Spaulding W D
Department of Psychology, University of Nebraska-Lincoln 68588-0308, USA.
Psychiatry. 1997 Winter;60(4):341-6. doi: 10.1080/00332747.1997.11024811.
There is a gap in scientific understanding of psychiatric disorders such as schizophrenia, between neurophysiological models of etiology and the behavioral expressions of the disorders. More complete cognitive models are needed to fill that gap. Such models would set neurophysiological models in a more meaningful context, would show how biological processes produce social-behavioral impairments, and would inform both biological and psychosocial treatment strategies. To be fully functional, however, cognitive models must address two key principles: diathesis-stress in the course of schizophrenia, and the nature of reciprocal causality in complex, self-regulating biosystems.
在诸如精神分裂症等精神疾病的科学理解方面，病因的神经生理学模型与这些疾病的行为表现之间存在差距。需要更完整的认知模型来填补这一差距。这样的模型将把神经生理学模型置于更有意义的背景中，展示生物过程如何导致社会行为障碍，并为生物治疗和心理社会治疗策略提供信息。然而，要想充分发挥作用，认知模型必须解决两个关键原则：精神分裂症病程中的素质-应激，以及复杂的自我调节生物系统中相互因果关系的本质。
