Department of Neurology, Oregon Health & Science University, Portland, OR, USA; Department of Neurology, VA Portland Health Care System, Portland, OR, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA.
Department of Biostatistics, Washington University School of Medicine, St. Louis, MO, USA; Department of Biostatistics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Mult Scler Relat Disord. 2024 Apr;84:105494. doi: 10.1016/j.msard.2024.105494. Epub 2024 Feb 11.
Diffusion basis spectrum imaging (DBSI) extracts multiple anisotropic and isotropic diffusion tensors, providing greater histopathologic specificity than diffusion tensor imaging (DTI). Persistent black holes (PBH) represent areas of severe tissue damage in multiple sclerosis (MS), and a high PBH burden is associated with worse MS disability. This study evaluated the ability of DBSI and DTI to predict which acute contrast-enhancing lesions (CELs) would persist as T hypointensities (i.e. PBHs) 12 months later. We expected that a higher radial diffusivity (RD), representing demyelination, and higher DBSI-derived isotropic non-restricted fraction, representing edema and increased extracellular space, of the acute CEL would increase the likelihood of future PBH development.
In this prospective cohort study, relapsing MS patients with ≥1 CEL(s) underwent monthly MRI scans for 4 to 6 months until gadolinium resolution. DBSI and DTI metrics were quantified when the CEL was most conspicuous during the monthly scans. To determine whether the CEL became a PBH, a follow-up MRI was performed at least 12 months after the final monthly scan.
The cohort included 20 MS participants (median age 33 years; 13 women) with 164 CELs. Of these, 59 (36 %) CELs evolved into PBHs. At Gd-max, DTI RD and AD of all CELs increased, and both metrics were significantly elevated for CELs which became PBHs, as compared to non-black holes (NBHs). DTI RD above 0.74 conferred an odds ratio (OR) of 7.76 (CI 3.77-15.98) for a CEL becoming a PBH (AUC 0.80, CI 0.73-0.87); DTI axial diffusivity (AD) above 1.22 conferred an OR of 7.32 (CI 3.38-15.86) for becoming a PBH (AUC 0.75, CI 0.66-0.83). DBSI RD and AD did not predict PBH development in a multivariable model. At Gd-max, DBSI restricted fraction decreased and DBSI non-restricted fraction increased in all CELs, and both metrics were significantly different for CELs which became PBHs, as compared to NBHs. A CEL with a DBSI non-restricted fraction above 0.45 had an OR of 4.77 (CI 2.35-9.66) for becoming a PBH (AUC 0.74, CI 0.66-0.81); a CEL with a DBSI restricted fraction below 0.07 had an OR of 9.58 (CI 4.59-20.02) for becoming a PBH (AUC 0.80, 0.72-0.87).
Our findings suggest that greater degree of edema/extracellular space in a CEL is a predictor of tissue destruction, as evidenced by PBH evolution.
扩散基础谱成像（DBSI）提取多个各向异性和各向同性扩散张量，比弥散张量成像（DTI）提供更高的组织病理学特异性。持续黑洞（PBH）代表多发性硬化症（MS）中严重的组织损伤区域，较高的 PBH 负担与更严重的 MS 残疾相关。本研究评估了 DBSI 和 DTI 预测急性对比增强病变（CEL）中哪些病变将在 12 个月后持续为 T 低信号（即 PBH）的能力。我们预计，急性 CEL 的径向扩散度（RD）升高（代表脱髓鞘）和 DBSI 衍生的各向同性无限制分数升高（代表水肿和细胞外空间增加），会增加未来 PBH 发展的可能性。
在这项前瞻性队列研究中，≥1 个 CEL（s）的复发型 MS 患者接受了 4 至 6 个月的每月 MRI 扫描，直到钆增强消退。当 CEL 在每月扫描中最明显时，对 DBSI 和 DTI 指标进行了量化。为了确定 CEL 是否会变成 PBH，在最后一次每月扫描后至少 12 个月进行了随访 MRI。
该队列包括 20 名 MS 参与者（中位年龄 33 岁；13 名女性），共 164 个 CEL。其中，59 个（36%）CEL 演变为 PBH。在 Gd-max，所有 CEL 的 DTI RD 和 AD 均增加，且成为 PBH 的 CEL 的这两项指标均显著高于非黑洞（NBH）。RD 高于 0.74 的 DTI 为 CEL 成为 PBH 的比值比（OR）为 7.76（CI 3.77-15.98）（AUC 0.80，CI 0.73-0.87）；AD 高于 1.22 的 DTI 为 CEL 成为 PBH 的 OR 为 7.32（CI 3.38-15.86）（AUC 0.75，CI 0.66-0.83）。在多变量模型中，DBSI RD 和 AD 均不能预测 PBH 的发展。在 Gd-max，所有 CEL 的 DBSI RD 和 AD 均降低，且成为 PBH 的 CEL 的这两项指标均显著低于 NBH。DBSI 非限制分数高于 0.45 的 CEL 成为 PBH 的 OR 为 4.77（CI 2.35-9.66）（AUC 0.74，CI 0.66-0.81）；DBSI 限制分数低于 0.07 的 CEL 成为 PBH 的 OR 为 9.58（CI 4.59-20.02）（AUC 0.80，0.72-0.87）。
我们的研究结果表明，CEL 中更大程度的水肿/细胞外空间是组织破坏的预测因子，这一点从 PBH 的演变中可以看出。
