![]() ![]() ![]() These types of findings are particularly exciting as they might allow for a better focus on the neurocircuits involved in pathological anxiety. Some recent work had even suggested that there might be separate fear and anxiety systems orchestrated through the central nucleus of the amygdala and the BNST, respectively ( Davis, 2006). Animal work using in vivo electrophysiological recording, tracing and lesions/reversible inactivation techniques was indispensable in acquiring this knowledge. These basic components of fear circuitry are well preserved across species and likely support similar functions in humans. Some key findings from animal literature, such as the central role of amygdaloid nuclei in the acquisition of fear conditioning and expression of fear responses, the involvement of the hippocampus in contextual processing, and the importance of the infralimbic cortex in extinction recall, have been replicated across different studies and laboratories. These regions have their respective roles in the various components of fear processing such as the perception of threat or of unconditioned stimuli, the pairing of an unconditioned stimulus and conditioned response (learning/conditioning), the execution of efferent components of fear response, and the modulation of fear responses through potentiation, contextual modulation, or extinction. Key components of fear circuitry including the amygdala (and its subnuclei), nucleus accumbens (including bed nucleus of stria terminalis BNST), hippocampus, ventromedial hypothalamus, periaqueductal gray, a number of brain stem nuclei, thalamic nuclei, insular cortex, and some prefrontal regions (mainly infralimbic cortex) have been identified in these studies (for recent reviews see Davis, 2006 Maren, 2008 Quirk and Mueller, 2008). A large volume of experimental work has examined the neurocircuitry associated with fear responses, mainly in rodents, using primarily fear conditioning, inhibitory avoidance, and fear-potentiated startle models. Given that excessive fear is a key component of anxiety disorders, it is not surprising that the search for the neurocircuitry of anxiety disorders has its roots in and has been closely intertwined with studies of fear circuits in animal models. In the future, neuroimaging studies of anxiety disorders may also prove to be clinically helpful in the prediction of treatment response. Given that anxiety disorders are a significant problem in the community, recent neuroimaging research has focused on determining the brain circuits that underlie them to inform the use of existing treatments and guide the possible development of new treatments. Anxiety disorders are associated with impaired workplace performance and hefty economic costs ( Greenberg et al, 1999), as well as an increased risk of cardiovascular morbidity and mortality ( Albert et al, 2005 Kawachi et al, 1994 Smoller et al, 2007). According to a recent epidemiological study, the lifetime prevalence of any anxiety disorder is 28.8% ( Kessler et al, 2005). Additional research will be needed to (1) clarify the exact role of each component of the fear circuitry in the anxiety disorders, (2) determine whether functional abnormalities identified in the anxiety disorders represent acquired signs of the disorders or vulnerability factors that increase the risk of developing them, (3) link the findings of functional neuroimaging studies with those of neurochemistry studies, and (4) use functional neuroimaging to predict treatment response and assess treatment-related changes in brain function.Īnxiety disorders are marked by excessive fear (and avoidance), often in response to specific objects or situations and in the absence of true danger, and they are extremely common in the general population. Unlike other anxiety disorders, post-traumatic stress disorder is associated with diminished responsivity in the rostral anterior cingulate cortex and adjacent ventral medial prefrontal cortex. Activation in the insular cortex appears to be heightened in many of the anxiety disorders. In general, these studies have reported relatively heightened amygdala activation in response to disorder-relevant stimuli in post-traumatic stress disorder, social phobia, and specific phobia. We review this research, as well as neuroimaging studies of anxiety disorders. Research on the neurocircuitry of anxiety disorders has its roots in the study of fear circuits in animal models and the study of brain responses to emotional stimuli in healthy humans. Anxiety disorders are a significant problem in the community, and recent neuroimaging research has focused on determining the brain circuits that underlie them. ![]()
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