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再谈精神分裂症素质。

Schizotaxia revisited.

作者信息

Meehl P E

机构信息

Department of Psychiatry, University of Minnesota, Minneapolis.

出版信息

Arch Gen Psychiatry. 1989 Oct;46(10):935-44. doi: 10.1001/archpsyc.1989.01810100077015.

Abstract

A conjectured neural integrative defect (schizotaxia), due to a dominant schizogene completely penetrant for a parametric aberration in synaptic signal selectivity (hypokrisia), gives rise under ordinary social learning regimens to schizotypy, a personality showing ambivalence, aversive drift, dereism, autism, and cognitive slippage. Given unfavorable polygenic potentiators (eg, introversion, hypohedonia, and anxiety) and adverse life experiences (eg, childhood trauma or adult misfortune), around 10% develop schizophrenia. That schizophrenia is basically a neurologic disorder does not contradict whatever is known about its psychodynamics, nor preclude efficacy for psychotherapy or other psychosocial interventions. Research should concentrate on soft neurology and psychophysiology as indicators, being closer in the causal chain to the schizogene than psychometric, social, or high-level cognitive processes. Taxometric statistics are appropriate to testing a major locus model not simplistically formulated.

摘要

一种推测的神经整合缺陷(精神分裂倾向),由一个显性精神分裂基因引起,该基因对突触信号选择性的参数畸变(机能减退)具有完全的穿透性,在普通的社会学习模式下会导致分裂型人格,这种人格表现出矛盾情绪、厌恶倾向、怪异行为、孤独症及认知失误。若存在不利的多基因增强因素(如内向、快感缺乏及焦虑)和不良生活经历(如童年创伤或成人不幸),约10%的人会发展为精神分裂症。精神分裂症本质上是一种神经疾病,这与已知的其心理动力学并不矛盾,也不排除心理治疗或其他社会心理干预的有效性。研究应集中于软神经病学和心理生理学指标,在因果链上比心理测量、社会或高级认知过程更接近精神分裂基因。分类统计适用于检验一个并非简单构建的主要基因座模型。

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