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综述
儿童髓鞘少突胶质细胞糖蛋白抗体相关疾病的MRI研究进展
李婷 陈欣 王浩入 何玲

Cite this article as: Li T, Chen X, Wang HR, et al. Research progress of MRI on myelin oligodendrocyte glycoprotein antibody disease in children[J]. Chin J Magn Reson Imaging, 2022, 13(9): 123-126.本文引用格式:李婷, 陈欣, 王浩入, 等. 儿童髓鞘少突胶质细胞糖蛋白抗体相关疾病的MRI研究进展[J]. 磁共振成像, 2022, 13(9): 123-126. DOI:10.12015/issn.1674-8034.2022.09.029.


[摘要] 髓鞘少突胶质细胞糖蛋白抗体相关疾病(myelin oligodendrocyte glycoprotein antibody associated disorder, MOGAD)是儿童中枢神经系统特发性炎性脱髓鞘疾病(idiopathic inflammatory demyelinating diseases, IIDDs)的一组新亚型,可累及脑、视神经和脊髓。MOGAD需要个体化的临床管理和特定的治疗方案,但其临床表现与IIDDs的其他亚型存在一定重叠,临床鉴别较为困难。MRI软组织分辨率较高,具有多参数、多序列成像的优势,能够更好显示MOGAD与IIDDs其他亚型的神经影像学特征的差异,在MOGAD的诊断与鉴别诊断中发挥着重要作用。近年来有关MOGAD的研究主要集中于MRI常规序列上脑、视神经和脊髓病灶影像学特征的总结归纳,新序列、新技术在儿童MOGAD中的研究较少。因此,本文综述了儿童MOGAD的临床及MRI研究进展,以期提高对该病的认识水平。
[Abstract] Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is a new subtype of idiopathic inflammatory demyelinating disease (IIDDs) of the central nervous system in children, involving the brain, optic nerve and spinal cord. MOGAD requires individualized clinical management and specific treatment regimens, but its clinical manifestations overlap with other subtypes of IIDDs, making clinical identification difficult. MRI has the advantages of high soft tissue resolution and multi-parameter and multi-sequence imaging, which can better display the differences of neuroimaging characteristics between MOGAD and other subtypes of IIDDs, and plays an important role in the diagnosis and differential diagnosis of MOGAD. In recent years, studies on MOGAD have mainly focused on the summary and induction of imaging features of brain, optic nerve and spinal cord lesions based on MRI conventional sequences, while few studies on new sequences and new technologies have been performed on MOGAD in children. Therefore, this paper reviews the clinical and MRI research progress of MOGAD in children, in order to improve the level of understanding of the disease.
[关键词] 儿童;脱髓鞘疾病;髓鞘少突胶质细胞糖蛋白抗体相关疾病;磁共振成像
[Keywords] children;demyelinating diseases;myelin oligodendrocyte glycoprotein antibody disease;magnetic resonance imaging

李婷    陈欣    王浩入    何玲 *  

重庆医科大学附属儿童医院放射科,国家儿童健康与疾病临床医学研究中心,儿童发育疾病研究教育部重点实验室,儿科学重庆市重点实验室,重庆 400014

*何玲,E-mail:heling508@sina.com

作者利益冲突声明:全体作者均声明无利益冲突。


基金项目: 重庆市教育委员会科学技术研究项目 KJQN202000440 重庆市渝中区基础研究与前沿探索项目 20200155
收稿日期:2022-05-16
接受日期:2022-07-26
中图分类号:R445.2  R744.5 
文献标识码:A
DOI: 10.12015/issn.1674-8034.2022.09.029
本文引用格式:李婷, 陈欣, 王浩入, 等. 儿童髓鞘少突胶质细胞糖蛋白抗体相关疾病的MRI研究进展[J]. 磁共振成像, 2022, 13(9): 123-126. DOI:10.12015/issn.1674-8034.2022.09.029

