视神经脊髓炎患者默认网络及额顶网络功能连接的研究
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摘要
目的采用独立成分分析(independent component analysis,ICA)方法分析静息态功能磁共振成像(resting-state functional magnetic resonance imaging,rsf MRI)数据,观察视神经脊髓炎(neuromyelitis optica,NMO)患者大脑默认网络(default mode network,DMN)及额顶网络(frontoparietal network,FPN)功能连接的异常以及与临床评分的相关性。材料与方法对我院20例NMO患者(NMO组)及20名健康对照者(正常对照组)行静息态f MRI扫描,所得数据利用DPARSFA软件预处理,然后利用GIFT软件行ICA分析,并用SPM8比较两组默认网络及额顶网络功能连接的差异,同时分析有差异脑区的时间序列信号与临床扩展残疾状态量表评分及病程的相关性。结果与对照组比较,NMO组DMN功能连接增强的脑区包括双侧舌回,延伸到右侧顶上小叶及左侧辅助运动区;功能连接减弱的脑区包括右侧额中回及右侧枕中回;NMO组FPN功能连接减弱的脑区为双侧楔叶,无功能连接增强的脑区。右侧舌回与病程呈正相关(r=0.682,P<0.05)。结论 NMO患者静息态DMN、FPN均存在功能连接异常,提示患者的脊髓及视神经病变不仅引起患者相应的临床症状,局部结构损伤所致的功能改变也不仅仅局限于病变对应的区域,脑功能网络是一个复杂的互相关联的网络,存在损伤与代偿的复杂过程。
Objective: To evaluate the difference of brain default mode network(DMN) and frontoparietal network(FPN) connectivity of neuromyelitis optica(NMO) by using independent component analysis(ICA), and the correlation with clincal score. Materials and Methods: Twenty NMO patients(NMO group) and twenty healthy controls(control group) underwent rest-state f MRI. The f MRI data were analyzed by using GIFT software, and the differences of functional connectivity(FC) between the two groups were compared with SPM8. The correlation between altered parameters of FC and expanded disability status scale(EDSS) scores, disease duration were further explored using the Pearson correlation coefficients. Results: Compared with the control group, the FC score of DMN in NMO group significantly decreased in the right middle frontal cortex and right middle occipital cortex, while increased in bilateral lingual gyrus, extended to right superior parietal lobule and left supplementary motor area; the FC score of FPN decreased in bilateral cuneus cortex, while no FC score increased area. In addition, the FC score changes of right lingualgyrus correlated with disease duration. Conclusion: The FC abnormalities in DMN and FPN in NMO patients may beprovide an evidence that the spinal cord and optic neuritis caused not only corresponding clincal symptoms but also brain hidden and widespread damage. Altered functional changes in multiple brain regions may be caused by the secondary spinal cord lesions of retrograde sensorimotor cortex lesions, demonstrate that the brain functional network is a complex interconnected network with both the process of damage and compensation.
Objective: To evaluate the difference of brain default mode network(DMN) and frontoparietal network(FPN) connectivity of neuromyelitis optica(NMO) by using independent component analysis(ICA), and the correlation with clincal score. Materials and Methods: Twenty NMO patients(NMO group) and twenty healthy controls(control group) underwent rest-state f MRI. The f MRI data were analyzed by using GIFT software, and the differences of functional connectivity(FC) between the two groups were compared with SPM8. The correlation between altered parameters of FC and expanded disability status scale(EDSS) scores, disease duration were further explored using the Pearson correlation coefficients. Results: Compared with the control group, the FC score of DMN in NMO group significantly decreased in the right middle frontal cortex and right middle occipital cortex, while increased in bilateral lingual gyrus, extended to right superior parietal lobule and left supplementary motor area; the FC score of FPN decreased in bilateral cuneus cortex, while no FC score increased area. In addition, the FC score changes of right lingualgyrus correlated with disease duration. Conclusion: The FC abnormalities in DMN and FPN in NMO patients may beprovide an evidence that the spinal cord and optic neuritis caused not only corresponding clincal symptoms but also brain hidden and widespread damage. Altered functional changes in multiple brain regions may be caused by the secondary spinal cord lesions of retrograde sensorimotor cortex lesions, demonstrate that the brain functional network is a complex interconnected network with both the process of damage and compensation.
引文
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[18]Liu Y,Liang P,Duan Y,et al.Abnormal baseline brain activity in patients with neuromyelitis optica:A resting-state f MRI study.Eur J of Radiol,2011,80(2):407-411.
[19]Menon V,Uddin LQ.Saliency,switching,attention and control:A network model of insula function.Brain Struct Funct,2010,214(5-6):655-667.
