Kimhy David, Goetz Ray, Yale Scott, Corcoran Cheryl, Malaspina Dolores
Department of Psychiatry, Columbia University, New York, NY 10032, USA.
Psychopathology. 2005 Nov-Dec;38(6):338-44. doi: 10.1159/000089455. Epub 2005 Nov 1.
Delusions are a central feature of schizophrenia, yet our understanding of their neurobiology is limited. Attempt to link dimensions of psychopathology to putative neurobiological mechanisms depends on careful delineation of symptoms. Previous factor analytic studies of delusions in schizophrenia were limited by several methodological problems, including the use of patients medicated with antipsychotics, inclusion of nondelusion symptoms in the analyses, and/or inclusion of patients with psychotic disorders other than schizophrenia. These problems may have possibly biased the resulting factor structure and contributed to the inconclusive findings regarding the neurobiology of positive symptoms. Our goal is to examine the factor structure of delusions in antipsychotic-free individuals with diagnoses of schizophrenia/schizoaffective disorder.
We assessed 83 antipsychotic-free individuals with DSM-IV diagnoses of schizophrenia/schizoaffective disorder. A principal component analysis was conducted on the delusions symptoms of the SAPS.
The principal component analysis resulted in three distinct and interpretable factors explaining 58.3% of the variance. The Delusions of Influence factor was comprised by delusions of being controlled, thought withdrawal, thought broadcasting, thought insertion, and mind reading. The Self-Significance Delusions factor was comprised by delusions of grandeur, reference, religious, and delusions of guilt/sin. The Delusions of Persecution factor was comprised solely by persecutory delusions. The three factors displayed distinct associations with hallucinations, bizarre behavior, attention, positive formal thought disorder, and avolition/apathy.
The results indicate that delusions are best described by three distinct subtypes. The authors propose a novel model linking the three delusion subtypes, attributions to self/other, and putative neurobiological mechanisms. Implications for future research are discussed, as well as links to cognitive-behavioral conceptualizations of delusions.
妄想是精神分裂症的核心特征，然而我们对其神经生物学的理解有限。将精神病理学维度与假定的神经生物学机制联系起来的尝试依赖于对症状的仔细界定。先前对精神分裂症妄想的因素分析研究受到若干方法学问题的限制，包括使用接受抗精神病药物治疗的患者、在分析中纳入非妄想症状和/或纳入精神分裂症以外的精神障碍患者。这些问题可能使所得的因素结构产生偏差，并导致关于阳性症状神经生物学的研究结果尚无定论。我们的目标是研究未服用抗精神病药物、诊断为精神分裂症/分裂情感性障碍的个体的妄想因素结构。
我们评估了83名未服用抗精神病药物、诊断为精神分裂症/分裂情感性障碍的个体。对阳性与阴性症状量表（SAPS）中的妄想症状进行了主成分分析。
主成分分析产生了三个不同且可解释的因素，解释了58.3%的方差。影响妄想因素包括被控制妄想、思维被夺、思维播散、思维插入和心灵感应。自我重要性妄想因素包括夸大妄想、牵连观念、宗教妄想和罪恶妄想。迫害妄想因素仅由被害妄想组成。这三个因素与幻觉、怪异行为、注意力、阳性形式思维障碍及意志缺乏/淡漠表现出不同的关联。
结果表明，妄想最好用三种不同的亚型来描述。作者提出了一个将三种妄想亚型、自我/他人归因及假定的神经生物学机制联系起来的新模型。讨论了对未来研究的启示以及与妄想的认知行为概念化的联系。
