Kumar Shivram, Lanzino Giuseppe, Brinjikji Waleed, Hocquard Kate W, Flemming Kelly D
Department of Neurology, Mayo Clinic, Rochester, Minnesota.
Department of R, Mayo Clinic, Rochester, Minnesota.
J Stroke Cerebrovasc Dis. 2019 Jun;28(6):1662-1667. doi: 10.1016/j.jstrokecerebrovasdis.2019.02.025. Epub 2019 Mar 14.
Sporadic brain cavernous malformations commonly correlate with developmental venous anomalies; however, developmental venous anomalies may exist without cavernous malformations. Infratentorial location and specific angioarchitectural features of the developmental venous anomaly increase the odds of a concomitant malformation. Animal data also suggest chronic inflammatory disease, oxidative stress, and angiogenesis promote cavernous malformation development. We sought to determine potential clinical and radiologic factors promoting development of sporadic cavernous malformations.
One hundred and forty-five patients with sporadic, nonradiation-induced brain cavernous malformations (63 with radiologic-apparent and 82 with radiologic-occult developmental venous anomalies) were compared to developmental venous anomaly controls without associated malformation. Data collection included demographic information, comorbidities, medications at diagnosis, and location of the developmental venous anomaly and/or malformation. Logistic regression with likelihood ratios, odds ratios and 95% confidence intervals were calculated comparing malformation cases with controls. A similar analysis compared malformations with radiologic-apparent anomalies to controls.
Compared to controls, cases were more likely to have had a major infectious illness (10.3% versus 2.3%; P = .0003 and/or chronic inflammatory disease (31.7% versus 21.3%; P = .0184) prior to diagnostic magnetic resonance imaging. Infratentorial location was more common in cavernous malformation cases (31.7% versus 15.7% controls; P ≤ .0001) with similar findings in cavernous malformation with radiologic-apparent developmental venous anomalies versus controls.
Infratentorial developmental venous anomalies location, major infectious illness, and chronic inflammatory disorders increase the odds of sporadic cavernous malformation formation. Inflammation may promote local thrombosis of developmental venous anomalies, trigger angiogenic response through increased vascular permeability, or promote cavernous malformation through Toll-like receptor 4.
散发性脑海绵状血管畸形通常与发育性静脉异常相关;然而,发育性静脉异常可能在没有海绵状血管畸形的情况下存在。幕下位置以及发育性静脉异常的特定血管构筑特征增加了合并畸形的几率。动物数据也表明慢性炎症性疾病、氧化应激和血管生成会促进海绵状血管畸形的发展。我们试图确定促进散发性海绵状血管畸形发展的潜在临床和放射学因素。
将145例散发性、非辐射诱导的脑海绵状血管畸形患者(63例伴有影像学可见的发育性静脉异常,82例伴有影像学隐匿的发育性静脉异常)与无相关畸形的发育性静脉异常对照组进行比较。数据收集包括人口统计学信息、合并症、诊断时的用药情况以及发育性静脉异常和/或畸形的位置。计算似然比、比值比和95%置信区间的逻辑回归,将畸形病例与对照组进行比较。类似的分析将有影像学可见异常的畸形与对照组进行比较。
与对照组相比,病例在诊断性磁共振成像之前更有可能患有重大感染性疾病(10.3%对2.3%;P = 0.0003)和/或慢性炎症性疾病(31.7%对21.3%;P = 0.0184)。幕下位置在海绵状血管畸形病例中更常见(31.7%对15.7%对照组;P≤0.0001),在伴有影像学可见发育性静脉异常的海绵状血管畸形与对照组中也有类似发现。
幕下发育性静脉异常位置、重大感染性疾病和慢性炎症性疾病增加了散发性海绵状血管畸形形成的几率。炎症可能促进发育性静脉异常的局部血栓形成,通过增加血管通透性触发血管生成反应,或通过Toll样受体4促进海绵状血管畸形。