首页> 外文期刊>Progress in Neuro-Psychopharmacology & Biological Psychiatry: An International Research, Review and News Journal >Lorazepam reduces the serum brain-derived neurotrophic factor level in schizophrenia patients with catatonia
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Lorazepam reduces the serum brain-derived neurotrophic factor level in schizophrenia patients with catatonia

机译:劳拉西m可降低精神分裂症合并卡塔尼亚患者的血清脑源性神经营养因子水平

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Catatonia is a common neuropsychiatric syndrome that can occur in schizophrenia, major depression and general medical conditions (Taylor and Fink, 2003). Previous studies revealed that catatonia could be from low gama-aminobutyric acid (GABA)-A receptor binding, dopamine hypoactivity and glutamate hyperactivity (Northoff, 2002; Carroll et al., 2007). Lorazepam and electroconvulsive therapy have been well established as the first-line choices for treating catatonia, and a related treatment algorithm has also been suggested (Taylor and Fink, 2003; Huang, 2005; Carroll et al., 2007). However, the real mechanism of catatonia was still unknown.Recently, we also found that patients with catatonic schizophrenia had lower serum brain-derived neurotrophic factor (BDNF) protein levels than patients with paranoid or residual schizophrenia in a previous cross-section study (Huang and Lee, 2006). The results supported us to investigate the changes of serum BDNF levels after the treatment of catatonia#
机译:卡塔顿尼亚是一种常见的神经精神病综合症,可发生于精神分裂症,重度抑郁症和一般医疗状况中(Taylor和Fink,2003)。先前的研究表明,卡塔尼亚可能来自于低γ-氨基丁酸(GABA)-A受体结合,多巴胺功能不足和谷氨酸过度活跃(Northoff,2002; Carroll et al。,2007)。劳拉西m和电惊厥疗法已被公认是治疗卡塔顿的一线选择,并且也提出了相关的治疗方法(Taylor和Fink,2003; Huang,2005; Carroll等,2007)。然而,卡塔尼亚症的真正机制仍然未知。最近,我们还发现,在先前的一项横断面研究中,卡塔克精神分裂症患者的血清脑源性神经营养因子(BDNF)蛋白水平低于偏执或残留精神分裂症患者和Lee,2006年)。结果支持我们研究卡塔尼亚治疗后血清BDNF水平的变化#

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