Striatal Functional Alteration During Incentive Anticipation in Pediatric Anxiety Disorders

Abstract

Objective Behavioral inhibition is an early childhood temperament recently associated with altered striatal response in adolescence to incentives of increasing magnitudes. Since early childhood behavioral inhibition is also associated with risk for adolescent social phobia, a similar pattern of striatal activation may manifest in social phobia. The present study compares striatal function in healthy adolescents, adolescents with social phobia, and adolescents with generalized anxiety disorder. Method Blood-oxygen-level-dependent signal in striatal regions was examined in 58 medication-free adolescents—14 with social phobia, 18 with generalized anxiety disorder but not social phobia, and 26 with no psychiatric disorder—matched on sex, age, puberty, IQ, and socioeconomic status. During functional magnetic resonance imaging, participants responded to incentive cues depicting potential monetary gains or losses of varying magnitudes. Results While anticipating incentives of increasing magnitude, adolescents with social phobia showed increasingly heightened caudate and putamen activation at a level greater than that seen in the healthy comparison and generalized anxiety disorder groups. The generalized anxiety disorder group showed a unique valence-specific putamen response relative to the healthy comparison or social phobia group. Both patient groups displayed more complex patterns in the nucleus accumbens than in the caudate or putamen. Conclusions Caudate and putamen hypersensitivity to incentives of increasing magnitudes characterizes adolescent social phobia, relative to activation in this region in adolescents with generalized anxiety disorder as well as healthy adolescents. Thus, these findings resemble the pattern previously found in adolescents with early childhood behavioral inhibition, thereby implicating similar neural responses to anticipation of incentives in both early childhood behavioral inhibition and adolescent social phobia.

A Preliminary Study of the Infl uence of Age of Onset and Childhood Trauma on Cortical Thickness in Major Depressive Disorder

“…The putamen, which belongs to the basal ganglia, has widely spread functional connections with cortical and subcortical areas in the brain [44]. The putamen has been suggested to be related to a number of anxiety disorders and anxiety symptoms, such as GAD [45], social anxiety disorder [45], posttraumatic stress disorder [46], panic disorder [47], obsessivecompulsive disorder [48], lactated-induced anxiety [49] and anxiety symptoms in Parkinson disease [50]. Besides, GAD patients often accompany with somatic symptoms which are associated with sympathetic dysregulation [51].…”

Longitudinal Associations Between Preschool Disruptive Mood Dysregulation Disorder Symptoms and Neural Reactivity to Monetary Reward During Preadolescence

“…Additional research is, therefore, needed to better understand the pathophysiology of DMDD and reward processing. Altered reward functioning is apparent in multiple psychiatric disorders, including depressive (Russo and Nestler 2013), bipolar (Nusslock et al 2012), substance use (Koob and Volkow 2010), and, possibly, anxiety (Guyer et al 2012) disorders, and may contribute to multiple behavioral, social, and emotional outcomes (Forbes and Goodman 2014). Identifying longitudinal associations between DMDD symptoms in early childhood and reward-processing disruptions in preadolescence may shed light on the processes linking DMDD to the development of other forms of psychopathology and adverse functional outcomes in adolescence and adulthood.…”

Pediatric anxiety disorders: from neuroscience to evidence-based clinical practice

“…These dysfunctional processes can be classified into five groups of information-processing functions: 1) threatattention interaction (a tendency for anxious children to automatically orient their attention towards or away from threats) 72 ; 2) threat appraisal (a tendency for anxious children to classify and respond to neutral or harmless stimuli as if they are dangerous) 73 ; 3) memory and learning processes (a tendency for anxious individuals to learn different associations among safe and dangerous stimuli, as presented in fear conditioning and extinction experiments) [73][74][75] ; 4) social evaluative processes (a tendency for anxious children to become concerned about peer evaluation) 76 ; 5) increased sensitivity to rewards (a tendency for anxiety children to more strongly alter their behavior when trying to achieve rewards). 77,78 This set of findings suggests that anxiety disorders involve dysfunctional processes in various emotional and cognitive processes, each of which is in turn regulated by several brain regions that may support anxiety disorder pathophysiology. 31,71 Some of the regions include: the amygdala, several portions of the prefrontal cortexparticularly the ventrolateral and dorsomedial divisionsand dysfunctions in the basal ganglia, particularly in patients with OCD.…”