Deficient Inhibitory Cortical Networks in Antipsychotic-Naive Subjects at Risk of Developing First-Episode Psychosis and First-Episode Schizophrenia Patients: A Cross-Sectional Study
Deficient Inhibitory Cortical Networks in Antipsychotic-Naive Subjects at Risk of Developing First-Episode Psychosis and First-Episode Schizophrenia Patients: A Cross-Sectional Study
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DOI：
10.1016/j.biopsych.2012.03.005
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发表时间：
2012-11-01
影响因子：
10.6
通讯作者：
Bechdolf, Andreas
中科院分区：
文献类型：
--
作者：
Hasan, Alkomiet;Wobrock, Thomas;Bechdolf, Andreas
背景资料：受损的皮层抑制是精神分裂症患者的一个公认的发现，并已与功能障碍的γ-氨基丁酸（GABA）能传递。然而，有没有以前的研究调查皮质兴奋性，特别是关于皮质内抑制网络抗精神病药初治受试者的风险，发展首发psychosis.Methods：共18例受试者的风险，18例首发精神分裂症患者，和18名健康对照组被纳入本研究。经颅磁刺激左侧初级运动皮层被用来确定短潜伏期内抑制，皮层内促进，和对侧沉默期（CSP）。短潜伏期皮层内抑制可以被认为是GABA A型（GABA（A））介导的抑制的一个参数，并且已经提出CSP可以测试GABA B型（GABA（B））介导的抑制性皮层内网络。与其他两组相比，首次发作患者的CSP持续时间延长，这意味着GABA（B）失衡仅发生在精神病患者中。分析并没有显示组内facilitation.Conclusions差异：这些结果表明，在抑制性皮质网络的风险和首次发作的患者在受试者的具体改变。看来，已经有一个皮质抑制赤字在风险的个人。这些结果表明，在疾病过程的早期可能存在GABA（A）功能障碍，而GABA（B）功能的改变似乎发生在疾病进展的后期。未来的纵向研究将需要澄清这种抑制缺陷及其与精神病转变的关系。
Background: Impaired cortical inhibition is a well-established finding in schizophrenia patients and has been linked to dysfunctional gamma-aminobutyric acid (GABA)ergic transmission. However, there have been no previous studies investigating cortical excitability with particular regard to intracortical inhibitory networks in antipsychotic-naive subjects at risk of developing first-episode psychosis.Methods: A total of 18 subjects at risk, 18 first-episode schizophrenia patients, and 18 healthy control subjects were included in this study. Transcranial magnetic stimulation over the left primary motor cortex was used to determine short-latency intracortical inhibition, intracortical facilitation, and the contralateral silent period (CSP). Short-latency intracortical inhibition can be considered as a parameter of GABA type A (GABA(A))-mediated inhibition and it has been proposed that CSP can test GABA type B (GABA(B))-mediated inhibitory intracortical networks.Results: Subjects at risk and first-episode patients showed a reduced short-latency intracortical inhibition compared with healthy control subjects, suggesting reduced GABA(A)-mediated inhibition. First-episode patients had a prolonged CSP duration compared with the other two groups, implying a GABA(B) imbalance only in patients with full-blown psychosis. Analyses did not reveal group differences for intracortical facilitation.Conclusions: These results indicate specific alterations in inhibitory cortical networks in subjects at risk and in first-episode patients. It appears that there is already a cortical inhibitory deficit in at-risk individuals. These results suggest a possible GABA(A) dysfunction early in the disease course, whereas alterations in GABA(B) functionality seem to occur later in the disease's progression. Future longitudinal studies will be needed to clarify this inhibitory deficit and its relation to the transition to psychosis.