Fukushima Yutaka, Nakahara Ichiro, Ohta Tsuyoshi, Matsumoto Shoji, Ishibashi Ryota, Gomi Masanori, Miyata Haruka, Nishi Hidehisa, Watanabe Sadayoshi
Department of Neurosurgery, Kokura Memorial Hospital, Kokurakita-ku, Kitakyushu, Japan
Department of Neurosurgery, Kokura Memorial Hospital, Kokurakita-ku, Kitakyushu, Japan.
Interv Neuroradiol. 2015 Feb;21(1):72-9. doi: 10.15274/inr-2014-10099.
We experienced a rare complication after carotid artery stenting (CAS) characterized by transient neurological symptoms with no evidence of distal emboli or hyperperfusion. Using neuroimaging, we investigated the pathogenesis of the complication that occurred after CAS in three patients who developed neurological symptoms over a period of ten hours after CAS and improved within two days. None of the three patients showed signs of fresh infarctions on diffusion-weighted imaging or hyperperfusion on single-photon emission computed tomography. However, high signal intensity was observed in the leptomeningeal zone of the cerebral hemisphere on the stent side in all three patients and in the leptomeningeal zone of the contralateral anterior cerebral artery territory in one patient. These areas were assessed using fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging without gadolinium administration. The high signal intensity in the leptomeningeal zone disappeared as the symptoms improved. Based on the transient nature of the neurological disorders and the normalization of FLAIR imaging findings in these patients, the pathogenesis of this complication might have been vasogenic edema due to vasoparalysis of the local vessels caused by the hemodynamic changes occurring after CAS.
我们在颈动脉支架置入术(CAS)后经历了一种罕见的并发症,其特征为短暂性神经症状,无远端栓子或血流过度灌注的证据。我们利用神经影像学方法,对3例在CAS术后10小时内出现神经症状且在两天内症状改善的患者CAS术后发生并发症的发病机制进行了研究。这3例患者在弥散加权成像上均未显示新鲜梗死迹象,在单光子发射计算机断层扫描上也未显示血流过度灌注。然而,所有3例患者在支架侧大脑半球的软脑膜区域均观察到高信号强度,1例患者在对侧大脑前动脉区域的软脑膜区域也观察到高信号强度。这些区域采用未注射钆剂的液体衰减反转恢复(FLAIR)磁共振成像进行评估。随着症状改善,软脑膜区域的高信号强度消失。基于这些患者神经功能障碍的短暂性以及FLAIR成像结果的正常化,该并发症的发病机制可能是CAS术后血流动力学变化导致局部血管麻痹引起的血管源性水肿。