From the Department of Neurology and Neurosurgery (H.V.D.B., L.O., G.J.B.), UMC Utrecht Brain Center; Department of Radiology (S.P., J.C.S., T.A., J.H., J.J.Z.), Center for Image Sciences, University Medical Center Utrecht; Spinoza Centre for Neuroimaging Amsterdam (J.C.S.); Image Sciences Institute (H.K.), University Medical Center Utrecht, the Netherlands; Brain Research Imaging Centre (J.M.W.), Centre for Clinical Brain Sciences, UK Dementia Research Institute Centre at the University of Edinburgh, United Kingdom; Institute for Stroke and Dementia Research (M.D.), University Hospital, LMU Munich; Munich Cluster for Systems Neurology (SyNergy) (M.D.); and German Center for Neurodegenerative Disease (DZNE) (M.D.), Germany.
Neurology. 2024 Mar 12;102(5):e209136. doi: 10.1212/WNL.0000000000209136. Epub 2024 Feb 6.
Cerebral small vessel disease (cSVD) is a major cause of stroke and dementia, but little is known about disease mechanisms at the level of the small vessels. 7T-MRI allows assessing small vessel function in vivo in different vessel populations. We hypothesized that multiple aspects of small vessel function are altered in patients with cSVD and that these abnormalities relate to disease burden.
Patients and controls participated in a prospective observational cohort study, the ZOOM@SVDs study. Small vessel function measures on 7T-MRI included perforating artery blood flow velocity and pulsatility index in the basal ganglia and centrum semiovale, vascular reactivity to visual stimulation in the occipital cortex, and reactivity to hypercapnia in the gray and white matter. Lesion load on 3T-MRI and cognitive function were used to assess disease burden.
Forty-six patients with sporadic cSVD (mean age ± SD 65 ± 9 years) and 22 matched controls (64 ± 7 years) participated in the ZOOM@SVDs study. Compared with controls, patients had increased pulsatility index (mean difference 0.09, = 0.01) but similar blood flow velocity in basal ganglia perforating arteries and similar flow velocity and pulsatility index in centrum semiovale perforating arteries. The duration of the vascular response to brief visual stimulation in the occipital cortex was shorter in patients than in controls (mean difference -0.63 seconds, = 0.02), whereas reactivity to hypercapnia was not significantly affected in the gray and total white matter. Among patients, reactivity to hypercapnia was lower in white matter hyperintensities compared with normal-appearing white matter (blood-oxygen-level dependent mean difference 0.35%, = 0.001). Blood flow velocity and pulsatility index in basal ganglia perforating arteries and reactivity to brief visual stimulation correlated with disease burden.
We observed abnormalities in several aspects of small vessel function in patients with cSVD indicative of regionally increased arteriolar stiffness and decreased reactivity. Worse small vessel function also correlated with increased disease burden. These functional measures provide new mechanistic markers of sporadic cSVD.
脑小血管病（cSVD）是中风和痴呆的主要病因，但人们对小血管疾病机制知之甚少。7T-MRI 可活体评估不同血管群的小血管功能。我们假设 cSVD 患者的小血管功能多个方面发生改变，且这些异常与疾病负担相关。
患者和对照者参与了一项前瞻性观察队列研究，即 ZOOM@SVDs 研究。7T-MRI 下的小血管功能测量包括基底节和半卵圆中心穿支动脉血流速度和搏动指数、枕叶皮质视觉刺激血管反应性和灰白质碳酸反应性。3T-MRI 上的病变负荷和认知功能用于评估疾病负担。
46 例散发性 cSVD 患者（平均年龄 ± 标准差 65 ± 9 岁）和 22 例匹配对照者（64 ± 7 岁）参与了 ZOOM@SVDs 研究。与对照者相比，患者的搏动指数增加（平均差值 0.09， = 0.01），但基底节穿支动脉的血流速度和半卵圆中心穿支动脉的血流速度和搏动指数相似。枕叶皮质短暂视觉刺激的血管反应持续时间较对照者短（平均差值-0.63 秒， = 0.02），而灰质和全白质的碳酸反应性无显著差异。在患者中，与正常外观白质相比，白质高信号区的碳酸反应性较低（血氧水平依赖平均差值 0.35%， = 0.001）。基底节穿支动脉血流速度和搏动指数及短暂视觉刺激反应性与疾病负担相关。
我们观察到 cSVD 患者的几个小血管功能方面存在异常，提示区域性小动脉僵硬增加和反应性降低。小血管功能更差也与疾病负担增加相关。这些功能测量为散发性 cSVD 提供了新的机制标志物。
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