脑淀粉样血管病中皮质微梗死与皮质浅表性红斑的时空关联

摘要(中文译文)

脑淀粉样血管病（CAA）是一种以出血性和非出血性脑损伤为特征的小血管疾病。虽然皮质脑微梗死（CMI）与皮质表面铁沉积（cSS）相关，但连接这些病变的机制仍不清楚。本研究旨在确定CAA中皮质CMI与cSS之间的时空关系，假设cSS可促进局部缺血性损伤。从马萨诸塞州总医院一项基于前瞻性记忆门诊的队列中招募了很可能CAA（波士顿标准v2.0）且无既往症状性颅内出血或CAA相关炎症的患者。在基线和24个月随访时通过3特斯拉MRI量化CAA相关影像学表现——包括皮质CMI和cSS。应用多变量逻辑回归和广义线性模型评估基线影像学特征与影像学进展之间的关联。我们还比较了有和无cSS覆盖区域中皮质CMI的局部密度。在74例很可能CAA患者（年龄：73.0 [67.9-78.2]岁；38%女性）中，26例（35%）有皮质CMI（n = 135，39%位于cSS下方）。与CMI阴性CAA相比，CMI阳性者的cSS患病率更高（73% vs 40%；= 0.006）、cSS体积更大（1.3 [0.1-8.3] vs 0 [0-0.5] mL；< 0.001）、脑叶腔隙灶计数更多（50% vs 19%；= 0.005）。在基线时，皮质CMI计数与cSS体积（Exp(B) = 1.12 [95% CI 1.07-1.18]；< 0.001）及脑叶腔隙灶计数（Exp(B) = 1.65 [95% CI 1.52-1.80]；< 0.001）呈非线性关联。cSS覆盖区域的CMI密度显著高于非cSS区域（中位数：20.84 [0.00-56.95] vs 0.49 [0.11-0.89]个皮质CMI/1,000 cm²；= 0.010）。随访扫描（n = 36）发现23个新发皮质CMI（43%位于cSS下方）。基线cSS体积与新发CMI独立相关（OR：1.41 [95% CI 1.02-1.95]；= 0.036），而基线CMI负荷与cSS进展无关。我们的研究结果证明皮质CMI与cSS之间存在密切相互作用，其时空关系支持凸面蛛网膜下腔出血及可能由此产生的cSS可触发局部缺血性损伤的假设。鉴于纵向队列的样本量，我们认为这些数据具有假设生成性。进一步研究应证实这一关联并确定驱动性病理生理机制，这可能代表预防cSS相关皮质损伤的新治疗靶点。

Abstract

Cerebral amyloid angiopathy (CAA) is a small vessel disease characterized by hemorrhagic and nonhemorrhagic brain injuries. While cortical cerebral microinfarcts (CMI) have been associated with cortical superficial siderosis (cSS), the mechanisms linking these lesions remain unknown. This study aims to determine the spatiotemporal relationship between cortical CMI and cSS in CAA, with the hypothesis that cSS can promote local ischemic injury. Patients with probable CAA (Boston Criteria v2.0) without previous symptomatic intracerebral hemorrhage or CAA-related inflammation were recruited from a prospective memory clinic-based cohort at Massachusetts General Hospital. CAA-related radiologic manifestations-including cortical CMI and cSS-were quantified at baseline and at the 24-month follow-up on 3-Tesla MRI. Multivariable logistic regression and generalized linear models were applied to assess associations between baseline radiologic features and radiologic progression. We also compared the local density of cortical CMIs in regions with and without overlaid cSS. Among 74 patients with probable CAA (age: 73.0 [67.9-78.2] years; 38% female), 26 (35%) had cortical CMIs (n = 135, 39% underlying cSS). Compared with CMI-negative CAA, those with CMI had a higher cSS prevalence (73% vs 40%; = 0.006), cSS volume (1.3 [0.1-8.3] vs 0 [0-0.5] mL; < 0.001), and lobar lacunes count (50% vs 19%; = 0.005). At baseline, cortical CMI count demonstrated a nonlinear association with cSS volume (Exp(B) = 1.12 [95% CI 1.07-1.18]; < 0.001) and with lobar lacunes count (Exp(B) = 1.65 [95% CI 1.52-1.80]; < 0.001). The CMI density was markedly higher in cSS-covered vs non-cSS regions (median: 20.84 [0.00-56.95] vs 0.49 [0.11-0.89]n° cortical CMI/1,000 cm2; = 0.010). Follow-up scans (n = 36) revealed 23 incident cortical CMIs (43% underlying cSS). Baseline cSS volume was independently associated with incident CMI (OR:1.41 [95% CI 1.02-1.95]; = 0.036), whereas baseline CMI burden was not associated with cSS progression. Our findings demonstrate a close interplay between cortical CMI and cSS, with the spatiotemporal relationship supporting the hypothesis that convexity subarachnoid hemorrhage, and potentially resultant cSS, may trigger local ischemic injury. Given the sample size of the longitudinal cohort, we consider these data hypothesis-generating. Further studies should confirm this association and identify the driving pathophysiology, which may represent a new therapeutic target for preventing cSS-associated cortical injury.

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