Meta-analyses of fear conditioning studies, a related experimental model that focuses on predictable (rather than unpredictable) threats, have also reported resulting hyperactivation in the dorsal anterior cingulate cortex and left and right anterior insula ( 28, 29), and a recent meta-analysis investigated shared neural correlates across mood and anxiety disorders ( 30). Meta-analyses and systematic reviews exploring the neural circuitry of different anxiety disorders suggest that many of the same regions have been implicated ( 22– 25) however, differences across disorders have not been investigated in the past decade ( 26, 27). Induced anxiety via unpredictable threat paradigms has been shown to involve brain regions involved in emotional-processing, decision-making, and reward circuitry, such as the amygdala, anterior cingulate cortex, medial prefrontal cortex, bed nucleus of the stria terminalis (BNST), insula, and striatum ( 17– 21), but this has not been systematically meta-analyzed. Critically, for the “experimental psychopathology” ( 7) approach to be valid, the assumption that induced anxiety evokes (at least some of) the same neurobiological mechanisms as pathological anxiety must be met, particularly on emotion-related paradigms, where the literature suggests that they lead to similar changes in cognitive performance ( 14). What remains insufficiently explored, however, is the extent to which underlying neurobiological mechanisms overlap, and whether ostensibly similar symptoms are driven by dissociable underlying mechanisms. Induced and pathological anxiety therefore overlap at the level of symptoms, as both promote functions and states that promote harm avoidance. A growing body of literature shows that, in addition to clear increases in subjective and physiological reports of anxiety ( 13), threat of shock results in cognitive and psychophysiological changes mirroring pathological anxiety ( 14– 16). This approach is well validated ( 10) and is reliable both for self-report and task performance ( 11), and, critically, it is also fully translational: a close paradigm is used in animal models ( 12). This adaptive anxiety can be reliably induced in healthy individuals in the laboratory by exposing them to unpredictable threat of rare electrical shocks. It occurs naturally in every individual-when walking down a dark alley at night, for instance. Anxiety enhances vigilance to threat and primes defense mechanisms ( 9), which allows the individual to react faster in dangerous situations. This experimental approach is possible because anxiety, perhaps uniquely among psychiatric symptoms, is also an adaptive behavior with a benefit to survival. More precisely, using the same techniques to induce anxiety in healthy individuals and animal models should enable us to both better understand the neurobiological basis of anxiety and provide an intermediate route to screen the efficacy of candidate interventions prior to full clinical trial ( 8). It has recently been argued, therefore, that models of anxiety (as defined by aversive anticipation and apprehension of perceived potential but unpredictable threats) in healthy humans could help us bridge this gap and facilitate therapeutic progress ( 7). Response rates to existing treatments usually range between 40% and 60% ( 4), which leaves a large number of people with debilitating symptoms and a high probability of relapse ( 5).ĭevelopment of new treatments for symptoms of anxiety has stagnated for several decades ( 6), however, partly as a result of the difficulty of establishing robust translational links between models of fear and anxiety in rodents and clinical anxiety in humans. Anxiety disorders constitute the most prevalent mental health condition ( 1), with a lifetime prevalence of 17% ( 2), resulting in significant individual and social impairment ( 1) and a considerable overall burden of disease, ranking ninth among causes of years lived with disability in the world in 2015 ( 3).
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