SENSORY GATING DEFICITS IN PSYCHIATRIC-INPATIENTS - RELATION TO CATECHOLAMINE METABOLITES IN DIFFERENT DIAGNOSTIC GROUPS
SENSORY GATING DEFICITS IN PSYCHIATRIC-INPATIENTS - RELATION TO CATECHOLAMINE METABOLITES IN DIFFERENT DIAGNOSTIC GROUPS
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DOI：
10.1016/0006-3223(90)90443-6
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发表时间：
1990-03-01
影响因子：
10.6
通讯作者：
FREEDMAN, R
中科院分区：
文献类型：
--
作者：
BAKER, NJ;STAUNTON, M;FREEDMAN, R
急性精神病住院患者接受了感觉门控缺陷的检查，测量结果是未能抑制对第二对刺激的听觉诱发反应的P50波。此前，我们已经发现，在躁狂症中，这种感觉门控缺陷与去甲肾上腺素能代谢物3-甲氧基，4-羟基苯甘醇(PMHPG)的血浆游离水平升高有关，而在精神分裂症中，这与儿茶酚胺代谢无关。为了评估这些发现的概括性，我们检查了具有更广泛诊断范围的住院患者，包括那些具有多个DSM III-R轴I、II和III诊断的患者。这些患者被分成三个诊断谱进行分析：精神分裂症、躁狂症和抑郁症。在精神分裂症患者中，pMHPG或其他儿茶酚胺代谢产物与感觉门控缺陷无关。然而，在躁狂症患者中，pMHPG水平与感觉门控缺陷再次观察到正相关。这种关系没有延伸到抑郁症患者，他们独特地表现出与疾病严重程度负相关的感觉门控缺陷。数据表明，感觉门控缺陷在这三种诊断光谱中是共同的，但每组的缺陷与儿茶酚胺代谢和症状严重程度的关系不同，这可能反映了这些疾病潜在的神经病理生理学的差异。
Acutely ill psychiatric inpatients were examined for a deficit in sensory gating, measured as failure to suppress the P50 wave of the auditory-evoked response to the second of paired stimuli. Previously, we had found that in mania, this sensory gating deficit is correlated with increased plasma-free levels of the noradrenergic metabolite 3-methoxy, 4-hydroxyphenylglycol (pMHPG), whereas in schizophrenia, there is no correlation with catecholamine metabolism. To assess the generalizability of these findings, we examined inpatients with a broader range of diagnoses, including those with multiple DSM III-R Axis I, II, and III diagnoses. The patients were grouped into three diagnostic spectra for analysis: schizophrenic, manic, and depressive. In the schizophrenic patients, there was no relationship between pMHPG or other catecholamine metabolites and the sensory gating deficit. In manic patients, however, a positive correlation between pMHPG level and the sensory gating deficit was again observed. This relationship did not extend to the depressive patients, who uniquely showed sensory gating deficits that correlated negatively with the severity of their illness. The data suggest that sensory gating deficits are common to these three diagnostic spectra, but the deficits in each group have different relationships to catecholamine metabolism and symptoms severity that may reflect differences in the underlying neuronal pathophysiology of these illnesses.