29] and might support aversive feelings by evaluating arousal responses [28, 30, 31].
However, although these areas have been repeatedly shown to be associated with the processing of disorder-relevant stimuli in SAD and other anxiety disorders , reported brain activation patterns are rather inconsistent across studies with most studies describing different areas to be involved. Furthermore, there are only few symptom provocation studies as compared to the large number of studies that investigated the neural correlates during the processing of social stimuli such as facial expressions in SAD patients. Remarkably, even though disorder-related stimuli such as emotional faces do not induce reliable anxiety symptoms in patients, they seem to activate parts of an emotional network. However, findings are variable and strongly depend on task conditions [8, 9] and time course parameters [18, 33].
Reliable anxiety responses are induced by symptom provocation designs such as actual or anticipated public performance. Furthermore, findings from anxiety symptom provocation studies should provide stronger evidence which regions are involved in anxiety symptoms in SAD. While some symptom provocation studies reported increased amygdala activation during public speaking in patients with SAD [11–14, 34], studies using other symptom provocation tasks did not [35–37]. Similarly, there are also inconsistencies regarding the involvement of the insula (see [10, 12, 13, 35–38]) and prefrontal regions in SAD [12–14, 34, 36, 37].
Obviously, threat-related brain activation in SAD depends on various factors, which are not well understood yet. For example, some symptom provocation tasks such as overt speaking tasks are associated with active performance but are also inherently susceptible to brain imaging-relevant artefacts such as head movements and performance differences between patients and controls. Moreover, in different tasks, different functions of the threat-processing network might be involved. Furthermore and most importantly, brain activation was shown to vary over time in response to anticipatory anxiety in social anxiety (see ) and some variability in previous findings may be due to different time courses of brain activation. Accordingly, there is general evidence that indicates different time courses of several brain areas within the defense cascade (for example, [39, 40]). Thus, while the amygdala has been suggested to be primarily relevant during the initial period of threat processing in healthy participants and patients with phobias (for example, [39–42]), the insula and prefrontal areas were shown to be associated with explicit and more sustained fear responses [39, 40, 42–44]. In SAD, the time course of activation in different brain areas during symptom provocation is largely unknown. A recent study found increased amygdala activation only during the first half of an anticipatory threat interval in SAD .
In the present study, we used a novel symptom provocation design in SAD by presenting disorder-related and neutral video clips. We developed a new set of video stimuli for symptom provocation in SAD, based on evidence that the use of short film clips represents one of the most effective and reliable methods to induce emotions in laboratory settings [45–47]. The study aimed to investigate increased brain activation in several areas that have been identified to be important in SAD during symptom provocation (amygdala, insula, ACC, and dmPFC). Activation was modelled to account (a) for the full time course of the video clips, and (b) specifically, for the first and (c) second half of the clips. If the amygdala bears specific relevance for initial threat processing, effects should be most pronounced during the first half of the video clips. In contrast, responses in other areas should also be manifest during the second half of the video clips or may occur specifically during the second half of the clips.