SENSORY PHYSIOLOGY AND CATECHOLAMINES IN SCHIZOPHRENIA AND MANIA
SENSORY PHYSIOLOGY AND CATECHOLAMINES IN SCHIZOPHRENIA AND MANIA
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DOI：
10.1016/0165-1781(90)90099-q
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发表时间：
1990-01-01
影响因子：
11.3
通讯作者：
FREEDMAN R
中科院分区：
文献类型：
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作者：
ADLER L E;GERHARDT G A;FREEDMAN R
对感觉刺激敏感是精神分裂症和躁狂症的显著特征。神经生理学记录表明，中枢神经感觉门控机制存在共同缺陷，该机制调节对重复听觉刺激的敏感性。多巴胺和去甲肾上腺素被认为在这些疾病中起主要作用，但它们在异常感觉处理中的作用尚未得到证实。儿茶酚胺对感觉加工的影响的推定证据来自对受到兴奋剂挑战的正常受试者的心理生理学研究，这些受试者显示感觉门控减少，以及对接受抗精神病药物治疗的精神病患者表现出功能改善的研究。对动物类似现象的研究表明，儿茶酚胺对感觉加工的影响类似，无论是在行为上还是在单个神经元水平上都是如此。在这项研究中，在治疗这两种疾病的过程中，听觉诱发电位(EPs)的门控与血浆多巴胺和去甲肾上腺素代谢产物进行了比较。对服药和未服药状态的比较表明，精神分裂症患者在感觉门控方面存在固定的缺陷，这是一种家族特征，药物治疗不会改变这一缺陷。在急性疾病期间，他们对刺激有额外的一过性超敏反应，表现为较小的EP，这似乎是由多巴胺介导的。躁狂症患者只有感觉门控缺陷，这是短暂的，似乎是由去甲肾上腺素调节的。因此，这两种精神病相似的神经生理缺陷与不同的生化异常有关，这可能解释了急性症状的相似之处和疾病其他方面的差异，如对治疗的反应。
Hypersensitivity to sensory stimulation is a prominent characteristic of both schizophrenia and mania. Neurophysiological recordings suggest a common deficit in a central neuronal sensory gating mechanism which regulates sensitivity to repeated auditory stimuli. Dopamine and norepinephrine are hypothesized to have major roles in these illnesses, but their role in aberrant sensory processing has not yet been proved. Presumptive evidence for effects of catecholamines on sensory processing comes from psychophysiological studies of normal subjects challenged with stimulants who show decreased sensory gating, and studies of psychotic patients treated with neuroleptics who show improved function. Studies of similar phenomena in animals show comparable effects of catecholamines on sensory processing, both behaviorally and at the single neuron level. In this study, gating of auditory evoked potentials (EPs) during treatment of both illnesses was compared with plasma dopamine and norepinephrine metabolites. Comparisons of medicated and unmedicated states showed that schizophrenic patients have a fixed deficit in sensory gating, which is a familial trait, unchanged by medication. During acute illness, they have an additional transient hypersensitivity to stimuli, manifested as smaller EPs, which seems to be mediated by dopamine. Manic patients have only the deficit in sensory gating, which is transient and seems to be mediated by norepinephrine. Thus, similar neurophysiological deficits in the two psychoses are associated with different biochemical abnormalities, which may explain similarities in acute symptoms and differences in other aspects of the illnesses, such as their response to treatment.