An 18-year-old man was admitted to our department showing the symptoms of blurriness. A 1-year history was reported on blurriness and visual indistinctness that had progressively worsened over the past 2 weeks. He has a record of tuberculosis and takes anti-TB drugs on a regular basis. Neurologic examinations at the time of admission revealed no focal neurologic deficits except for oculomotor paralysis. Magnetic resonance imaging (MRI) indicated that the diameter of intracranial segment in the left internal carotid artery was significantly dilated, the inner diameter was approximately 14 mm, the left anterior cerebral artery, and the starting point of the MCA were slightly dilated as well, and the structure of the left cavernous sinus area lacked clarity. There was a circular liquid signal shadow spotted under the inner wall of the left maxillary sinus, the diameter of which was about 16 mm (Fig. 1). Further cerebral angiography indicated that the left internal carotid artery GSA was about 48.61 mm x 23.40 mm in size, 4.65 mm in diameter of proximal vessels, and 3.16 mm in diameter of distal vessels (Fig. 2).  
His family was informed of these conditions and signed a consent form prior to the operation. The balloon occlusion test conducted previous to surgery indicated that the anterior communicating artery was open and the contralateral internal carotid artery had a good compensatory blood supply, as a result of which direct trapping of the parent artery was taken as an alternative method. However, ipsilateral MA has a potential of further growth which could lead to paralysis of facial nerve compression, which is due to higher blood flow to the external carotid artery. His family members rejected this traumatic treatment method and thus the insertion of stents was chosen to reconstruct the original structure of the vessel. Therefore, the following surgery was performed: antiplatelet therapy (100 mg aspirin +  75 mg clopidogrel daily) was carried out at least 3 days prior to the operation, and he underwent surgery after being diagnosed with anesthesia. Firstly, a LEO (6.5 mm x 75 mm) stent was put through an Echelon-10 catheter located in the MCA, and then the stent was released at a slow pace and completely through the GSA. Meanwhile, the head was anchored at the distal end of the parent artery. Subsequently, the trans 300 floppy guidewire was switched to the marksman on the MCA. The Tubridge flow diverter (6.5 mm x 45 mm) was easily placed into the designated position where it was attached to the LEO stent that was well anchored before. With the assistance of X-ray, the Tubridge flow diverter was slowly released to overlap with the LEO stent wall and the aneurysm neck was completely covered. Ultimately, digital subtraction angiography (DSA) revealed obvious retention of contrast agent in GSA, and three-dimensional vascular reconstruction demonstrated that the walls of the parent artery were reconstructed by both Tubridge and LEO stent (Fig. 3). Then, the guide catheter to the external carotid artery was replaced, liquid glue (50%, 1.5 ml) was injected, and three coils were released through the microcatheter. Finally, the right femoral artery with an 8F Angio-Seal vascular occlude was blocked. The patient needed to avoid stent thrombosis by taking aspirin for a long period of time, although the thrombo-elastography (TEG) test indicated that arachidonic acid inhibition rate (AA%) and inhibition rate on ADP receptor of clopidogrel (ADP%) were within the normal range. After a follow-up observation for 1 year, DSA revealed that the aneurysms were almost completely occluded and the abnormal serpentine channels disappeared. Meanwhile, the MA disappeared as well. The two stents overlapped in the parent artery with excellent adhesion, and no stenosis or displacement was discovered. Three-dimensional revascularization indicated a significant reduction in aneurysm volume, and the mass effect was reduced as shown by CT scan (Fig. 4).