       儿童中枢神经系统特发性炎性脱髓鞘疾病(idiopathic inflammatory demyelinating diseases, IIDDs)是一组单相或多相发作的中枢神经系统自身免疫性脱髓鞘炎症疾病,主要包括临床孤立综合征(clinically isolated syndrome, CIS)、急性播散性脑脊髓炎(acute disseminated encephalomyelitis, ADEM)、多发性硬化(multiple sclerosis, MS)和视神经脊髓炎谱系疾病(neuromyelitis optica spectrum disorders, NMOSD)[1, 2]。随着对髓鞘少突胶质细胞糖蛋白免疫球蛋白G抗体(myelin oligodendrocyte glycoprotein-IgG, MOG-IgG)在IIDDs发生发展中的认识逐渐加深,髓鞘少突胶质细胞糖蛋白抗体相关疾病(myelin oligodendrocyte glycoprotein antibody associated disorder, MOGAD)是近年来提出的一种免疫介导的中枢神经系统炎性脱髓鞘疾病,是IIDDs的一组新亚型,而MOG-IgG可能是其致病性抗体[3]。MOGAD常累及脑、脊髓和视神经,需要个体化的临床管理和特定的治疗方案[4, 5]。MOGAD主要通过临床表现、实验室检查和影像学联合诊断,但由于MOGAD的临床表现与IIDDs的其他亚型存在一定重叠,MOGAD易误诊为其他亚型的IIDDs[6]。MRI有较高的软组织分辨率,具有多参数、多序列成像的特点,能够更好显示MOGAD与IIDDs其他亚型神经影像学特征的差异。近年来有关MOGAD的研究主要集中于MRI常规序列上MOGAD的脑、视神经和脊髓病灶影像学特征的总结归纳,而新序列、新技术在儿童MOGAD中的研究较少。因此,本文综述了儿童MOGAD的临床及MRI研究进展,以期望提高对该病的认识。

1 临床表现

1.1 首次发作

       MOGAD在儿童的各个年龄段均可发生,但主要发生在年幼儿童,中位年龄为6岁,男女患病比率无明显差异[7]。儿童MOGAD起病多为单相过程,但也可出现复发—缓解的类型,部分可缓慢进展,从而出现不可逆的神经损害[8, 9]。MOGAD的临床表型与几种已知的儿童IIDDs具有一定重叠,主要包括ADEM样表型、视神经炎(optic neuritis, ON)表型、脊髓炎表型、水通道蛋白-4(aquaporin-4, AQP4)-IgG阴性的NMOSD表型等[10]。MOGAD发病时的临床表型与患儿首次发作时的年龄密切相关。对于9岁以下的患儿,MOGAD首次发作时的临床表现倾向于ADEM[11]。研究报道,约40%的ADEM和近100%的多时相ADEM均存在MOG-IgG[12]。而对于9岁以上的患儿,MOGAD首次发作时的临床表现更倾向于ON、脊髓炎和NMOSD[13]。当患儿以脑病为主要症状时,可出现脑膜刺激征、颅内压升高的表现。依据颅内病变部位不同,患儿可出现局灶性神经和精神功能障碍,如癫痫发作、嗜睡和共济失调等症状[14]。当累及视神经时,患儿可出现视力障碍、眼球运动疼痛等症状[15]。当脊髓受累时,患儿可出现双下肢运动感觉功能障碍、尿潴留或排便困难[13]。近年来,越来越多的MOGAD临床表型在不同的研究中广泛报道。其中,皮质脑炎(cerebral cortical encephalitis, CCE)是MOGAD的一个新表型,属于自身免疫性脑炎的范畴,好发于年幼儿童[16]。有研究发现MOG-IgG是儿童自身免疫性脑炎最常见的自身抗体,约占儿童自身免疫性脑炎的13%,超过其他所有神经元抗体的总和[17]。此外,还有一些非典型MOGAD临床表型的病例报道,如MRI仅表现为孤立的基底节或丘脑受累,或轻微脑部异常但伴随难治性癫痫持续状态[18]。在以往的临床诊疗中,除ADEM以外,其他的疑似自身免疫性脑炎患者极少检测MOG-IgG,因此了解MOGAD的不同临床表型有助于患者的早期诊断和早期治疗[8]。近年来,MOGAD罕见的临床表型被不断发现,扩展了MOGAD的疾病谱,但仅为个案报道,尚未被系统阐述。

1.2 治疗后复发

       儿童MOGAD治疗后复发的比例约为26%,其中75%的患儿在首次发作一年内复发[19]。MOGAD复发时可出现与初次发作时不同的临床表型,主要包括多时相ADEM、ADEM相关性ON(acute disseminated encephalomyelitis-optic neuritis, ADEM-ON)、NMOSD和复发性ON,但以ON最为常见,其中年幼患儿复发时的临床表型常为多时相ADEM[18,20]

