{"title":"Anxious-depressive attack and rejection sensitivity-Toward a new approach to treatment-resistant depression.","authors":"Hisanobu Kaiya","doi":"10.1002/npr2.12399","DOIUrl":null,"url":null,"abstract":"<p><p>This paper aimed to find clues to treatment-resistant depression (TRD) solutions. Depression comorbid with anxiety is often treatment-resistant where anxious-depressive attack (ADA) often lurks. ADA is a recently proposed clinical idea for just a psychological version of a panic attack. It mostly begins with an abrupt surge of intense anxiety followed by uninterrupted intrusive thoughts; lasting ruminations about regret or worry produced by violent anxiety, agitation, and loneliness. Acting-out behaviors such as deliberate self-injury and over-dose may also be observed during the attack. As the basic psychopathology of ADA, rejection sensitivity (RS) was revealed by a structural equation model. It is said that the presence of RS in depressive disorders implies a poor prognosis. The following biological markers for RS were reviewed in the literature: first, the involvement of the μ-opioid receptor function in RS and, secondly, hypersensitivity of the dopamine D4 receptor (DRD4) in the medial prefrontal cortex. The latter has been suggested in fear-conditioned animal experiments. Manipulation of the μ-opioid receptor function together with the DRD4 function may culminate in a treatment for RS, which could contribute to the development of a treatment for TRD via the improvement of ADA.</p>","PeriodicalId":19137,"journal":{"name":"Neuropsychopharmacology Reports","volume":" ","pages":"17-28"},"PeriodicalIF":2.0000,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10932773/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuropsychopharmacology Reports","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/npr2.12399","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/12/7 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
This paper aimed to find clues to treatment-resistant depression (TRD) solutions. Depression comorbid with anxiety is often treatment-resistant where anxious-depressive attack (ADA) often lurks. ADA is a recently proposed clinical idea for just a psychological version of a panic attack. It mostly begins with an abrupt surge of intense anxiety followed by uninterrupted intrusive thoughts; lasting ruminations about regret or worry produced by violent anxiety, agitation, and loneliness. Acting-out behaviors such as deliberate self-injury and over-dose may also be observed during the attack. As the basic psychopathology of ADA, rejection sensitivity (RS) was revealed by a structural equation model. It is said that the presence of RS in depressive disorders implies a poor prognosis. The following biological markers for RS were reviewed in the literature: first, the involvement of the μ-opioid receptor function in RS and, secondly, hypersensitivity of the dopamine D4 receptor (DRD4) in the medial prefrontal cortex. The latter has been suggested in fear-conditioned animal experiments. Manipulation of the μ-opioid receptor function together with the DRD4 function may culminate in a treatment for RS, which could contribute to the development of a treatment for TRD via the improvement of ADA.