In support, previous studies investigating the content of patients’ descriptions of their OCD symptoms have revealed that physiological changes associated with fear and anxiety, such as a racing heart, play a key role in triggering a variety of obsessions and compulsions [38]. Difficulties with top-down cognitive appraisal, such as interpreting one’s own thoughts and feelings as evidence that an unlikely event occurred, likely also play a role in perpetuating obsessive symptoms. Consistent with these clinical observations, neuroimaging studies have reported increased amygdala activity, reduced dorsal prefrontal activity and reduced prefrontal-amygdala functional connectivity during the provocation and cognitive reappraisal of stimuli that provoke OCD symptoms and increase physiological arousal [36, 39]. Together, these findings suggest that hyperactive limbic fear responses and insufficient recruitment of dorsal prefrontal top-down control are involved in the production and/or maintenance of fear in the context of OCD triggers. There is also evidence that individuals with OCD have difficulty extinguishing learned fear responses [37, 40–42], likely due to impaired “safety-signaling” functions of the vmPFC [40], which may further contribute to the maintenance of fear-related OCD symptoms.
