Maher Brendan
Harvard University, USA.
Integr Physiol Behav Sci. 2005 Jul-Sep;40(3):136-46. doi: 10.1007/BF03159710.
A hypothesis is presented regarding the genesis of paranoid delusion that attempts to take into account certain data. The data of interest are (a) the failure to find evidence of cognitive impairment in diagnosed paranoid patients, (b) the evidence of perceptual disorder as a primary and prior condition in the natural history of the clinical development of delusions and the empirical relationship of the perceptual disorder to presence of "thought disorder," (c) the failure to find evidence supporting universal psychodynamic patterns of etiology, (d) appearance of "delusional" phenomena in normal subjects in situations of deviant sensory experience, and (e) the reports of articulate patients writing of their experiences. This hypothesis suggests that there exists a group of patients who suffer from primary perceptual anomalies, fundamentally biological in nature although probably fluctuating with current stresses, and that these anomalies involve vivid and intense sensory input. These experiences demand explanation which the patient develops through the same cognitive mechanisms that are found in normal and scientific theory-building. As the data that are available to the patient are crucially different from those available to an observer, the latter judges the explanation to be bizarre and pathological. Being unable to check the validity of the patient's descriptions of his sensory experience the assumption is made that the patient is having the same experience as the observer but is defective in reality-testing and/or inferential thinking. As the evidence for the presence of perceptual disorder is stronger than the direct evidence for cognitive impairment, the hypothesis outlined here places central importance on the former. In brief, it is suggested that for many paranoid patients the delusion should be seen as the reaction of a normal, "sane" individual to abnormal but genuine perceptual experiences.
本文提出了一个关于偏执妄想起源的假说,该假说试图考虑某些数据。这些相关数据包括:(a) 在已确诊的偏执患者中未发现认知障碍的证据;(b) 在妄想临床发展的自然史中,感知障碍作为主要和先前存在的状况的证据,以及感知障碍与“思维障碍”存在之间的经验关系;(c) 未找到支持普遍病因心理动力学模式的证据;(d) 在异常感官体验的情况下,正常受试者中出现“妄想”现象;(e) 有表达能力的患者对其经历的书面报告。这个假说表明,存在一群患有原发性感知异常的患者,这些异常本质上是生物学性的,尽管可能会随当前压力而波动,并且这些异常涉及生动而强烈的感官输入。这些体验需要解释,患者通过与正常和科学理论构建中相同的认知机制来进行解释。由于患者可获得的数据与观察者可获得的数据截然不同,后者将这种解释判断为怪异和病态的。由于无法检验患者对其感官体验描述的有效性,于是假设患者与观察者有相同的体验,但在现实检验和/或推理思维方面存在缺陷。由于存在感知障碍的证据比认知障碍的直接证据更强,这里概述的假说将重点置于前者。简而言之,有人认为,对于许多偏执患者来说,妄想应被视为一个正常、“理智”的个体对异常但真实的感知体验的反应。