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[基于近期神经生物学发现对妄想本质的一些疑问]

[Some questions about the essence of delusions in the light of recent neurobiological findings].

作者信息

Murawiec Sławomir

机构信息

Centrum Zdrowia Psychicznego IPiN w Warszawie.

出版信息

Psychiatr Pol. 2009 Jul-Aug;43(4):403-10.

Abstract

Formation of delusions in the phase of acute psychosis is based on two subsequent processes. The first one is dopamine hyperactivity in mesolimbic neural pathways, the second one is a cognitive process of up-down attribution of meanings of this subjectively perceived state of mind by the higher levels of brain. After the successful antipsychotic treatment, the subjectivity of patients changes. When the state of acute psychosis resolves patients must re-interpret this new emerging subjective experience. These interpretations are often incorrect and bizarre. In most cases they are regarded as delusions (sometimes "chronic delusions"). The question asked in the presented paper is whether they are truly delusions. The essence of delusion must include in the same time an active neurobiological basis of delusion (hyperdopaminergic state) and its cognitive level. It's not clear what is the proper term for the phenomenon when only incorrect or bizarre cognitive convictions are present after successful treatment of psychosis, but without dopaminergic hyperactivity.

摘要

急性精神病阶段妄想的形成基于两个相继的过程。第一个是中脑边缘神经通路中的多巴胺功能亢进,第二个是大脑高级区域对这种主观感知的心理状态进行意义的上下归因的认知过程。在成功进行抗精神病治疗后,患者的主观性会发生变化。当急性精神病状态消退时,患者必须重新解释这种新出现的主观体验。这些解释往往是不正确且怪异的。在大多数情况下,它们被视为妄想(有时是“慢性妄想”)。本文所提出的问题是,它们是否真的是妄想。妄想的本质必须同时包括妄想的活跃神经生物学基础(多巴胺能亢进状态)及其认知层面。目前尚不清楚在精神病成功治疗后仅存在不正确或怪异的认知信念但没有多巴胺能亢进时,该现象的恰当术语是什么。

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