伴药源性肥胖的精神分裂症患者事件相关电位P300、血清脑源性神经营养因子及胰岛素抵抗的研究  

Event related potential P300,serum level of brain-derived neurotrophic factor and insulin resistance in schizophrenics with obesity induced by antipsychotics

作　　者：吴爱菊[1] 张文跃[1] 韩晓东[1] 朱强[1] 马俊峰[1] 杜向东[2] WU Ai-ju;ZHANG Wen-yue;HAN Xiao-dong;ZHU Qiang;MA Jun-feng;DU Xiang-dong(the Third People's Hospital of Taicang,Taicang 215400,China)

机构地区：[1]江苏省太仓市第三人民医院精神科,215400 [2]苏州大学附属广济医院

出　　处：《临床精神医学杂志》2018年第5期297-300,共4页Journal of Clinical Psychiatry

基　　金：苏州市2017产业技术创新专项(民生科技─医疗卫生应用基础研究)项目(SYSD2017024);苏州市精神疾病临床医学中心项目(Szzx201509);2017年度苏州市精神疾病临床医学中心青年科技项目(gjyy201711)

摘　　要：目的:探讨伴药源性肥胖精神分裂症患者事件相关电位P300特征、血清脑源性神经营养因子(BDNF)水平及胰岛素抵抗的状况。方法:对伴药源性肥胖的精神分裂症患者32例(肥胖组)、不伴药源性肥胖的精神分裂症患者47例(非肥胖组)及正常人42名(正常组)。以事件相关电位P300评价其认知功能,酶免疫法测定血清BDNF水平,常规检测血脂及胰岛素抵抗指数(HOMA-IR)。结果:肥胖组P300潜伏期较非肥胖组和正常组延长(P均<0. 01),非肥胖组P300潜伏期也较正常组延长(P <0. 01);肥胖组P300波幅较非肥胖组和正常组下降(P均<0. 01),非肥胖组P300波幅也较正常组下降(P <0. 01);肥胖组、非肥胖组及正常组之间血清BDNF水平差异无统计学意义(F=1. 81,P>0. 05);肥胖组HOMA-IR高于非肥胖组及正常组(均P <0. 01);精神分裂症患者中P300潜伏期与HOMA-IR呈正相关(r=0. 34,P <0. 01),P300波幅与HOMA-IR呈负相关(r=-0. 29,P <0. 05)。结论:伴药源性肥胖的精神分裂症有更明显的认知功能缺陷,并与BDNF无关;胰岛素抵抗可能参与了药源性肥胖相关认知损害的病理生理过程。Objective:To explore the characteristics of event related potential P300,the change of serum level of brain-derived neurotrophic factor(BDNF)and the status of insulin resistance in schizophrenics with obesity induced by antipsychotics. Method:32 schizophrenics with obesity induced by antipsychotics(obesity group),47 schizophrenics without obesity induced by antipsychotics(non-obesity group)and 42 normal subjects(normal group)were enrolled.Cognitive function in all subjects was evaluated with event related potential P300.Serum level of BDNF in all subjects was measured by enzyme immunoassays.Blood lipids and homeostasis model assessment of insulin resistance(HOMA-IR)in all subjects were routinely detected.Results:P300 latency in obesity group was longer than that in non-obesity group and normal group(all P<0.01).P300 latency in non-obesity group was also longer than that in normal group(P<0.01).P300 amplitude in obesity group was lower than that in non-obesity group and normal group(all P<0.01).P300 amplitude in non-obesity group was also lower than that in normal group(P<0.01).No significant difference was observed in serum level of BDNF among obesity group,non-obesity group and normal group(F=1.81,P>0.05).HOMA-IR in obesity group was higher than that in non-obesity group and normal group(all P<0.01).P300 latency was positively correlated with HOMA-IR in schizophrenics(r=0.34,P<0.01).P300 amplitude was negatively correlated with HOMA-IR in schizophrenics(r=-0.29,P<0.05).Conclusion:Schizophrenics with obesity induced by antipsychotics has more obvious cognitive deficit,which is not correlated with BDNF.Insulin resistance may be involved in the pathophysiological process of cognitive impairment associated with obesity induced by antipsychotics.

关 键 词：药源性肥胖 精神分裂症 事件相关电位 脑源性神经营养因子 胰岛素抵抗 

分 类 号：R749.3[医药卫生—神经病学与精神病学]