BACKGROUND Slow-burning inflammation is putatively associated with lesion expansion and leads to progressive loss of axons and disability worsening. OBJECTIVE To investigate the incidence and extent of chronic white matter lesion expansion in relapsing-remitting multiple sclerosis (RRMS) patients and to evaluate its relationship with biomarkers of disease progression. METHODS Pre- and post-gadolinium T1, fluid-attenuated inversion recovery (FLAIR) and diffusion tensor images were acquired from 33 patients. Lesional activity were analysed between baseline and 48 months using custom-designed software. RESULTS A total of 569 lesions were identified as chronic at baseline, of which 261 were expanding, 236 were stable and 72 were shrinking. In addition, 139 new lesions (both confluent and free-standing) were observed. Chronic lesion expansion was associated with patient's age and accounted for the bulk (67.3%) of total brain lesion volume increase, while only 32.7% was attributable to new lesion formation. Change in chronic lesion volume correlated with the rate of brain atrophy (r = -0.57, p = 0.001), change of Expanded Disability Status Scale (EDSS; r = 0.38, p = 0.03) and an increase of isotropic diffusivity inside the lesions (r = 0.75, p < 0.001). CONCLUSION Expansion of chronic lesions in RRMS patients is the primary determinant of increased T2 total lesion load. It significantly contributes to disease progression and partially driving axonal loss inside the lesions and brain damage outside of lesional tissue.

中文翻译：

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慢性病灶的扩大与复发缓解型多发性硬化症患者的疾病进展有关

背景缓慢燃烧的炎症被推定与病灶扩大有关并导致轴突的进行性丧失和残疾恶化。目的 调查复发缓解型多发性硬化症 (RRMS) 患者慢性白质病变扩张的发生率和程度，并评估其与疾病进展的生物标志物的关系。方法 从 33 名患者中获取钆前后 T1、流体衰减反转恢复 (FLAIR) 和扩散张量图像。使用定制设计的软件分析基线和 48 个月之间的病变活动。结果基线时共有569个病灶被确定为慢性病灶，其中261个病灶在扩大，236个病灶稳定，72个病灶缩小。此外，还观察到 139 个新病灶（融合的和独立的）。慢性病灶扩大与患者的年龄有关，占脑总病灶体积增加的大部分（67.3%），而只有 32.7% 可归因于新病灶的形成。慢性病灶体积的变化与脑萎缩率 (r = -0.57, p = 0.001)、扩展残疾状态量表 (EDSS; r = 0.38, p = 0.03) 和病灶内各向同性扩散的增加​​相关 ( r = 0.75，p < 0.001）。结论 RRMS 患者慢性病灶的扩大是 T2 总病灶负荷增加的主要决定因素。它显着促进疾病进展并部分驱动病变内部的轴突损失和病变组织外部的脑损伤。7% 归因于新病灶的形成。慢性病灶体积的变化与脑萎缩率 (r = -0.57, p = 0.001)、扩展残疾状态量表 (EDSS; r = 0.38, p = 0.03) 和病灶内各向同性扩散的增加​​相关 ( r = 0.75，p < 0.001）。结论 RRMS 患者慢性病灶的扩大是 T2 总病灶负荷增加的主要决定因素。它显着促进疾病进展并部分驱动病变内部的轴突损失和病变组织外部的脑损伤。7% 归因于新病灶的形成。慢性病灶体积的变化与脑萎缩率 (r = -0.57, p = 0.001)、扩展残疾状态量表 (EDSS; r = 0.38, p = 0.03) 和病灶内各向同性扩散的增加​​相关 ( r = 0.75，p < 0.001）。结论 RRMS 患者慢性病灶的扩大是 T2 总病灶负荷增加的主要决定因素。它显着促进疾病进展并部分驱动病变内部的轴突损失和病变组织外部的脑损伤。结论 RRMS 患者慢性病灶的扩大是 T2 总病灶负荷增加的主要决定因素。它显着促进疾病进展并部分驱动病变内部的轴突损失和病变组织外部的脑损伤。结论 RRMS 患者慢性病灶的扩大是 T2 总病灶负荷增加的主要决定因素。它显着促进疾病进展并部分驱动病变内部的轴突损失和病变组织外部的脑损伤。