McCarley R W, Faux S F, Shenton M E, Nestor P G, Adams J
Harvard Medical School, Department of Psychiatry, Brockton VAMC, MA 02401.
Schizophr Res. 1991 Mar-Apr;4(2):209-31. doi: 10.1016/0920-9964(91)90034-o.
Evidence is growing that schizophrenic patients show significant structural damage in the temporal lobe limbic system. We review event-related potentials abnormalities (ERPs) in schizophrenia that may be related to dysfunction in this brain region or its inputs; ERPs discussed include the N100/P200, P300 and N400 components. Additional CT and clinical data have led our laboratory to a unifying working hypothesis of the presence of temporal lobe damage in schizophrenics that is evinced electrophysiologically as ERP alterations, structurally as tissue loss/derangement, and clinically as positive symptoms. The final section of this paper presents a new model of at least one form of schizophrenic pathology that, while speculative, incorporates experimentally based data from both our ERP work and from basic cellular physiology and pharmacology. The model proposes that positive symptoms of schizophrenia are related to limbic system pathology and in particular to a dysregulation of the NMDA form of excitatory amino acid transmission, potentiated by stress, and leading to cell damage and death due to 'excitotoxicity'.
越来越多的证据表明，精神分裂症患者的颞叶边缘系统存在明显的结构损伤。我们回顾了精神分裂症中可能与该脑区或其输入功能障碍相关的事件相关电位异常（ERP）；所讨论的ERP包括N100/P200、P300和N400成分。额外的CT和临床数据使我们实验室得出一个统一的工作假设，即精神分裂症患者存在颞叶损伤，在电生理上表现为ERP改变，在结构上表现为组织丢失/紊乱，在临床上表现为阳性症状。本文的最后一部分提出了至少一种精神分裂症病理形式的新模型，该模型虽然具有推测性，但整合了来自我们ERP研究以及基础细胞生理学和药理学的实验数据。该模型提出，精神分裂症的阳性症状与边缘系统病理有关，特别是与应激增强的兴奋性氨基酸NMDA形式传递失调有关，并由于“兴奋性毒性”导致细胞损伤和死亡。