2 儿童MOGAD的MRI研究进展

2.1 儿童MOGAD脑部MRI表现

       儿童MOGAD脑部最常见的影像学表现类似于ADEM,主要累及双侧大脑半球脑白质和脑灰质,病灶分布多不对称、多灶性、直径较大(轴位≥2 cm),最常见的好发部位是皮质和皮质旁下白质,其次为深部白质和深部灰质,脑干和小脑病变较为少见[7]。病变边缘模糊,大部分病灶不强化,少数病灶强化,这可能是由于血脑屏障的破坏程度不同。强化的病灶大多呈边界不清的强化,活动性病灶还可出现散在的线状和结节状强化[21]。Zhou等[9]研究发现约81.43%的MOGAD患儿出现脑部病灶,其中约54.35%的出现幕上白质病变的患儿具有ADEM样病灶。与非MOG-IgG相关的ADEM不同,MOGAD患儿脑部病灶更多表现为大的、累及双侧大脑半球的模糊的典型病灶,小的、边界清楚的不典型病灶几率更小。并且,MOGAD患儿小脑病变数显著高于非MOGAD患儿,但合并脊髓炎的发生率小于非MOGAD患儿,累及脊髓时多表现为纵向广泛横贯性脊髓炎(longitudinal extensive transverse myelitis, LETM)[12,22]。一部分MOGAD患者仅累及脊髓和/或视神经,脑部MRI显示正常,或脑部MRI表现为分布于皮质下白质或深层白质的边界不清的非特异性病变,且临床往往不出现脑病的表现[23]。MOGAD也可以为孤立的脑干受累,MRI常出现边界不清的脑干病变,通常位于桥脑、延髓或小脑脚[4]

       CCE也是儿童MOGAD自身免疫性脑炎的重要组成部分,表现为单侧或双侧皮质病变[24]。在液体衰减反转恢复(fluid attenuated inversion recovery, FLAIR)序列上观察病变最明显,表现为受累皮质高信号,不出现皮质旁白质受累或其他部位受累,没有扩散受限,但部分患者可出现病变皮质旁软脑膜强化[25]

       部分年幼儿童初次发作或ADEM样反复发作时,患儿脑部病灶可类似于脑白质营养不良样的MRI表现,呈脑室周围广泛的融合白质异常,分布基本对称,增强可出现结节状强化,但在随访时可消退,提示为炎性脱髓鞘病灶[26]。脑部病灶范围累及较大,如出现脑白质营养不良样病灶、广泛CCE时,可出现脑萎缩的影像学表现[17]。患者MRI表现为全脑萎缩、多灶性模糊病变和脑白质营养不良样病灶时,常常隐匿发作并缓慢进展,且治疗后症状改善不明显[8]。尽管既往文献对MOGAD的脑部MRI影像学特征进行了详细描述,然而仍有较大比例的患者存在着非典型病变。这些非典型病变丰富着MOGAD的影像谱,需要随着研究不断深入。

2.2 儿童MOGAD视神经MRI表现

       MOGAD累及视神经时常出现T2WI高信号伴视神经肿胀,或出现纵向广泛的视神经强化病灶,其中眼眶段最易受累,其次为视神经管内段和前视交叉,而视交叉和视束较少受累[27]。视神经常出现强化,表现为视神经鞘及周围脂肪组织的强化,周围强化是MOGAD特征性表现,有助于区分AQP4-IgG阳性的NMOSD或MS[28]。视神经强化的常见部位与最常累及的部位相同,以眼眶段受累最多见,其次为视神经管内段,颅内段强化最为少见[29]。与AQP4-IgG阳性的NMOSD出现视神经受累时的表现不同,MOGAD患者视神经病变累及的范围更大、更靠前,累及视盘时出现水肿多见,较少累及视交叉[30]。而AQP4-IgG阳性的NMOSD疾病出现视神经受累时,常累及后段视神经,视交叉常受累[31]。在IDDs首次发作的患儿中,出现双侧视神经同时受累是一种罕见的表现,但40%的MOGAD视神经受累患者可表现为双侧视神经受累,而AQP4-IgG阳性的NMOSD和MS累及视神经时常表现为单侧病变[32, 33]

