Anterior cingulate neurochemistry in social anxiety disorder: 1H-MRS at 4???Tesla

Neuroreport ◽  
2005 ◽  
Vol 16 (2) ◽  
pp. 183-186 ◽  
Author(s):  
K. Luan Phan ◽  
Daniel A. Fitzgerald ◽  
Bernadette M. Cortese ◽  
Navid Seraji-Bozorgzad ◽  
Manuel E. Tancer ◽  
...  
Keyword(s):  
Anxiety Disorder ◽  
Social Anxiety ◽  
Social Anxiety Disorder ◽  
Anterior Cingulate ◽  
1H Mrs

scholarly journals Anterior cingulate cortex activity as a candidate biomarker for treatment selection in social anxiety disorder

BJPsych Open ◽  
2018 ◽  
Vol 4 (3) ◽  
pp. 157-159 ◽  
Author(s):  
Andreas Frick ◽  
Jonas Engman ◽  
Kurt Wahlstedt ◽  
Malin Gingnell ◽  
Mats Fredrikson ◽  
...  
Keyword(s):  
Anxiety Disorder ◽  
Social Anxiety ◽  
Anterior Cingulate Cortex ◽  
Social Anxiety Disorder ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Cingulate Cortex ◽  
Demographic Variables ◽  
Treatment Selection ◽  
Anterior Cingulate ◽  
Potential Biomarker

SummaryWe aimed to identify biomarkers to guide the decision to add selective serotonin reuptake inhibitors (SSRI) to psychological treatment for social anxiety disorder (SAD). Forty-eight patients with SAD underwent functional magnetic resonance imaging and collection of clinical and demographic variables before treatment with cognitive–behavioural therapy, combined on a double-blind basis with either escitalopram or placebo for 9 weeks. Pre-treatment neural reactivity to aversive faces in the dorsal anterior cingulate cortex (ACC), but not clinical/demographic variables, moderated clinical outcomes. Cross-validated individual-level predictions accurately identified 81% of responders/non-responders. Dorsal ACC reactivity is thus a potential biomarker for SAD treatment selection.Declaration of interestNone.

scholarly journals Interoceptive active inference and self-representation in social anxiety disorder (SAD): exploring the neurocognitive traits of the SAD self

2020 ◽  
Author(s):  
Philip Gerrans ◽  
Ryan J Murray
Keyword(s):  
Anxiety Disorder ◽  
Social Anxiety ◽  
Social Anxiety Disorder ◽  
Anterior Cingulate ◽  
Affective Processing ◽  
Prediction Errors ◽  
Active Inference ◽  
Symptom Profile ◽  
Insula Cortex ◽  
High Level

Abstract This article provides an interoceptive active inference (IAI) account of social anxiety disorder (SAD). Through a neurocognitive framework, we argue that the cognitive and behavioural profile of SAD is best conceived of as a form of maladaptive IAI produced by a negatively biased self-model that cannot reconcile inconsistent tendencies to approach and avoid social interaction. Anticipated future social interactions produce interoceptive prediction error (bodily states of arousal). These interoceptive states are transcribed and experienced as states of distress due to the influence of inconsistent and unstable self-models across a hierarchy of interrelated systems involved in emotional, interoceptive and affective processing. We highlight the role of the insula cortex, in concert with the striatum, amygdala and dorsal anterior cingulate in the generation and reduction of interoceptive prediction errors as well as the resolution of social approach-avoidance conflict. The novelty of our account is a shift in explanatory priority from the representation of the social world in SAD to the representation of the SAD self. In particular, we show how a high-level conceptual self-model of social vulnerability and inadequacy fails to minimize prediction errors produced by a basic drive for social affiliation combined with strong avoidant tendencies. The result is a cascade of interoceptive prediction errors whose attempted minimization through action (i.e. active inference) yields the symptom profile of SAD. We conclude this article by proposing testable hypotheses to further investigate the neurocognitive traits of the SAD self with respect to IAI.