[20]Rocca MA,Agosta F,Mezzapesa DM,et al.A functional MRI study of movement-associated cortical changes in patients with Devic's neuromyelitis optica.Neuroimage,2004,21(3):1061-1068.
[21]Dobryakova E,Rocca MA,Valsasina P,et al.Abnormalities of the executive control network in multiple sclerosis phenotypes:An f MRI effective connectivity study.Hum Brain Mapp,2016,37(6):2293-2304.
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[23]Tomasi D,Volkow ND.Functional connectivity density mapping.PNAS,2010,107(21):9885-9890.
[2]Zhang N,Li YJ,Fu Y,et al.Cognitive impairment in Chinese neuromyelitis optica.Mult Scler,2015,21(14):1839-1846.
[3]Liu Y,Fu Y,Schoonheim MM,et al.Structural MRI substrates of cognitive impairment in neuromyelitis optica.Neurology,2015,85(17):1491-1499.
[4]Rueda Lopes FC,Doting T,Martins C,et al.The role of demyelination in neuromyelitis optica damage:difusion-tensor MR imaging study.Radiology,2012,263(1):235-242.
[5]Wingerchuk DM,Lennon VA,Pittock SJ,et a1.Revised diagnostic criteria for neuromyelitis optica.Neurology,2006,66(10):1485-1489.
[6]Yan CG,Zang YF.DPARSF:A MATLAB toolbox for"pipeline"data analysis of resting-state f MRI.Front Syst Neurosci,2010,4(2):13.
[7]Yah CG,Cheung B,Kelly C,et al.A comprehensive assessment of regional variation in the impact of head micromovements on functional connectomics.Neuroimage,2013,76(8):183-201.
[8]Beckmann CF,Smith SM.Tensorial extensions of independent component analysis for multisubject FMRI analysis.Neuroimage,2005,25(1):294-311.
[9]Damoiseaux JS,Rombouts SA,Barkhof F,et al.Consistent resting-state networks across healthy subjects.PNAS,2006,103(37):13848-13853.
[10]Mantini D,Perrueei MG,Gratta CD,et al.Electrophysiological signatures of resting state networks in the human brain.PNAS,2007,104(32):13170-13175.
[11]Beckmann CF,Mackay C,Filippin N,et al.Group comparison of resting-state FMRI data using multi-subject ICA and dual regression.Neuroimage,2009,47(Suppl 1):S148.
[12]Figueroa M,Guo Y,Tselis A,et al.Paraneoplastic neuromyelitis optica spectrum disorder associated with metastaticcarcinoid expressing aquaporin-4.JAMA Neurol,2014,71(4):495-498.
[13]Wingerchuk DM,Lennon VA,Lucchinetti CF,et al.The spectrum of neuromyelitis optica.Lancet Neurol,2007,6(9):805-815.
[14]DM Wingerchuk,BG Weinshenker.Neuromyelitis optica clinical predictors of a relapsing course and survival.Neurology,2003,60(5):848-853.
[15]Paul F,Jarius S,Aktas O,et al.Antibody to aquaporin 4 in the diagnosis of neuromyelitis optica.PLo S Med,2007,4(4):133.
[16]Mc Keown MJ,Makeig S,Brown GG,et al.Analysis of f MRI data by blind separation into independent spatial components.Hum Brain Mapp,1998,6(3):160-188.
[17]Buckner RL,Andrews-Hanna JR,Schacter DL.The brain's default network:Anatomy,function,and relevance to disease.Ann N Y Acad Sci,2008,1124(10):1-38.
[18]Liu Y,Liang P,Duan Y,et al.Abnormal baseline brain activity in patients with neuromyelitis optica:A resting-state f MRI study.Eur J of Radiol,2011,80(2):407-411.
[19]Menon V,Uddin LQ.Saliency,switching,attention and control:A network model of insula function.Brain Struct Funct,2010,214(5-6):655-667.
[20]Rocca MA,Agosta F,Mezzapesa DM,et al.A functional MRI study of movement-associated cortical changes in patients with Devic's neuromyelitis optica.Neuroimage,2004,21(3):1061-1068.
[21]Dobryakova E,Rocca MA,Valsasina P,et al.Abnormalities of the executive control network in multiple sclerosis phenotypes:An f MRI effective connectivity study.Hum Brain Mapp,2016,37(6):2293-2304.
[22]Seeley WW,Menon V,Schatzberg AF,et al.Dissociable intrinsic connectivity networks for salience processing and executive control.J Neurosci,2007,27(9):2349-2356.
[23]Tomasi D,Volkow ND.Functional connectivity density mapping.PNAS,2010,107(21):9885-9890.