Measurement of cortical thickness asymmetry in carotid occlusive disease.

Measurement of cortical thickness asymmetry in carotid occlusive disease.
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DOI:
10.1016/j.nicl.2016.09.013
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发表时间:
2016
影响因子:
4.2
通讯作者:
Marshall, Randolph S.
Marshall, Randolph S.
中科院分区:
医学2区
文献类型:
--
作者:
Asllani, Iris;Slattery, Pamelia;Fafard, Alexander;Pavol, Marykay;Lazar, Ronald M.;Marshall, Randolph S.

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尽管皮层厚度被认为是与神经元密度直接相关的重要解剖参数,但在人脑体内研究中并未常规评估皮层厚度。这种缺乏很大程度上是由于人类皮质的大小和复杂的形状,这使得开发能够有效、可靠地测量皮质厚度的自动化算法变得困难。自 2000 年 Fischl 和 Dale 开发出这种算法以来,研究大脑皮质厚度与其他生理参数之间关系的研究数量一直在增加。然而,还没有研究根据已知的血管解剖学验证皮质不对称性。为此,我们使用高分辨率 MRI 测量了单侧高度颈动脉闭塞性疾病患者(n = 29,年龄 = 74 ± 10 岁)的初级运动皮层 (M1) 和初级视觉皮层 (V1) 的皮层厚度和体积。这些区域的选择基于这样的假设:在闭塞的颈动脉供应的区域中,M1 的皮质厚度将会变薄,而 V1 将不会表现出不对称性,因为它的血液供应是由未受影响的后动脉提供的。为了测试惯用手的影响,还测量了健康志愿者(n = 8,年龄 = 37 ± 13 岁)的皮质厚度和体积。在患者中,我们发现闭塞侧 M1 的皮质较薄(平均值 = 2.07 ± 0.19 mm 与 2.15 ± 0.20 mm,p = 0.0008),但 V1 没有半球差异(闭塞侧为 1.80 ± 0.17 mm,未闭塞侧为 1.78 ± 0.16 mm, p = 0.31)。尽管闭塞半球的 M1 平均皮质体积也较低,但差异并未达到统计学显着性 (p = 0.09)。同样,在健康对照中,结果显示任一区域的皮质厚度或体积均不存在半球不对称性 (p > 0.1)。为了测试该方法中的方向偏差,将图像从神经方向翻转到放射方向,重复进行分析。虽然该算法没有对两个方向产生相同的结果,但这种效果并没有改变研究结果。这些结果提供了一种在受试者体内验证颈动脉闭塞性疾病对人类皮质的病理生理学影响的方法,并值得进一步研究潜在机制。研究了无症状单侧颈动脉闭塞性疾病的皮质厚度不对称性。闭塞半球的初级运动皮层明显变薄。根据血管解剖学的假设,视觉皮层的厚度没有表现出不对称性。对照组的初级皮质或视觉皮质没有皮质厚度不对称。对于患者和对照组,任一 ROI 的体积没有半球差异。
Despite being considered an important anatomical parameter directly related to neuronal density, cortical thickness is not routinely assessed in studies of the human brain in vivo. This paucity has been largely due to the size and convoluted shape of the human cortex, which has made it difficult to develop automated algorithms that can measure cortical thickness efficiently and reliably. Since the development of such an algorithm by Fischl and Dale in 2000, the number of studies investigating the relationship between cortical thickness and other physiological parameters in the brain has been on the rise. There have been no studies however that have validated cortical asymmetry against known vascular anatomy. To this aim, using high-resolution MRI, we measured cortical thickness and volume in the primary motor (M1) and primary visual (V1) cortex in patients with unilateral, high-grade carotid occlusive disease (n = 29, age = 74 ± 10 years). These regions were selected based on the hypothesis that there will be thinning of the cortical thickness of M1 in the territory supplied by the occluded carotid artery, whereas V1 will show no asymmetry since its blood supply is provided by unaffected posterior arteries. To test for an effect of handedness, cortical thickness and volume were also measured in healthy volunteers (n = 8, age = 37 ± 13 years). In patients, we found thinner cortex in M1 on the occluded side (mean = 2.07 ± 0.19 mm vs 2.15 ± 0.20 mm, p = 0.0008) but no hemispheric difference in V1 (1.80 ± 0.17 mm in occluded vs 1.78 ± 0.16 mm in unoccluded, p = 0.31). Although the mean cortical volume of M1 in the occluded hemisphere was also lower, the difference did not reach statistical significance (p = 0.09). Similarly, in healthy controls, the results showed no hemispheric asymmetry in either cortical thickness or volume in either region (p > 0.1). To test for an orientation bias in the method, the analysis was repeated with images flipped from neurological to radiological orientation. While the algorithm did not yield identical results for the two orientations, the effect did not alter the findings of the study. These results provide a method for within-subject validation of a pathophysiological effect of carotid occlusive disease on the human cortex and warrant further investigation for underlying mechanisms. Cortical thickness asymmetry in asymptomatic unilateral carotid occlusive disease was studied. Significant thinning was seen in the primary motor cortex in the occluded hemisphere. As hypothesized based on vascular anatomy, thickness of the visual cortex showed no asymmetry. There was no cortical thickness asymmetry in either primary or visual cortices in controls. For both patients and controls, there was no hemispheric difference in the volume of either ROI.
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发表时间: 1999-02-01
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期刊: NEUROIMAGE
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发表时间: 2016-01-01
期刊: Alzheimer's & dementia (Amsterdam, Netherlands)
影响因子: --
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