Freedman R, Adler L E, Gerhardt G A, Waldo M, Baker N, Rose G M, Drebing C, Nagamoto H, Bickford-Wimer P, Franks R
Dept. of Psychiatry, University of Colorado Health Sciences Center, Denver 80262.
Schizophr Bull. 1987;13(4):669-78. doi: 10.1093/schbul/13.4.669.
The sensory disturbance in schizophrenia is often described as an inability to filter out extraneous noise from meaningful sensory inputs. The neurobiological basis of this inability to filter has been examined using auditory evoked potentials, which are computerized averages of the brain's electrical response to sound. The sounds are presented in pairs to test the ability of the brain to inhibit, or gate, its response to a repeated stimulus. Schizophrenic patients lack the ability to gate the neuronal response shown by a particular wave, the P50 wave. The measurement of this deficit in human subjects and the exploration of its neurobiology in animals has produced evidence about several issues in the pathophysiology of schizophrenia: (1) the role of dopamine in improvement of sensory function in schizophrenic patients treated with neuroleptic drugs, (2) the interaction between familial or genetic deficits in sensory functioning in schizophrenic patients and possible abnormalities in dopamine metabolism, and (3) a mechanism by which noradrenergic hyperactivity in mania and other psychiatric illnesses might mimic some pathophysiological deficits in schizophrenia.
精神分裂症中的感觉障碍通常被描述为无法从有意义的感觉输入中滤除无关噪声。这种无法过滤的神经生物学基础已通过听觉诱发电位进行研究，听觉诱发电位是大脑对声音的电反应的计算机化平均值。声音以成对形式呈现，以测试大脑抑制或控制其对重复刺激反应的能力。精神分裂症患者缺乏控制特定波（P50波）所显示的神经元反应的能力。在人类受试者中测量这种缺陷并在动物中探索其神经生物学，已经产生了关于精神分裂症病理生理学中几个问题的证据：（1）多巴胺在接受抗精神病药物治疗的精神分裂症患者感觉功能改善中的作用；（2）精神分裂症患者感觉功能的家族性或遗传性缺陷与多巴胺代谢可能异常之间的相互作用；（3）躁狂症和其他精神疾病中去甲肾上腺素能亢进可能模拟精神分裂症某些病理生理缺陷的机制。