2.3 儿童MOGAD脊髓MRI表现

       在MOGAD的脊髓病变中,通常出现两种脊髓受累模式:(1)LETM,在脊柱矢状位上表现为超过三个或更多椎体的脊髓损害;(2)短节段脊髓炎,矢状位图像上范围小于3个椎体水平的脊髓病变或小片状病变[34]。在MOGAD的脊髓病变中,两种脊髓受累模式可以同时出现,但LEMT比短小的病变更常见,且病变多不连续。病灶可累及灰质和白质,主要累及中央灰质部位,典型者呈H型中央灰质分布,增强呈部分轻度增强[35]。就病变部位而言,MOGAD可以影响脊髓的任何节段,且常累及一个以上脊髓区域,颈、胸段脊髓是最常累及的节段,相比于其他中枢神经系统炎性脱髓鞘疾病更容易累及脊髓圆锥[14]。MS、AQP4-IgG阳性的NMOSD最常好发于颈髓。AQP4-IgG阳性的NMOSD常累及脊髓中央灰质,表现为长节段的连续中央病灶,较MOG-IgG相关脊髓炎更常出现强化[36],MS多表现为非对称性脊髓病灶[37]。大部分研究表明,MOGAD更常累及颈段和胸段脊髓,然而部分研究发现MOGAD累及腰段脊髓和脊髓圆锥更为常见[7]。因此MOGAD最常累及的节段仍存在部分争议,需要扩大样本量进行研究。

3 鉴别诊断

       MOGAD诊断依赖于临床、实验室检查和影像学表现。当患者出现脑炎相关的临床症状,脑脊液中淋巴细胞增多时可能被误诊为病毒性脑炎[38]。对于不能排除病毒感染导致的脑炎患者,应避免使用皮质类固醇,但MOGAD患者在急性期使用皮质类固醇可减轻患者的神经功能障碍、减少复发,因此早期鉴别两者有助于患者的及时治疗,从而改善预后[21,39]。单纯疱疹病毒(herpes simplex virus, HSV)脑炎是儿童急性散发性脑炎最常见的类型。与MOGAD常累及幕上深部白质、皮层及皮质下白质不同,HSV脑炎病灶主要累及颞叶皮质和白质区域,且病灶内大量脑结构损伤,因此扩散加权成像和增强的信号强度常明显增高[40, 41]

       此外,MOGAD还需要与IDDs其他亚型相鉴别。AQP4-IgG可以介导大多数NMOSD,MOG-IgG介导的NMOSD仅出现无AQP4-IgG患者中。MOGAD可表现为反复发作的单侧、双侧ON和脊髓炎,脑部仍可出现病变[42, 43]。AQP4-IgG相关NMOSD的脑部病灶主要出现在AQP4存在较多的区域,如第三脑室周围区域、导水管周围灰质和邻近第四脑室的背侧脑干[44]。MOGAD患者在大脑中AQP4丰富的区域分布后也会有损伤,表现出邻近第四脑室的脑干或小脑脚边界不清的病灶,即存在“NMOSD特异性”区域的病变[45, 46]。但在AQP4-IgG阳性的NMOSD患者中较少出现ADEM样病变,且T1低信号病变更多见[31]。与AQP4-IgG阳性的NMOSD相比,双侧丘脑病变在MOGAD发病时很常见,约60%的患者可以观察到。小脑脚病变仅在MOGAD儿童中发现[26]

4 小结与展望

       MOGAD作为近年来提出的一组IDDs新亚型,相关研究主要围绕在疾病的治疗、转归以及MRI影像特征的总结归纳,但相关的影像学诊断标准目前尚未形成。随着MOGAD的病理生理研究不断深入,以及新的临床表型不断被发现,MRI新技术有望从病灶功能及代谢方面提供更多的关于疾病诊断及预后的特异性信息[47]。目前,DTI是最常用的量化脑白质纤维结构变化的技术[48]。此外,其他新技术,如磁转化成像、髓鞘水成像、磁化率图等也可以量化脱髓鞘的程度[49]。磁共振波谱能从代谢方面量化脱髓鞘病灶内轴突损伤及脱髓鞘、髓鞘再生的程度[50]。但是,目前MRI新技术在儿童MOGAD中运用相对较少。随着MRI新技术的不断发展,这些新技术将有助于MOGAD的精准诊断与预后评估。

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