Altered fusiform connectivity during processing of fearful faces in social anxiety disorder

Abstract

Social anxiety disorder (SAD) has been associated with hyper-reactivity in limbic brain regions like the amygdala, both during symptom provocation and emotional face processing tasks. In this functional magnetic resonance imaging study we sought to examine brain regions implicated in emotional face processing, and the connectivity between them, in patients with SAD (n=14) compared with healthy controls (n=12). We furthermore aimed to relate brain reactivity and connectivity to self-reported social anxiety symptom severity. SAD patients exhibited hyper-reactivity in the bilateral fusiform gyrus in response to fearful faces, as well as greater connectivity between the fusiform gyrus and amygdala, and decreased connectivity between the fusiform gyrus and ventromedial prefrontal cortex. Within the SAD group, social anxiety severity correlated positively with amygdala reactivity to emotional faces, amygdala-fusiform connectivity and connectivity between the amygdala and superior temporal sulcus (STS). These findings point to a pivotal role for the fusiform gyrus in SAD neuropathology, and further suggest that altered amygdala-fusiform and amygdala-STS connectivity could underlie previous findings of aberrant socio-emotional information processing in this anxiety disorder.

Facial emotion processing in patients with social anxiety disorder and Williams–Beuren syndrome: an fMRI study

“…This result is consistent with those of an earlier study of SAD that found fusiform hypoactivation in response to faces. 60 However, other studies in this context have reported fusiform hyperactivity [61][62][63] or no fusiform activation at all. 64,65 Recently, Frick and colleagues 63 found increased reactivity in the bilateral fusiform gyrus in response to fearful as opposed to neutral faces as well as greater fusiform connectivity with the right amygdala in patients with SAD compared with controls.…”

“…67 Taken together our findings suggest that fusiform hypoactivation may reflect the use of avoidance strategies and/or diminished gaze fixation to facial stimuli during the task by patients with SAD. This would further explain inconsistencies in the results regarding fusiform reactivity, both among previous studies [60][61][62][63] and within individual studies, 61 since this reactivity may vary depending on the use of avoidant strategies and the type of paradigm adopted. 61 Further studies using eye-tracking methodology are necessary to confirm this hypothesis.…”

“…64,65 Recently, Frick and colleagues 63 found increased reactivity in the bilateral fusiform gyrus in response to fearful as opposed to neutral faces as well as greater fusiform connectivity with the right amygdala in patients with SAD compared with controls. At first sight, it may seem that our results contradict those reported by Frick and colleagues 63 ; however, in our study, people with SAD showed decreased fusiform activation and decreased amygdala reactivity under the angry condition (i.e., precisely in response to an expression that is particularly threatening to individuals with SAD).…”

Systems Neuroscience of Psychosis: Mapping Schizophrenia Symptoms onto Brain Systems

“…Also, the frontal and temporal components of the language system have been shown to exert mutual inhibitory control [22], thus presenting the features of a balanced loop. fMRI studies suggest the existence of similar domain-specific long-range connections between specialized cortical regions and the limbic system, e.g., for emotional face processing, between the fusiform gyrus, the amygdala, and the orbitofrontal cortex [23, 24]. In the motor domain, the capacity to recognize nonverbal information such as hand gestures is strongly linked to the performance of hand gestures [25], suggesting a parallel organization with direct connections between brain areas of action perception and those of action planning [26].…”

Hjärnan formas av psykologisk behandling

“…Heightened neural reactivity in SAD is also reported in the insula (Klumpp, Post, Angstadt, Fitzgerald, & Phan, 2013b), and the ACC (Amir et al, 2005;Klumpp, Angstadt, & Phan, 2012). There are also a few studies demonstrating that the connectivity between brain regions differentiates SAD individuals from healthy controls, e.g., more positive connectivity between the dACC and the amygdala (Robinson et al, 2014); the amygdala and the fusiform gyrus (Frick, Howner, Fischer, Kristiansson, & Furmark, 2013b); and the left hippocampus-temporal pole (Pantazatos, Talati, Schneier, & Hirsch, 2014). This suggests that the amygdala and the fear circuitry may be major players in processing emotional facial expressions, but still, the amygdala works collaboratively, and these studies suggest that amygdala couplings may also differentiate individuals with SAD from healthy controls.…”