Cerebrovascular Reactivity Has Negligible Contribution to Hemodynamic Lag After Stroke: Implications for Functional Magnetic Resonance Imaging Studies.

Cerebrovascular Reactivity Has Negligible Contribution to Hemodynamic Lag After Stroke: Implications for Functional Magnetic Resonance Imaging Studies.
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DOI:
10.1161/strokeaha.122.041880
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发表时间:
2023-04
期刊:
影响因子:
8.3
通讯作者:
Geranmayeh F
Geranmayeh F
中科院分区:
医学1区
文献类型:
--
作者:
Braban A;Leech R;Murphy K;Geranmayeh F

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功能磁共振成像被广泛用于研究中风后的恢复。然而,fMRI衍生的血流动力学反应易受血管损伤的影响,这可能导致血流动力学反应功能(HRF)的幅度降低和时间延迟(滞后)。HRF滞后的病因仍然存在争议,需要更好地了解它,以确保准确的解释中风后的fMRI研究。在这项纵向研究中,我们探讨了脑卒中后血流动力学滞后与脑血管反应性(CVR)之间的关系。在两个时间点(卒中后约2周和约4个月)和两种条件下(静息状态和屏气),计算27名健康对照和59名卒中患者相对于平均灰质参考信号的体素滞后图。屏气条件还用于计算高碳酸血症时的CVR。HRF滞后计算两种条件下跨组织区室:病变,病灶周围组织,未受影响的组织的病变半球,和它们的同源区域在未受影响的半球。CVR和滞后图相关。使用ANOVA分析评估组、条件和时间效应。与平均灰质信号相比,在静息状态下的初级感觉运动皮层和屏气状态下的双侧下顶叶皮层观察到相对血流动力学领先。全脑血流动力学滞后显着相关的条件下,无论组,与区域差异的条件下,提示神经网络模式。患者在受损半球表现出相对滞后,随着时间的推移显著减少。在对照组、病变半球内的患者或右半球的病变和病变周围组织的同源区域内,屏气导出的滞后和CVR没有显著的体素相关性(平均r<0.1)。CVR改变对HRF滞后的影响可以忽略不计。我们认为,HRF滞后在很大程度上是独立的CVR,并可以部分反映内在的神经网络动态等因素。
Functional MRI is ubiquitously used to study post-stroke recovery. However, the fMRI-derived haemodynamic responses are vulnerable to vascular insult which can result in reduced magnitude and temporal delays (lag) in the haemodynamic response function (HRF). The aetiology of HRF lag remains controversial, and a better understanding of it is required to ensure accurate interpretation of post-stroke fMRI studies. In this longitudinal study, we investigate the relationship between haemodynamic lag and cerebrovascular reactivity (CVR) following stroke. Voxelwise lag maps were calculated relative to a mean grey matter reference signal for 27 healthy controls and 59 patients with stroke across two timepoints (~2 weeks and ~4 months post-stroke), and two conditions: resting-state and breath-holding. The breath-holding condition was additionally used to calculate CVR in response to hypercapnia. HRF lag was computed for both conditions across tissue compartments: lesion, perilesional tissue, unaffected tissue of the lesioned hemisphere, and their homologue regions in the unaffected hemisphere. CVR and lag maps were correlated. Group, condition, and time effects were assessed using ANOVA analyses. Compared with the average grey matter signal, a relative haemodynamic lead was observed in the primary sensorimotor cortices in resting-state and bilateral inferior parietal cortices in breath-holding condition. Whole-brain haemodynamic lag was significantly correlated across conditions irrespective of group, with regional differences across conditions suggestive of a neural network pattern. Patients showed relative lag in the lesioned hemisphere which significantly reduced over time. Breath-hold derived lag and CVR had no significant voxel-wise correlation in controls, or patients within the lesioned hemisphere or the homologous regions of the lesion and perilesional tissue in the right hemisphere (mean r<0.1). The contribution of altered CVR to HRF lag was negligible. We suggest that HRF lag is largely independent of CVR, and could partly reflect intrinsic neural network dynamics amongst other factors.