Fotiadis Panagiotis, Pasi Marco, Charidimou Andreas, Warren Andrew D, Schwab Kristin M, Rosand Jonathan, van der Grond Jeroen, van Buchem Mark A, Viswanathan Anand, Gurol M Edip, Greenberg Steven M
Department of Neurology, J.P. Kistler Stroke Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Department of Neuroscience, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
J Stroke. 2021 May;23(2):223-233. doi: 10.5853/jos.2020.04280. Epub 2021 May 31.
Cerebral amyloid angiopathy (CAA) is a common pathology of the leptomeningeal and cortical small vessels associated with hemorrhagic and non-hemorrhagic brain injury. Given previous evidence for CAA-related loss of cortical thickness and white matter volume, we hypothesized that CAA might also cause tissue loss in the basal ganglia.
We compared basal ganglia volumes expressed as a percentage of total intracranial volume (pBGV) of non-demented patients with sporadic and hereditary CAA to age-matched healthy control (HC) and Alzheimer's disease (AD) cohorts.
Patients with sporadic CAA had lower pBGV (n=80, 1.16%±0.14%) compared to HC (n=80, 1.30%±0.13%, P<0.0001) and AD patients (n=80, 1.23%±0.11%, P=0.001). Similarly, patients with hereditary CAA demonstrated lower pBGV (n=25, 1.26%±0.17%) compared to their matched HC (n=25, 1.36%±0.15%, P=0.036). Using a measurement of normalized basal ganglia width developed for analysis of clinical-grade magnetic resonance images, we found smaller basal ganglia width in patients with CAA-related lobar intracerebral hemorrhage (ICH; n=93, 12.35±1.47) compared to age-matched patients with hypertension-related deep ICH (n=93, 13.46±1.51, P<0.0001) or HC (n=93, 15.45±1.22, P<0.0001). Within the sporadic CAA research cohort, decreased basal ganglia volume was independently correlated with greater cortical gray matter atrophy (r=0.45, P<0.0001), increased basal ganglia fractional anisotropy (r=-0.36, P=0.001), and worse performance on language processing (r=0.35, P=0.003), but not with cognitive tests of executive function or processing speed.
These findings suggest an independent effect of CAA on basal ganglia tissue loss, indicating a novel mechanism for CAA-related brain injury and neurologic dysfunction.
脑淀粉样血管病（CAA）是一种常见于软脑膜和皮质小血管的病理状态，与出血性和非出血性脑损伤相关。鉴于先前有证据表明CAA会导致皮质厚度和白质体积减少，我们推测CAA可能也会导致基底神经节组织丢失。
我们将散发型和遗传型CAA的非痴呆患者的基底神经节体积表示为总颅内体积的百分比（pBGV），并与年龄匹配的健康对照（HC）和阿尔茨海默病（AD）队列进行比较。
与HC（n = 80，1.30%±0.13%，P < 0.0001）和AD患者（n = 80，1.23%±0.11%，P = 0.001）相比，散发型CAA患者的pBGV较低（n = 80，1.16%±0.14%）。同样，与匹配的HC（n = 25，1.36%±0.15%，P = 0.036）相比，遗传型CAA患者的pBGV较低（n = 25，1.26%±0.17%）。使用为分析临床级磁共振图像而开发的标准化基底神经节宽度测量方法，我们发现与年龄匹配的高血压相关性深部脑出血患者（n = 93，13.46±1.51，P < 0.0001）或HC（n = 93，15.45±1.22，P < 0.0001）相比，CAA相关性脑叶脑出血（ICH；n = 93，12.35±1.47）患者的基底神经节宽度较小。在散发型CAA研究队列中，基底神经节体积减少与更大程度的皮质灰质萎缩独立相关（r = 0.45，P < 0.0001），基底神经节分数各向异性增加（r = -0.36，P = 0.001），以及语言处理能力较差（r = 0.35，P = 0.003），但与执行功能或处理速度的认知测试无关。
这些发现表明CAA对基底神经节组织丢失有独立影响，提示了一种与CAA相关的脑损伤和神经功能障碍的新机制。
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