PROSPECTIVE STUDY OF RELAPSE PREDICTORS IN PANIC DISORDER

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。恐慌症的病因尚不清楚。然而，对恐惧的神经科学研究和对焦虑的临床研究数据的汇总表明，恐慌症可能是由基因决定的大脑恐惧通路的超敏反应和压力生活事件的影响的结合来解释的。从动物和人类的研究中也有大量的证据表明，压力生活事件会影响大脑恐惧通路的功能，并与恐慌症的发展、发作和复发有关。我们之前已经证明了惊恐障碍患者心血管和呼吸功能测量的显著异常。对心脏和肺部的控制受到大脑中与压力反应和焦虑发展有关的区域的影响。我们现在计划调查压力生活事件，大脑对心血管和呼吸功能的控制，以及成功治疗后恐慌症复发的可能性之间的关系。使用非侵入性方法，我们将获得恐慌症患者心血管和呼吸功能的测量，以及对压力生活事件的严格历史评估。然后，我们将使用认知行为疗法和抗抑郁药舍曲林的组合，这两种疗法对治疗惊恐障碍都有良好的疗效，并在治疗期间和之后反复测量压力、心血管和呼吸。急性治疗期为3个月，维持治疗期为3个月，随访无治疗期为12个月。本研究旨在检验惊恐障碍患者是否容易受到生活压力事件的影响，以及治疗前、治疗中、治疗后心血管和呼吸功能与惊恐复发的关系。这些关系可能为指导治疗方法提供重要数据，并允许临床医生测试对恐慌障碍的易感性。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The etiology of panic disorder remains unknown. Yet a convergence of data from neuroscience research on fear and clinical research on anxiety suggests panic disorder may be explained by a combination of genetically determined hypersensitivity of the brains fear pathways and the influence of stressful life events. There is also abundant evidence from both animal and human studies that stressful life events can impact on functioning of the brain's fear pathways and are associated with development, onset, and relapse of panic disorder. We have previously demonstrated significant abnormalities in cardiovascular and respiratory function measures in individuals with panic disorder. The control of the heart and lungs is affected by regions of the brain involved in the response to stress and the development of anxiety. We now plan to investigate the relationships of stressful life events, the brain's control of cardiovascular and respiratory function, and the potential for relapse after successful treatment of panic disorder. Using non-invasive methods, we will obtain measures of cardiovascular and respiratory function in panic disorder patients along with a rigorous historical assessment of stressful life events. We will then use a combination of cognitive behavioral therapy and the antidepressant sertraline, both with well-validated efficacy for the treatment of panic disorder, and obtain repeated stress, cardiovascular, and respiratory measures during and after such treatment. The acute treatment phase is 3 months, the maintenance treatment phase is another 3 months, and the follow-up, no-treatment phase is 12 months. This investigation will enable us to test whether patients with panic disorder are vulnerable to the impact of stressful life events and what are the relationships with cardiovascular and respiratory function and panic relapse before, during, and after treatment. These relationships may offer important data for directing treatment approaches and allowing clinicians to test for vulnerability to panic disorder.