Common and differential alterations of general emotion processing in obsessive-compulsive and social anxiety disorder

2016 ◽  
Vol 46 (7) ◽  
pp. 1427-1436 ◽  
Author(s):  
S. Weidt ◽  
J. Lutz ◽  
M. Rufer ◽  
A. Delsignore ◽  
N. J. Jakob ◽  
...  
Keyword(s):  
Anxiety Disorder ◽  
Social Anxiety ◽  
Social Anxiety Disorder ◽  
Patient Group ◽  
Emotional Valence ◽  
Anterior Cingulate ◽  
Emotional Stimuli ◽  
Obsessive Compulsive ◽  
Compulsive Disorder ◽  
Biased Perception

BackgroundObsessive compulsive disorder (OCD) and social anxiety disorder (SAD) are characterized by biased perception and processing of potentially threatening stimuli. A hyper-reactivity of the fear-circuit [e.g. amygdala, anterior cingulate (ACC)] has been consistently reported using functional magnetic resonance imaging (fMRI) in SAD in comparison with healthy controls (HCs). Studies investigating the processing of specific emotional stimuli in OCD reported mainly orbitofrontal-striatal abnormalities. The goal of this study was to examine similar/common and differential neurobiological responses in OCD and SAD using unspecific emotional stimuli.MethodFifty-four subjects participated: two groups (each n = 18) of outpatients with a current diagnosis of OCD or SAD, and 18 HCs. All subjects underwent fMRI while anticipating and perceiving unspecific visual stimuli with prior announced emotional valence (e.g. positive).ResultsCompared to HCs, the combined patient group showed increased activation in amygdala, caudate and prefrontal/orbitofrontal cortex while anticipating unspecific emotional stimuli. Caudate was more active in the combined patient group during perception. A comparison between the OCD and the SAD samples revealed increased amygdala and decreased rostral ACC activation in OCD patients during perception, but no differences in the anticipation phase.ConclusionsOverall, we could identify common fronto-subcortical hyper-reactivity in OCD and SAD while anticipating and perceiving unspecific emotional stimuli. While differential neurobiological responses between OCD and SAD when processing specific stimuli are evident from the literature, differences were less pronounced using unspecific stimuli. This could indicate a disturbance of emotion regulation common to both OCD and SAD.

Neurobiological correlates of social anxiety disorder: an update

CNS Spectrums ◽  
2014 ◽  
Vol 20 (2) ◽  
pp. 100-111 ◽  
Author(s):  
Donatella Marazziti ◽  
Marianna Abelli ◽  
Stefano Baroni ◽  
Barbara Carpita ◽  
Carla E. Ramacciotti ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Anxiety Disorder ◽  
Social Anxiety ◽  
Social Anxiety Disorder ◽  
Anterior Cingulate ◽  
Therapeutic Interventions ◽  
Future Research ◽  
Special Focus ◽  
Brain Areas ◽  
Wide Range

Social anxiety disorder (SAD) is a condition characterized by pervasiveness and impairment in social functioning, with a prevalence in the general population between 1.9% and 12.1%. The most consistent findings on its neurobiological underpinnings involve a wide range of neurotransmitters (serotonin, norepinephrine, glutamate, and GABA) and neuropeptides (oxytocin), but no comprehensive hypothesis is yet available. In particular, oxytocin is becoming increasingly established as a “prosocial neuropeptide” and, as such, is a major focus of current research, with a great range of therapeutic applications including SAD treatment. Specifically, the amygdala plays a pivotal role in conditioning and processing of fear, and exaggerated amygdala responses in SAD patients have been observed during various social-emotional stimuli. In addition to the amygdala, other brain areas of interest in SAD-related circuitry are represented by the medial prefrontal cortex, dorsal raphe, striatum, locus coeruleus, prefrontal cortex, insular cortex, and anterior cingulate cortex. The aim of this review is to provide an update on neurobiological correlates of SAD, with a special focus on neurotransmitters and brain areas possibly involved, and suggestions for future research that could lead to more specific therapeutic interventions.

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