Introduction: Imagery rescripting is a method to rescript the imagery of fear memory to safety imagery. Although the mechanism of imagery rescripting is not clear, it has been thought to diminish fear memory through reconsolidation. Method: A search of Web of Science and Science Direct was conducted. The search term (“imagery rescripting” and “reconsolidation”) was used. Results: This review revealed that no study has indicated the relation between imagery rescripting and reconsolidation. Conclusions: Further research should (1) compare the late relapse of imagery rescripting and imaginal exposure, (2) compare the brain activities related to imagery rescripting and imaginal exposure, (3) compare the changes of the declarative contents of traumatic memory after imagery rescripting and imaginal exposure, and (4) compare the intervention effects of inserting imagery immediately after retrieval and 10 minutes after retrieval.

Classical conditioning plays an important role in developing anxiety related disorders. However, such role is not clearly specified in recent findings in learning psychology and clinical psychological practices. This paper aimed to discuss the method for applying the findings of classical conditioning in animals including humans and associative learning theories to clinical psychological practices. We described phenomena that are related to classical conditioning procedure from the perspective of “the factor other than conditioning trials affecting conditioned response (CR)” and “the factor causing relapse of CR after extinction”, and then discussed the possibility of these phenomena occurring in clinical settings. We also reviewed two associative learning theories, Rescorla–Wagner model and Bouton’s model, and then discussed whether these can be applied to clinical interventions. Finally, we discussed the importance of applying the findings of classical conditioning to cognitive behavior therapy.

Comorbid rates of anxiety disorders among patients with bipolar disorders are higher than those among general populations, although comorbid rates vary among studies because of heterogeneity. In addition, the scantiness of randomized controlled and double blind studies causes difficulty in formulating treatment guidelines for comorbid anxiety disorders among bipolar disorders. It is essential when trying to understand these complex relationships to take a comprehensive, broad view of psychiatric disorders including personality and neurodevelopmental disorders in addition to bipolar and anxiety disorders. The differential diagnosis between bipolar and borderline personality disorder has been debated, although specific psychotherapy is the choice of treatment for borderline personality disorder. Adults with autism spectrum disorder who did not meet the former narrow diagnostic criteria develop secondary psychiatric disorders such as bipolar and anxiety disorders because they had not received early intervention. In those cases, active psychiatric treatment rather than just empathic observations should be adopted. Broader perspectives and specific treatments are needed to resolve this clinical tasks how to understand and treat anxiety disorders among bipolar disorders.

The etiology of Panic disorder (PD) is related to some neuroanatomical pathways involving conditioned fear, “fear network.” Gorman et al. (2000) postulated that panic originated in an abnormally sensitive “fear network” since the physiological and behavioral consequences of response to a conditioned-fear stimulus appeared to be similar to a panic attack (Gorman et al., 2000). This “fear network” is centered in the amygdala and involves interaction with the hippocampus and medial prefrontal cortex (mPFC). The amygdala receives sensory information from two major pathways: downstream, from the brainstem structures and sensory thalamus, and upstream, from the sensory cortex and via corticothalamic relays, allowing for higher level neurocognitive processing and modulation of sensory information (Andrews et al., 2009; Gorman et al., 2000). Contextual information is stored in memory in the hippocampus and conveyed directly to the amygdala. Major different pathways of the amygdala relevant to anxiety include locus coeruleus (increases noradrenaline release, which contributes to physiological and behavioral arousal); the periaqueductal gray region (results in defensive behavior and postural freezing); the hypothalamic paraventricular nucleus (activates the hypothalamic–pituitary–adrenal axis, releasing adrenocorticoids); the hypothalamic lateral nucleus (activates the sympathetic nervous system); and the parabrachial nucleus (influences respiratory rate) (Andrews et al., 2009; Gorman et al., 2000). Extinction of conditioned fear involves increased activity in the rostral anterior cingulate gyrus and ventral mPFC and decreased activity in the amygdala (Etkin et al., 2006).

Anxious-depressive attack (ADA) is a symptom cluster, without a direct psychological cause, comprised of a sudden intense, distressing emotional fit; this is followed by the intrusion of ruminative thoughts, such as negative memories of several stories accompanied by severe agitation and worry. These symptoms result in coping behaviors, including acting out. ADA is seen in anxiety disorders, affective disorders, and some personality disorders. ADA mimics complex post-traumatic stress disorder (CPTSD) in terms of re-experiencing past negative events in the form of vivid memories accompanied by intense emotions, autonomic arousal, and hypervigilance. Disturbances in self-organization (DSO), which is a proposed hierarchical structure of CPTSD described in ICD-11, are also seen regularly in ADA. DSO affects dysregulation, negative self-concept, and relationship disturbances, which are also observed in patients with ADA. These are considered to be consequences of rejection sensitivity. This is because patients with ADA show a higher level of social anxiety. ADA differs from CPTSD in some ways; it comprises a definite symptom cluster that is seen trans-diagnostically. The ruminative intriguing thoughts of ADA are abundant and mostly not severe traumatic memories, sometimes, they are even anticipatory concerns or happy past events. Moreover, ADA and panic attacks appear alternatively in panic disorders. It is concluded that ADA is similar to, but has specific differences from CPTSD, as described in ICD-11.

The purpose of this study was to test the effects of cognitive-behavioral factors on job-hunting anxiety in university students. 181 Japanese university students in their junior year (55 males and 125 females, mean age＝20.95 years, SD＝0.74 years) completed assessments of cognitive-behavioral factors including automatic thoughts, problem-solving skills, and social skills, as well as job-hunting anxiety. Negative automatic thoughts were positively related to several aspects of job-hunting anxiety. On the other hand, problem-solving skills and social skills were negatively related to relatively limited aspects of job-hunting anxiety. However, positive automatic thoughts were not related to any aspects of job-hunting anxiety. These results suggest that cognitive-behavioral therapy focused on modification of negative automatic thoughts, problem solving skills, and social skills may reduce job-hunting anxiety in university students. Meanwhile, interventions focusing only on increasing positive thinking may not be effective in reducing job-hunting anxiety.