Harreld J H, Sabin N D, Rossi M G, Awwad R, Reddick W E, Yuan Y, Glass J O, Ji Q, Gajjar A, Patay Z
From the Departments of Radiological Sciences (J.H.H., N.D.S., R.A., W.E.R., J.O.G., Q.J., Z.P.)
From the Departments of Radiological Sciences (J.H.H., N.D.S., R.A., W.E.R., J.O.G., Q.J., Z.P.).
AJNR Am J Neuroradiol. 2014 Aug;35(8):1574-9. doi: 10.3174/ajnr.A3911. Epub 2014 Apr 3.
Hyperintense FLAIR signal in the cerebral sulci of anesthetized children is attributed to supplemental oxygen (fraction of inspired oxygen) but resembles FLAIR hypersignal associated with perfusion abnormalities in Moyamoya disease and carotid stenosis. We investigated whether cerebral perfusion, known to be altered by anesthesia, contributes to diffuse signal intensity in sulci in children and explored the relative contributions of supplemental oxygen, cerebral perfusion, and anesthesia to signal intensity in sulci.
Supraventricular signal intensity in sulci on pre- and postcontrast T2 FLAIR images of 24 propofol-sedated children (6.20 ± 3.28 years) breathing supplemental oxygen and 18 nonsedated children (14.28 ± 2.08 years) breathing room air was graded from 0 to 3. The Spearman correlation of signal intensity in sulci with the fraction of inspired oxygen and age in 42 subjects, and with dynamic susceptibility contrast measures of cortical CBF, CBV, and MTT available in 25 subjects, were evaluated overall and compared between subgroups. Factors most influential on signal intensity in sulci were identified by stepwise logistic regression.
CBV was more influential on noncontrast FLAIR signal intensity in sulci than the fraction of inspired oxygen or age in propofol-sedated children (CBV: r = 0.612, P = .026; fraction of inspired oxygen: r = -0.418, P = .042; age: r = 0.523, P = .009) and overall (CBV: r = 0.671, P = .0002; fraction of inspired oxygen: r = 0.442, P = .003; age: r = -0.374, P = .015). MTT (CBV/CBF) was influential in the overall cohort (r = 0.461, P = .020). Signal intensity in sulci increased with contrast in 45% of subjects, decreased in none, and was greater (P < .0001) in younger propofol-sedated subjects, in whom the signal intensity in sulci increased with age postcontrast (r = .600, P = .002).
Elevated cortical CBV appears to contribute to increased signal intensity in sulci on noncontrast FLAIR in propofol-sedated children. The effects of propofol on age-related cerebral perfusion and vascular permeability may play a role.
麻醉儿童脑沟内的FLAIR高信号归因于补充氧气(吸入氧分数),但其类似于烟雾病和颈动脉狭窄中与灌注异常相关的FLAIR高信号。我们研究了已知受麻醉影响的脑灌注是否会导致儿童脑沟内弥漫性信号强度增加,并探讨了补充氧气、脑灌注和麻醉对脑沟内信号强度的相对贡献。
对24名接受丙泊酚镇静、呼吸补充氧气的儿童(6.20±3.28岁)以及18名未镇静、呼吸室内空气的儿童(14.28±2.08岁),在增强前后的T2 FLAIR图像上,将脑沟内的室上信号强度从0到3进行分级。评估了42名受试者脑沟内信号强度与吸入氧分数和年龄的Spearman相关性,以及25名受试者可获得的皮质脑血流量(CBF)、脑血容量(CBV)和平均通过时间(MTT)的动态磁敏感对比测量值,并在亚组之间进行比较。通过逐步逻辑回归确定对脑沟内信号强度影响最大的因素。
在接受丙泊酚镇静的儿童中,CBV对脑沟内非增强FLAIR信号强度的影响大于吸入氧分数或年龄(CBV:r = 0.612,P = 0.026;吸入氧分数:r = -0.418,P = 0.042;年龄:r = 0.523,P = 0.009),总体情况也是如此(CBV:r = 0.671,P = 0.0002;吸入氧分数:r = 0.442,P = 0.003;年龄:r = -0.374,P = 0.015)。MTT(CBV/CBF)在总体队列中有影响(r = 0.461,P = 0.020)。45%的受试者脑沟内信号强度随增强而增加,无受试者信号强度降低,且在较年轻的丙泊酚镇静受试者中信号强度更高(P < 0.000),在这些受试者中,脑沟内信号强度随增强后的年龄增加而增加(r = 0.600,P = .002)。
皮质CBV升高似乎导致接受丙泊酚镇静的儿童非增强FLAIR脑沟内信号强度增加。丙泊酚对与年龄相关的脑灌注和血管通透性的影响可能起作用。