Diffusion basis spectrum imaging and diffusion tensor imaging predict persistent black hole formation in multiple sclerosis.
Diffusion basis spectrum imaging and diffusion tensor imaging predict persistent black hole formation in multiple sclerosis.
复制标题
扩散基谱成像和扩散张量成像预测多发性硬化症中持续黑洞的形成。
DOI：
10.1016/j.msard.2024.105494
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发表时间：
2024
影响因子：
4
通讯作者：
Cross,AnneH
中科院分区：
文献类型：
--
作者：
Wooliscroft,Lindsey;Salter,Amber;Adusumilli,Gautam;Levasseur,VictoriaA;Sun,Peng;Lancia,Samantha;Perantie,DanaC;Trinkaus,Kathryn;Naismith,RobertT;Song,Sheng-Kwei;Cross,AnneH
背景和目标扩散基础能谱成像 (DBSI) 可提取多个各向异性和各向同性扩散张量，提供比扩散张量成像 (DTI) 更高的组织病理学特异性。持续性黑洞 (PBH) 代表多发性硬化症 (MS) 中严重组织损伤的区域，高 PBH 负担与更严重的 MS 残疾相关。本研究评估了 DBSI 和 DTI 预测哪些急性对比增强病变 (CEL) 在 12 个月后将持续存在 T1 低强度（即 PBH）的能力。我们预计，急性 CEL 的较高径向扩散率 (RD)（代表脱髓鞘）和较高的 DBSI 衍生的各向同性非限制分数（代表水肿和细胞外间隙增加）将增加未来发生 PBH 的可能性。 方法在这项前瞻性队列研究中，CEL ≥1 的复发性 MS 患者每月接受 MRI 扫描，持续 4 至 6 个月，直至钆消退。当 CEL 在每月扫描期间最明显时，对 DBSI 和 DTI 指标进行量化。为了确定 CEL 是否成为 PBH，在最后一次每月扫描后至少 12 个月进行了随访 MRI。 结果 该队列包括 20 名 MS 参与者（中位年龄 33 岁；13 名女性），有 164 个 CEL。其中，59 个 (36%) CEL 演化为 PBH。在 Gd-max 时，所有 CEL 的 DTI RD 和 AD 均增加，并且与非黑洞 (NBH) 相比，成为 PBH 的 CEL 的两个指标均显着升高。 DTI RD 高于 0.74 使得 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）； DTI 轴向扩散率 (AD) 高于 1.22 时，成为 PBH 的 OR 为 7.32 (CI 3.38–15.86)（AUC 0.75，CI 0.66–0.83）。 DBSI RD 和 AD 不能在多变量模型中预测 PBH 的发展。在 Gd-max 时，所有 CEL 中的 DBSI 限制性分数下降，DBSI 非限制性分数增加，并且与 NBH 相比，对于成为 PBH 的 CEL，这两个指标均显着不同。 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）。结论我们的研究结果表明，CEL 中更大程度的水肿/细胞外间隙是组织破坏的预测因素，正如 PBH 进化所证明的那样。
Background and objectivesDiffusion 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 T1hypointensities (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.MethodsIn 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.ResultsThe 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).ConclusionOur findings suggest that greater degree of edema/extracellular space in a CEL is a predictor of tissue destruction, as evidenced by PBH evolution.