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The objective of this study was to analyze the neurostructural abnormalities of brain areas responsible for the acquisition and maintenance of fear in small animal phobia by comparing gray matter volume (GMV) in individuals with phobia and non-fearful controls. Structural magnetic resonance imaging was obtained from 62 adults (79% female) assigned to one of two groups: 31 were diagnosed with small animal phobia and 31 were non-fearful controls. To investigate structural alterations, a whole-brain voxel-based morphometry analysis was conducted to compare the GMV of the brain areas involved in fear between both groups. The results indicated that individuals with a small animal specific phobia showed smaller GMV in cortical regions, such as the orbitofrontal (OFC) and medial frontal cortex, and greater GMV in the putamen than non-fearful controls. These brain areas are responsible for avoidant behavior (putamen) and emotional regulation processes or inhibitory control (prefrontal cortex (PFC)), which might suggest a greater vulnerability of phobic individuals to acquiring non-adaptive conditioned responses and emotional dysregulation. The findings provide preliminary support for the involvement of structural deficits in OFC and medial frontal cortex in phobia, contributing to clarify the neurobiological substrates for phobias.

Cognitive behavioral therapy (CBT) packages for anxiety disorders, such as phobias, usually include gradual exposure to anxious contexts, positive self-verbalizations, and relaxation breathing. The objective of this research was to analyze the specific neural activation produced by the self-verbalizations (S) and breathing (B) included in CBT. Thirty participants with clinical levels of a specific phobia to small animals were randomly assigned to three fMRI conditions in which individuals were exposed to phobic stimuli in real images: a group underwent S as a technique to reduce anxiety; a second group underwent B; and a control group underwent exposure only (E). Simple effects showed higher brain activation comparing E > S, E > B, and S > B. In particular, in the E group, compared to the experimental conditions, an activation was observed in sensory-perceptive and prefrontal and in other regions involved in the triggering of emotion (i.e., amygdala, supplementary motor area, and cingulate gyrus) as well as an activation associated with interoceptive sensitivity (i.e., insula and cingulate cortex). According to the specific tool used, discrepancies in the neural changes of CBT efficacy were observed. We discuss the theoretical implications according to the dual model of CBT as a set of therapeutic tools that activate different processes.

Brain regions involved in small-animal phobia include subcortical and cortical areas. The present study explored the neuronal correlates of small-animal phobia through fMRI data to determine whether a manipulation of number and proximity parameters affects the neurobiology of the processing of feared stimuli. The participants were 40 individuals with phobia and 40 individuals without phobia (28.7% male and 71.3% female). They watched videos of real and virtual images of spiders, cockroaches and lizards in motion presented more or less nearby with one or three stimuli in the different conditions. The results suggested a differential brain activity between participants with and without phobia depending on the proximity and number of phobic stimuli. Proximity activated the motor response marked by the precentral gyrus and the cingulate gyrus. By contrast, the number of stimuli was associated with significant sensory activity in the postcentral gyrus and ventromedial prefrontal cortex. We also observed a greater activity in the occipital cortex when exploring the number compared to the proximity factor. Threatening stimuli presented nearby and those presented in greater numbers generated an intense phobic response, suggesting a different emotion regulation strategy. Based on these findings, exposure therapies might consider including proximity to the threat and number of stimuli as key factors in treatment.