广场恐怖症、惊恐障碍和广泛性焦虑障碍:最近进展的一些含义。

Psychiatric developments Pub Date : 1984-01-01
M Roth
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引用次数: 0

摘要

“恐慌症”、广场恐怖症和一般焦虑症之间关系的本质仍然是开放的。试图用生物学和心理学概念把它们联系起来的病因学理论没有考虑到相互矛盾的观察结果。“恐慌”发作并不局限于广场恐惧症和相关疾病,它与急性焦虑和恐惧症厌恶的发作难以区分,这些发作表现在广泛的焦虑和情感障碍中。广场恐惧症的发展过程中既有连续性,也有不连续性;受影响的患者在一系列发病前特征方面与其他疾病患者和对照受试者不同。这些变量包括家族史、生活发展、特质焦虑和其他人格特征,包括内向、神经质和可能对他人的情感依赖。并不是所有关于药物治疗和行为治疗的功效的说法都得到了证实。行为疗法取得的成功似乎可以持续数年。但是,所有形式的治疗之后的残障和缺陷以及患者选择和高辍学率所带来的问题没有得到足够的重视。广场恐惧症和相关疾病的病因学理论已经沿着生物医学、心理学和精神动力学的方向发展。每种理论都有一些证据支持。但没有一个与关于其现象学和进化的发现完全一致。最近的生物学研究在突触连接的变化、递质释放的增强以及分子结构的改变和基因表达的调节方面,导致了与预期性和慢性焦虑有关的假设的形成。现在下结论说这些发现可以为解释人类焦虑症提供一个统一的概念框架还为时过早。这类疾病的心理、行为和精神动力学方面在临床管理和科学调查中都应继续得到应有的重视。
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Agoraphobia, panic disorder and generalized anxiety disorder: some implications of recent advances.

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.

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