Roth M
Psychiatr Dev. 1984 Spring;2(1):31-52.
The nature of the relationship between 'panic disorder', agoraphobia and general anxiety disorder remains open. The aetiological theories which have tried to link them with the aid of biological and psychological concepts fail to take account of conflicting observations. 'Panic' attacks are not confined to agoraphobic and related disorders, being indistinguishable from the attacks of acute anxiety and phobic aversion manifest in a wide range of anxiety and affective disorders. There is continuity and discontinuity in the evolution of agoraphobia; those affected differ in respect of a range of premorbid features from patients with other disorders and control subjects. These variables include family history, life development, trait anxiety and other personality characteristics including introversion, neuroticism and probably emotional dependence on others. Not all the claims made on behalf of the efficacy of pharmacological treatment on the one hand and behavioural therapies on the other are substantiated. The success achieved by behavioural treatment appear to endure over some years. But the residual disabilities and defects that follow all forms of treatment and the problems posed by patient selection and high drop-out rates have received insufficient attention. Aetiological theories of agoraphobia and related conditions have been advanced along biomedical, psychological and psychodynamic lines. Some evidence supports each kind of theory. But none is wholly consistent with the findings regarding its phenomenology and evolution. Recent biological investigations have led to the formulation of hypotheses in relation to anticipatory and chronic anxiety in terms of changes in synaptic connections, enhancement of transmitter release as well as alterations in molecular configuration and regulation of gene expression. It would be premature to conclude that these findings can provide a unitary conceptual framework for the explanation of human anxiety disorders. The psychological, behavioural and psychodynamic aspects of this group of disorders should all continue to receive due attention both in clinical management and scientific investigation.
“惊恐障碍”、广场恐惧症和广泛性焦虑症之间关系的本质仍不明确。试图借助生物学和心理学概念将它们联系起来的病因学理论，未能考虑到相互矛盾的观察结果。“惊恐”发作并不局限于广场恐惧症及相关障碍，与广泛的焦虑症和情感障碍中出现的急性焦虑发作和恐惧性厌恶发作并无区别。广场恐惧症的演变过程既有连续性，也有不连续性；患者在一系列病前特征方面与其他疾病患者及对照组不同。这些变量包括家族史、生活发展、特质焦虑以及其他人格特征，如内向、神经质以及可能存在的对他人的情感依赖。一方面，并非所有关于药物治疗有效性的说法都得到了证实；另一方面，行为疗法的有效性也未得到充分证实。行为治疗所取得的成功似乎能持续数年。但是，各种治疗方式之后残留的残疾和缺陷，以及患者选择和高脱落率所带来的问题，都没有得到足够的关注。广场恐惧症及相关病症的病因学理论沿着生物医学、心理学和心理动力学的方向发展。每种理论都有一些证据支持。但没有一种理论能完全与关于其现象学和演变的研究结果相一致。最近的生物学研究已就预期性焦虑和慢性焦虑提出了一些假设，涉及突触连接的变化、递质释放的增强以及分子构型和基因表达调控的改变。现在就得出这些发现能够为解释人类焦虑症提供一个统一的概念框架的结论还为时过早。在临床管理和科学研究中，这组障碍的心理、行为和心理动力学方面都应继续得到应有的关注。
