Optical coherence tomography reflects brain atrophy in multiple sclerosis: A four-year study.

Optical coherence tomography reflects brain atrophy in multiple sclerosis: A four-year study.
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DOI:
10.1002/ana.24487
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发表时间:
2015-11
影响因子:
11.2
通讯作者:
Calabresi PA
Calabresi PA
中科院分区:
医学1区
文献类型:
--
作者:
Saidha S;Al-Louzi O;Ratchford JN;Bhargava P;Oh J;Newsome SD;Prince JL;Pham D;Roy S;van Zijl P;Balcer LJ;Frohman EM;Reich DS;Crainiceanu C;Calabresi PA

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这项工作的目的是确定特定视网膜层和大脑亚结构的萎缩是否随时间推移而相关,以进一步验证光学相干断层扫描(OCT)作为多发性硬化症(MS)患者神经元组织损伤指标的实用性。Cirrus高清晰度OCT(包括自动黄斑分割)每两年对107例MS患者进行一次(中位随访时间:46个月)。每年进行一次3特斯拉磁共振成像脑扫描(包括脑子结构体积测量)。视网膜和大脑测量的个体特异性变化率(用线性回归估计)相关,调整了年龄、性别、病程和视神经炎(ON)病史。神经节细胞+内丛状层(GCIP)和全脑(r = 0.45; p<0.001)、灰质(GM; r = 0.37; p<0.001)、白色物质(WM; r = 0.28; p = 0.007)和丘脑(r = 0.38; p < 0.001)萎缩的发生率相关。GCIP和全脑(以及GM和WM)萎缩率在进展型MS中(r = 0.67; p<0.001)比复发缓解型MS(RRMS; r = 0.33; p = 0.007)更强相关。然而,RRMS中GCIP和全脑(以及GM和WM)萎缩率之间的相关性随着逐步细化而逐渐增加,以排除ON效应;排除眼睛和患者(考虑表型效应),相关性分别增加至0.45和0.60,与效应修正一致。在RRMS中,病变累积率与GCIP(r =-0.30; p = 0.02)和内核层(r =-0.25; p = 0.04)萎缩率相关。随着时间的推移,GCIP萎缩似乎反映了全脑萎缩,尤其是GM萎缩,尤其是在进行性MS中,从而反映了潜在的疾病进展。我们的研究结果支持OCT用于临床监测,并作为研究性试验的结果。
The aim of this work was to determine whether atrophy of specific retinal layers and brain substructures are associated over time, in order to further validate the utility of optical coherence tomography (OCT) as an indicator of neuronal tissue damage in patients with multiple sclerosis (MS). Cirrus high-definition OCT (including automated macular segmentation) was performed in 107 MS patients biannually (median follow-up: 46 months). Three-Tesla magnetic resonance imaging brain scans (including brain-substructure volumetrics) were performed annually. Individual-specific rates of change in retinal and brain measures (estimated with linear regression) were correlated, adjusting for age, sex, disease duration, and optic neuritis (ON) history. Rates of ganglion cell + inner plexiform layer (GCIP) and whole-brain (r = 0.45; p<0.001), gray matter (GM; r = 0.37; p<0.001), white matter (WM; r = 0.28; p = 0.007), and thalamic (r = 0.38; p < 0.001) atrophy were associated. GCIP and whole-brain (as well as GM and WM) atrophy rates were more strongly associated in progressive MS (r = 0.67; p<0.001) than relapsing-remitting MS (RRMS; r = 0.33; p = 0.007). However, correlation between rates of GCIP and whole-brain (and additionally GM and WM) atrophy in RRMS increased incrementally with step-wise refinement to exclude ON effects; excluding eyes and then patients (to account for a phenotype effect), the correlation increased to 0.45 and 0.60, respectively, consistent with effect modification. In RRMS, lesion accumulation rate was associated with GCIP (r = −0.30; p = 0.02) and inner nuclear layer (r = −0.25; p = 0.04) atrophy rates. Over time GCIP atrophy appears to mirror whole-brain, and particularly GM, atrophy, especially in progressive MS, thereby reflecting underlying disease progression. Our findings support OCT for clinical monitoring and as an outcome in investigative trials.