![]() ![]() ![]() While the segregation has been translated into the Acute Threat (fear) and Potential Threat (anxiety) domains proposed in the Research Domain Criteria (RDoC) framework, accumulating evidence from neuroimaging studies in healthy individuals suggests a shared neurofunctional basis of anxiety, fear and general negative affect. Despite ongoing debates about the nosology of psychiatric disorders and overarching symptom domains, the neurobiological substrates underlying these conceptualizations remain unclear.Īnimal models and human neuroimaging studies have demonstrated that anxiety and fear are regulated by distinct neurobiological circuits such that the fear response is mediated by the central nucleus of the amygdala (CeA), and anxiety is mediated by the bed nucleus of the stria terminalis (BNST). Particularly, GAD and MDD exhibit symptomatic overlap (e.g., negative affect, worry) and common genetic factors. On the other hand, subcategories of AD are often highly co-morbid with each other as well as with other emotional (internalizing) disorders. This echoes findings on the psychopathological factor model in internalizing disorders indicating that SAD, SP, PD and AG originate from the higher-order “fear” dimension, whereas GAD and major depressive disorder (MDD) originate from the “anxious-misery” or “distress” dimension. Recent overarching conceptualizations based on the DSM-5 propose that AD can be placed along a fear–anxiety continuum ranging from excessive fear-based responses to imminent specific threats in fear-related anxiety disorders (FAD, e.g., social anxiety disorder, SAD specific phobias, SP panic disorder, PD and agoraphobia, AG) to a rather diffuse anxious apprehension of events in anxiety-related anxiety disorders such as generalized anxiety disorder (GAD). AD comprise a group of heterogeneous disorders that share features of excessive fear and anxiety. transcranial magnetic stimulation or neurofeedback).Īnxiety disorders (AD) constitute the most prevalent diagnostic group of mental disorder and cause considerable suffering, disability and economic costs. These findings may have implications for determining promising target regions for disorder-specific neuromodulation interventions (e.g. Our study is the first to provide meta-analytic evidence for distinct neuroanatomical abnormalities underlying the pathophysiology of anxiety-, fear-related and depressive disorders. No shared structural abnormalities were found. While FAD showed less robust alterations in lingual gyrus compared to controls, this group presented intact frontal integrity. ![]() Both GAD and MDD showed decreased prefrontal volumes compared to controls and FAD. Results showed that GAD exhibited disorder-specific altered volumes relative to FAD including decreased volumes in left insula and lateral/medial prefrontal cortex as well as increased right putamen volume. Given that a neurobiological evaluation is lacking, we conducted a Seed-based D-Mapping comparative meta-analysis including coordinates as well as original statistical maps to determine common and disorder-specific gray matter volume alterations in generalized anxiety disorder (GAD), fear-related anxiety disorders (FAD, i.e., social anxiety disorder, specific phobias, panic disorder) and major depressive disorder (MDD). Internalizing disorders encompass anxiety, fear and depressive disorders, which exhibit overlap at both conceptual and symptom levels. ![]()
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