From the Neurology Clinic and Policlinic (J.M., T.S., M.J.W., R.S., J.K., S.S., P.B., T.D., M.B., A.C., C.T., K.P., A.-K.P., S.R., L.K., C.G., O.Y.), Departments of Head, Spine and Neuromedicine, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel; Translational Imaging in Neurology (ThINk) Basel (J.M., S.S., M.B., A.C., C.T., K.P., C.G., O.Y.), Department of Biomedical Engineering, University Hospital Basel and University of Basel, Switzerland; Department of Biomedical Engineering (P.C., C.J., F.S., J.W., C.G.), University of Basel, Allschwil, Switzerland; Medical Imaging Analysis Center AG (M.A., J.W.); Section of Neuroradiology (T.L.), Clinic for Radiology & Nuclear Medicine, University Hospital Basel and University of Basel, Switzerland; Reha Rheinfelden (K.P.), Rheinfelden, Switzerland; NeuroCure Clinical Research Center and Experimental and Clinical Research Center (S.A., A.D., A.B., J.W., F.P.), Max Delbrueck Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Germany; Department of Neurology (A.B.), University of California, Irvine; Department of Neurology (K.R.), Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Martinos Center for Biomedical Imaging (N.H.), Massachusetts General Hospital and Harvard Medical School, Boston; Gillberg Neuropsychiatry Center (N.H.), Sahlgrenska Academy, University of Gothenburg, Sweden; Department of Neurology (S.F., M.W., K.M., T.M., N.I., J.-I.K.), Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan; Department of Neurology (J.-I.K.), Brain and Nerve Center, Fukuoka Central Hospital, International University of Health and Welfare, Fukuoka; and Translational Neuroscience Center (J.-I.K.), Graduate School of Medicine, and School of Pharmacy at Fukuoka, International University of Health and Welfare, Okawa, Japan.
Neurol Neuroimmunol Neuroinflamm. 2022 Feb 25;9(3). doi: 10.1212/NXI.0000000000001147. Print 2022 May.
The choroid plexus has been shown to play a crucial role in CNS inflammation. Previous studies found larger choroid plexus in multiple sclerosis (MS) compared with healthy controls. However, it is not clear whether the choroid plexus is similarly involved in MS and in neuromyelitis optica spectrum disorder (NMOSD). Thus, the aim of this study was to compare the choroid plexus volume in MS and NMOSD.
In this retrospective, cross-sectional study, patients were included by convenience sampling from 4 international MS centers. The choroid plexus of the lateral ventricles was segmented fully automatically on T1-weighted MRI sequences using a deep learning algorithm (Multi-Dimensional Gated Recurrent Units). Uni- and multivariable linear models were applied to investigate associations between the choroid plexus volume, clinically meaningful disease characteristics, and MRI parameters.
We studied 180 patients with MS and 98 patients with NMOSD. In total, 94 healthy individuals and 47 patients with migraine served as controls. The choroid plexus volume was larger in MS (median 1,690 µL, interquartile range [IQR] 648 µL) than in NMOSD (median 1,403 µL, IQR 510 µL), healthy individuals (median 1,533 µL, IQR 570 µL), and patients with migraine (median 1,404 µL, IQR 524 µL; all < 0.001), whereas there was no difference between NMOSD, migraine, and healthy controls. This was also true when adjusted for age, sex, and the intracranial volume. In contrast to NMOSD, the choroid plexus volume in MS was associated with the number of T2-weighted lesions in a linear model adjusted for age, sex, total intracranial volume, disease duration, relapses in the year before MRI, disease course, Expanded Disability Status Scale score, disease-modifying treatment, and treatment duration (beta 4.4; 95% CI 0.78-8.1; = 0.018).
This study supports an involvement of the choroid plexus in MS in contrast to NMOSD and provides clues to better understand the respective pathogenesis.
脉络丛在中枢神经系统炎症中起着至关重要的作用。先前的研究发现，多发性硬化症（MS）患者的脉络丛比健康对照组更大。然而，脉络丛是否同样参与 MS 和视神经脊髓炎谱系障碍（NMOSD）尚不清楚。因此，本研究旨在比较 MS 和 NMOSD 患者的脉络丛体积。
在这项回顾性、横断面研究中，通过便利抽样从 4 个国际 MS 中心纳入患者。使用深度学习算法（多维门控递归单元）对侧脑室的 T1 加权 MRI 序列进行脉络丛的全自动分割。应用单变量和多变量线性模型来研究脉络丛体积与临床上有意义的疾病特征和 MRI 参数之间的关联。
我们研究了 180 例 MS 患者和 98 例 NMOSD 患者。共有 94 名健康个体和 47 名偏头痛患者作为对照。MS 患者的脉络丛体积（中位数 1690µL，四分位距 [IQR] 648µL）大于 NMOSD（中位数 1403µL，IQR 510µL）、健康个体（中位数 1533µL，IQR 570µL）和偏头痛患者（中位数 1404µL，IQR 524µL；所有 <0.001），而 NMOSD、偏头痛和健康对照组之间无差异。在调整年龄、性别和颅内体积后也是如此。与 NMOSD 相反，在调整年龄、性别、总颅内体积、疾病持续时间、MRI 前 1 年的复发、疾病过程、扩展残疾状态量表评分、疾病修正治疗和治疗持续时间的线性模型中，MS 患者的脉络丛体积与 T2 加权病变数量相关（β 4.4；95%CI 0.78-8.1； = 0.018）。
本研究支持脉络丛参与 MS 而不参与 NMOSD，并提供线索以更好地理解各自的发病机制。
