Dysfunction of ventrolateral prefrontal cortex underlying social anxiety disorder: A multi-channel NIRS study (original) (raw)
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Brain Imaging and Behavior, 2013
Preliminary studies examining brain function associated with social anxiety suggest the possibility of right-sided prefrontal activation associated with phobic stimulation. Although most existing neuroimaging techniques preclude participants from engaging in ecologically valid social tasks during assessment, functional near-infrared spectroscopy (fNIRS) is a promising new technique that permits such assessment. The present study investigated the utility of the fNIRS procedure and explored frontal asymmetry during in vivo social challenge tasks among female undergraduate students who scored in top and bottom percentiles on a social anxiety screening measure. Results revealed that participants in both groups experienced a significant increase in concentration of blood volume and oxygenated hemoglobin in the right hemisphere compared to the left hemisphere while giving a speech. Non-hemispheric effects were also observed. In addition, the high anxiety group showed a non-significant trend toward greater right frontal activity than the low anxiety group. This study highlights the utility of the fNIRS device in successfully assessing real-time changes in cerebrovascular response as a function of naturalistic social behavior, and supports the potential utility of this technology in the study of the neurophysiology of social anxiety.
Comprehensive psychiatry, 2017
Neuroimaging findings suggest that social anxiety disorder (SAD) may be correlated with changes in regional- or network-level brain function. However, few studies have explored alterations in intrinsic resting cerebral function in patients with SAD at both the regional and network levels, particularly focusing on the theory of mind (ToM)-related regions. This study was performed to investigate changes in neural activity and functional connectivity (FC) in ToM-related regions during the resting state in SAD patients and to determine how these alterations are correlated with the clinical symptoms of SAD. Forty-three SAD patients and 43 matched healthy controls underwent resting-state functional magnetic resonance imaging (rsfMRI) scans. First, the amplitude of low-frequency fluctuation (ALFF) approach was used to explore regional activity. Then, the ToM-related region, i.e., the left precuneus, which showed altered ALFF values, was adopted as a seed for further FC analyses to assess n...
Neurocognitive Functions in Social Anxiety Disorder
Middle Black Sea Journal of Health Science, 2020
Objective: The purpose of this study was to assess the neurocognitive functions of patients with social phobia and to examine the relation between these functions and the severity of the disease. Methods: The study was performed with 30 patients under monitoring with a diagnosis of social phobia at the Ondokuz Mayıs University Psychiatry Clinic and 30 age- and sex-matched healthy controls. Patients were assessed using the Hamilton Anxiety Rating Scale (HARS), the State-Trait Anxiety Inventory (STAI), and the Liebowitz Social Anxiety Scale (LSAS). Both groups were administered the Wisconsin Card Sorting Test (WCST), the Stroop Test, the Auditory-Verbal Learning Test (AVLT), and the Trail Making Test (TMT) forms A and B, and the two groups’ neurocognitive performances were compared. Results: Social phobia patients exhibited significantly poorer performance than the control group in terms of total number of errors, number of perseverative errors and number of categories completed on th...
Social anxiety disorder: a critical overview of neurocognitive research
WIREs Cognitive Science, 2016
Social anxiety is a common disorder characterized by a persistent and excessive fear of one or more social or performance situations. Behavioral inhibition is one of the early indicators of social anxiety, which later in life may advance into a certain personality structure (low extraversion and high neuroticism) and the development of maladaptive cognitive biases. While there are several effective psycho‐ and pharmacotherapy options, a large number of patients benefit insufficiently from these therapies. Brain and neuroendocrine research can help uncover both the biological basis of social anxiety and potentially provide indicators, ‘biomarkers,’ that may be informative for early disease detection or treatment response, above and beyond self‐report data. Several large‐scale brain networks related to emotion, motivation, cognitive control, and self‐referential processing have been identified, and are affected in social anxiety. Social anxiety is further characterized by increased co...
Neural correlates of altered general emotion processing in social anxiety disorder
2011
Specific anxiety disorders are characterized by altered emotion processing of phobia-specific stimuli at the neurobiological level. Recent work has concentrated on specific anxietyprovoking stimuli; focusing on arousal-or fear-related brain areas such as the amygdala. We analyzed brain activation during the cued anticipation of unpleasant or uncertain emotional stimuli as a means of modeling an unspecific anxiety-laden situation. Sixteen patients with social anxiety disorder (SAD) and eighteen healthy control subjects completed a task during functional magnetic resonance imaging involving the anticipation of cued visual stimuli with prior known emotional valence (positive, negative, and neutral) or prior unknown/ambiguous emotional content. The anticipated stimuli had no social phobia specific content. During the anticipation of emotional stimuli of prior known negative and prior ambiguous emotional valence, brain activity in patients with SAD was increased in the upper midbrain/dorsal thalamus, the amygdala, and in temporo-occipital and parietal regions as compared to control subjects. Activity was decreased in SAD in left orbitofrontal cortex. Activations in the amygdala and in occipital regions correlated with trait anxiety and social anxiety measures. In conclusion, SAD was associated with enhanced activation in brain regions involved in emotional arousal as well as in attention and perception processing during the anticipation of non-specific, general emotional stimuli. Hence, our results suggest that patients with SAD not only have an altered processing of specific feared stimuli, but also a more generally disturbed emotion processing in basic neural pathways. These findings have implications for diagnostic models and the treatment of SAD.
