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Fearful Faces Paradigms

Several imaging studies of conscious and unconscious fear processing have examined reactivity to a standardized series of emotional facial expressions.33 These “target” (fearful or neutral) facial expressions are presented too briefly for conscious appreciation and then are immediately “masked” by a longer exposure to a neutral face. When subjects reported seeing only the neutral faces, the limbic system was found to have measurable blood-oxygen level dependent (BOLD) signal changes in reaction to the target images.34 Neural responsiveness to masked fearful faces consistently shows variances in the limbic system, which consists of several structures including the amygdala, hippocampus, cingulate gyrus, and parahippocampal gyrus, in both PTSD subjects and in healthy controls. Of the different regions of interest in PTSD, the amygdala has been most often shown to be hyperactivated during presentation of general emotionally laden stimuli.35,36 Furthermore, greater amygdala activation was shown to be highly associated with symptom severity in PTSD.6 This hyperactive amygdalar response to fearful faces is evident as early as 1 month following trauma and continues through the course of chronic PTSD.37 Fonzo and colleagues found increased amygdala and insula activation in response to fearful or angry versus happy faces in women with PTSD exposed to intimate partner violence (IPV) in comparison to healthy controls without a history of IPV. Additionally, the dACC and mPFC of individuals with IPV-PTSD were more active when presented with male faces versus female faces. Hyperactivation in these regions are also positively associated with hyperarousal symptoms.38 In a recent study, activation of the vmPFC and amygdala was significantly and consistently associated with early exposure to angry faces and symptom severity.7 Furthermore, vmPFC and amygdala activation was also found to be positively associated with recollection of fearful faces and symptom severity in individuals with PTSD.6 Finally, severity of symptoms, as measured by scores on the Clinician-Administered PTSD Scale (CAPS), the gold standard diagnostic interview for PTSD, was also positively related to insula and hippocampus activation, whereas dissociative symptoms had an inverse relationship with dACC activation.7 Hippocampal activation and its association with symptom severity has been noted in several additional studies.39,40

In an emotional-interference task,41 participants are presented with a pair of houses (distractors) and a pair of either fearful or neutral faces (target) and are instructed to either attend to or ignore the target. Studies using this paradigm have found that participants with PTSD exhibited increased amygdala activity in the presence of both fearful and neutral faces4 but higher insular activation only when fearful images were presented, thus implicating the insula in cognition and emotional processing, particularly to conscious attention to emotional content.4 Consistent with recent results,173842 the PTSD group also showed greater mPFC activity and less suppression of dACC activity during attentional avoidance of threatening cues.4 In an interesting cultural perspective on the neurocircuitry of PTSD, Kim et al. utilized the same emotional-interference task but replaced the Caucasian faces with Korean faces to adapt it to their sample of 12 survivors of the Taegu subway fire in 2003.43 No significant differences in amygdala response to fearful versus neutral faces were observed in either the PTSD or healthy control group.43 This finding was corroborated by a Japanese study that also incorporated cultural specificity into the facial stimuli.44

PTSD patients appear to be more reactive than nonclinical populations to exposure to masked fearful faces. In a study comparing genuine PTSD patients with trauma-exposed controls coached to simulate PTSD, Bryant and colleagues found that the PTSD subjects had lower mPFC and left amygdala activity than did simulators when the fearful faces were presented for long enough to be consciously observed, but stronger mPFC activation than simulators when the same fear signals were presented too quickly to be consciously noted. Consistent with previous findings that fear signals may engage cortical systems by way of bottom-up neural connections,37 it has been suggested that in patients with PTSD, neural fear signals that occur quickly, allowing for automatic alerting to possible hazards—especially unconscious fear signals—may be heightened.45

SCR used in combination with fMRI is also a valuable tool for examining unconscious fear response in PTSD. In a comparison of PTSD patients and matched controls with high versus low SCR to fearful facial stimuli, PTSD patients displayed increased bilateral activation of the amygdala relative to con- trols.46 Within the PTSD group, individuals with high SCR displayed elevated activation in the brainstem, amygdala, and mPFC system in contrast to PTSD responders with low SCR. Increased activation of these regions within the high SCR responders suggests that nonconscious fear perception in PTSD may depend on concurrent physiological arousal.46

 
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