To prepare the body to face this danger, these stimuli can evoke “freeze, flight, fight, fright” reactions ( Bracha 2004) or “tend-and-befriend” responses (such as turning to others for help or social support, or making a situation less tense, dangerous, or uncomfortable in some way) ( Taylor et al. Poor habituation and poor extinction are presented as dysfunctional mechanisms contributing to persistence of nonexperiential and experiential phobias, respectively.įear is an emotion of anticipation that is triggered when a situation that is at risk for our safety and/or the safety of others is perceived, through either exteroceptive inputs or the endocrine and autonomic nervous systems (interoceptive inputs). These fear mechanisms are also distinguished in specific phobias, which can indeed be nonexperiential (implicating innate, learning-independent mechanisms) or experiential (implicating learning-dependent mechanisms). Innate and learned fear mechanisms, particularly those involving the amygdala, are considered. The neurobiological basis of normal and pathological fear reactions is reviewed in this article. Although recognized as highly debilitating, pathological fear remains insufficiently treated, indicating the importance of research on fear processing. However, dysfunction in fear processing can lead to psychiatric disorders in which fear outweighs the danger or possibility of harm. Its role is to prepare the body to face this danger. Fear, which can be expressed innately or after conditioning, is triggered when a danger or a stimulus predicting immediate danger is perceived.
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