Neural Bases of Social Anxiety Disorder
Archives of General Psychiatry, 2009
Context: Social anxiety disorder is thought to involve emotional hyperreactivity, cognitive distortions, and ineffective emotion regulation. While the neural bases of emotional reactivity to social stimuli have been described, the neural bases of emotional reactivity and cognitive regulation during social and physical threat, and their relationship to social anxiety symptom severity, have yet to be investigated. Objective: To investigate behavioral and neural correlates of emotional reactivity and cognitive regulation in patients and controls during processing of social and physical threat stimuli. Design: Participants were trained to implement cognitivelinguistic regulation of emotional reactivity induced by social (harsh facial expressions) and physical (violent scenes) threat while undergoing functional magnetic resonance imaging and providing behavioral ratings of negative emotion experience. Setting: Academic psychology department. Participants: Fifteen adults with social anxiety disorder and 17 demographically matched healthy controls. Main Outcome Measures: Blood oxygen leveldependent signal and negative emotion ratings. Results: Behaviorally, patients reported greater negative emotion than controls during social and physical threat but showed equivalent reduction in negative emotion following cognitive regulation. Neurally, viewing social threat resulted in greater emotion-related neural responses in patients than controls, with social anxiety symptom severity related to activity in a network of emotion-and attention-processing regions in patients only. Viewing physical threat produced nobetween-groupdifferences.Regulationduringsocialthreat resulted in greater cognitive and attention regulation-related brain activation in controls compared with patients. Regulation during physical threat produced greater cognitive control-related response (ie, right dorsolateral prefrontal cortex) in patients compared with controls. Conclusions: Compared with controls, patients demonstrated exaggerated negative emotion reactivity and reduced cognitive regulation-related neural activation, specifically for social threat stimuli. These findings help to elucidate potential neural mechanisms of emotion regulation that might serve as biomarkers for interventions for social anxiety disorder.
Journal of Biomedical Optics, 2014
According to the valence asymmetry hypothesis, the left/right asymmetry of prefrontal cortex (PFC) activity is correlated with specific emotional responses to mental stress and personality traits. Here, we evaluated the relation between emotional state and asymmetry in PFC activity at rest by using near-infrared spectroscopy (NIRS). We measured spontaneous oscillation of oxyhemoglobin (oxy-Hb) concentrations in the bilateral PFC at rest in normal adults employing two-channel NIRS. In order to analyze left/right asymmetry of PFC activity at rest, we calculated the laterality index at rest (LIR) (see text). We investigated the correlation between the LIR and anxiety levels evaluated by the State-Trait Anxiety Inventory (STAI) test. We found that the right PFC was more active at rest than the left PFC, corresponding to a higher anxiety level measured by the STAI; that is, subjects with right-dominant activity at rest showed higher STAI scores, while those with leftdominant oxy-Hb changes at rest showed lower STAI scores. Aging had no significant effect on the relation. The present results obtained by NIRS are consistent with the valence asymmetry hypothesis. We emphasize NIRS may be a useful tool for objective assessment of anxiety levels.
Neurobiological correlates of social anxiety disorder: an update
CNS Spectrums, 2014
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.
Social anxiety disorder (SAD) is one of the most frequent anxiety disorders. The landmark meta-analysis of functional neuroimaging studies by Etkin & Wager (2007) revealed primarily the typical fear circuit as overactive in SAD. Since then, new methodological developments such as functional connectivity and more standardized structural analyses of grey and white matter have been developed. We provide a comprehensive update and a meta-analysis of neuroimaging studies in SAD since 2007 and present a new model of the neurobiology of SAD. We confirmed the hyperactivation of the fear circuit (amygdala, insula, anterior cingulate and prefrontal cortex) in SAD. In addition, task-related functional studies revealed hyperactivation of medial parietal and occipital regions (posterior cingulate, precuneus, cuneus) in SAD and a reduced connectivity between parietal and limbic and executive network regions. Based on the result of this meta-analysis and review, we present an updated model of SAD adopting a network-based perspective. The disconnection of the medial parietal hub in SAD extends current frameworks for future research in anxiety disorders.