Igarashi Suguru, Ando Toshihiko, Takahashi Tatsuhiko, Yoshida Jun, Kobayashi Masakazu, Yoshida Kenji, Terasaki Kazunori, Fujiwara Shunrou, Kubo Yoshitaka, Ogasawara Kuniaki
1Department of Neurosurgery and.
2Cyclotron Research Center, Iwate Medical University School of Medicine, Morioka, Japan.
J Neurosurg. 2021 Jan 1;135(4):1122-1128. doi: 10.3171/2020.7.JNS202353. Print 2021 Oct 1.
A primary cause of cognitive decline after carotid endarterectomy (CEA) is cerebral injury due to cerebral hyperperfusion. However, the mechanisms of how cerebral hyperperfusion induces cerebral cortex and white matter injury are not known. The presence of cerebral microbleeds (CMBs) on susceptibility-weighted imaging (SWI) is independently associated with a decline in global cognitive function. The purpose of this prospective observational study was to determine whether cerebral hyperperfusion following CEA leads to the development of CMBs and if postoperative cognitive decline is related to these developed CMBs.
During the 27-month study period, patients who underwent CEA for ipsilateral internal carotid artery stenosis (≥ 70%) also underwent SWI and neuropsychological testing before and 2 months after surgery, as well as quantitative brain perfusion SPECT prior to and immediately after surgery.
According to quantitative brain perfusion SPECT and SWI before and after surgery, 12 (16%) and 7 (9%) of 75 patients exhibited postoperative cerebral hyperperfusion and increased CMBs in the cerebral hemisphere ipsilateral to surgery, respectively. Cerebral hyperperfusion was associated with an increase in CMBs after surgery (logistic regression analysis, 95% CI 5.08-31.25, p < 0.0001). According to neuropsychological assessments before and after surgery, 10 patients (13%) showed postoperative cognitive decline. Increased CMBs were associated with cognitive decline after surgery (logistic regression analysis, 95% CI 6.80-66.67, p < 0.0001). Among the patients with cerebral hyperperfusion after surgery, the incidence of postoperative cognitive decline was higher in those with increased CMBs (100%) than in those without (20%; p = 0.0101).
Cerebral hyperperfusion following CEA leads to the development of CMBs, and postoperative cognitive decline is related to these developed CMBs.
颈动脉内膜切除术（CEA）后认知功能下降的主要原因是脑血流灌注过多导致的脑损伤。然而，脑血流灌注过多如何诱发大脑皮质和白质损伤的机制尚不清楚。磁敏感加权成像（SWI）上脑微出血（CMB）的存在与整体认知功能下降独立相关。这项前瞻性观察性研究的目的是确定CEA术后脑血流灌注过多是否会导致CMB的发生，以及术后认知功能下降是否与这些新出现的CMB有关。
在为期27个月的研究期间，因同侧颈内动脉狭窄（≥70%）接受CEA的患者在手术前和术后2个月均接受了SWI和神经心理学测试，以及手术前和手术后即刻的定量脑灌注单光子发射计算机断层扫描（SPECT）。
根据手术前后的定量脑灌注SPECT和SWI，75例患者中有12例（16%）和7例（9%）分别在术后出现同侧大脑半球脑血流灌注过多和CMB增加。术后脑血流灌注过多与CMB增加相关（逻辑回归分析，95%置信区间5.08 - 31.25，p < 0.0001）。根据手术前后的神经心理学评估，10例患者（13%）出现术后认知功能下降。CMB增加与术后认知功能下降相关（逻辑回归分析，95%置信区间6.80 - 66.67，p < 0.0001）。在术后出现脑血流灌注过多的患者中，CMB增加的患者术后认知功能下降的发生率（100%）高于未增加的患者（20%；p = 0.0101）。
CEA术后脑血流灌注过多会导致CMB的发生，且术后认知功能下降与这些新出现的CMB有关。
