Right posterior communicating artery aneurysm with multiple arterial stenoses and moyamoya disease: A case report

Abstract

Objective

To analyze the clinical features, diagnosis, and treatment of cerebral arteriovenous malformation with arterial stenosis and moyamoya disease.

Methods

A 50-year-old man with a 20-year history of hypertension and multiple cerebral infarctions was admitted following the detection of cerebral artery stenosis. Imaging revealed a right posterior communicating artery aneurysm, severe stenosis of the right internal carotid artery (C6 segment), bilateral middle cerebral artery occlusion, and moyamoya vessels. The diagnosis was confirmed by cerebral angiography. The patient underwent stent-assisted aneurysm coiling and carotid stenting with balloon angioplasty.

Results

Postoperative antiplatelet, antihypertensive, and lipid-lowering therapies were administered. The patient recovered well without new neurological deficits and was discharged in stable condition. Follow-up assessment is ongoing.

Conclusion

Digital subtraction angiography remains the gold standard for diagnosing such complex cerebrovascular diseases. Endovascular intervention combined with medication can improve clinical outcomes, and regular follow-up assessment is essential to prevent complications.

Clinical data

A 50-year-old man was admitted following the discovery of cerebral artery stenosis more than 9 months ago. On 18 July 2025, the patient experienced transient left-sided limb weakness. Follow-up cranial magnetic resonance angiography (MRA) revealed acute cerebral infarction in the right frontal lobe and multiple cerebral vascular stenoses. For further evaluation and management, the patient was admitted to the Department of Neurosurgery, Ganzhou Hospital of Guangdong Provincial People’s Hospital, on 25 July 2025. The patient had a 20-year history of hypertension, which was generally well controlled. Since September 2024, he had experienced recurrent cerebral infarctions and had been receiving long-term treatment with enteric-coated aspirin tablets, clopidogrel tablets, and multiple antihypertensive medications. He reported a smoking history of approximately 50 cigarettes daily and a family history of hypertension.

On admission, physical examination revealed a temperature of 36.4°C, pulse rate of 69 beats per minute, respiratory rate of 20 breaths per minute, and blood pressure of 153/92 mmHg. The patient was alert. Limb muscle strength was graded 5/5. Physiological reflexes were present, and no pathological signs were elicited. MRA performed at another hospital on 30 September 2024 demonstrated multiple cerebral vascular stenoses. MRA performed on 18 July 2025 revealed acute cerebral infarction in the right frontal lobe with multiple cerebral vascular stenoses. Electrocardiography performed on 19 July 2025 showed ST-segment elevation. Computed tomography perfusion (CTP) performed on 26 July 2025 demonstrated bilateral abnormal perfusion in multiple brain regions without evidence of core infarction. The admission diagnosis was cerebral arterial stenosis. To confirm the diagnosis, transradial cerebral angiography combined with aortic arch angiography was performed on 28 July 2025. Intraoperative digital subtraction angiography (DSA) revealed a cystic aneurysm measuring 2.5 × 3.0 mm in the right posterior communicating artery (Figure 1).

Figure 1.

Lateral view of the arterial angiography showing a posterior communicating artery aneurysm, stenosis of the C6 segment of the internal carotid artery, and a basal foggy abnormal vascular network (black arrows).

Postoperative revised diagnosis included moyamoya disease (MMD), right posterior communicating artery aneurysm, and severe bilateral middle cerebral artery stenosis. On 1 August 2025, under general anesthesia, the patient underwent transfemoral stent-assisted embolization of the right posterior communicating artery aneurysm, balloon angioplasty of internal carotid artery stenosis, and carotid artery stenting. Intraoperatively, guided by a Mudfish guidewire and a multifunctional catheter, an 8F guide catheter was advanced to the right internal carotid artery near the C2 segment. After confirmation of the working position via three-dimensional angiography, a microcatheter was used to deliver a Fastunnel 2.5 ×15-mm delivery balloon catheter (Jiaqi Bio 21 Series) to the stenotic segment of the right internal carotid artery. Balloon angioplasty was performed at a pressure of 3 atm, resulting in significant improvement of the stenosis. Subsequently, a C-shaped microcatheter was advanced into the aneurysm cavity, and two coils (2 mm × 4 cm and 1.0 mm × 1 cm; Jasper, Jiaqi Bio) were sequentially deployed, achieving relatively dense embolization of the aneurysm. A 4.5 × 14-mm stent was then delivered using balloon-expandable stent delivery catheter. Angiography demonstrated no aneurysm filling, with marked improvement in the stenotic segment of the parent artery (Figure 2). Postprocedural CT review was completed. On 7 August 2025, the patient was discharged with improved symptoms. Physical examination revealed an alert mental status and clear speech, with muscle strength graded as 5/5 in all limbs. No gastrointestinal discomfort or allergic reactions occurred during hospitalization.

Figure 2.

(a) Intraoperative path map showing the Fastunnel balloon catheter crossing the narrowed segment and the neck of the aneurysm, with the microcatheter superselected entering the aneurysmal cavity and (b) immediate postoperative angiography showing complete nonvisualization of the aneurysm, restoration of the aneurysmal arterial lumen, and smooth blood flow.

After discharge, the patient was prescribed long-term antiplatelet therapy with aspirin (100 mg/day) and clopidogrel (75 mg/day, to be adjusted after 7 November 2025), lipid-lowering therapy with atorvastatin (20 mg/night), and antihypertensive therapy with irbesartan–hydrochlorothiazide (300 mg/day) and amlodipine besylate (5 mg/day). The patient was instructed to monitor blood pressure regularly and to undergo complete blood count testing and liver and kidney function tests every 6 months.

At the first follow-up on 22 August 2025, a “personalized, stepwise” follow-up plan was established:

Short-term follow-up (1, 3, and 6 months postoperatively). Repeat cerebral angiography to assess aneurysm embolization status and bypass vessel patency as well as CTP to monitor cerebral perfusion, with close surveillance for complications such as transient ischemic attack and vasospasm;

Long-term follow-up (1–5 years postoperatively). Annual cerebral angiography to monitor lesion recurrence and progression of vascular stenosis. Cognitive function assessment using the Montreal Cognitive Assessment scale, together with cranial magnetic resonance imaging review every 2 years to screen for white matter lesions;

Lifelong management. Long-term adherence to antiplatelet therapy and control of underlying conditions, combined with rehabilitation training and patient education, including avoidance of strenuous exercise and management of emotional fluctuations to reduce the risk of aneurysm rupture and ischemic episodes.

Discussion

MMD is characterized by progressive stenosis or occlusion of the terminal segments of the bilateral internal carotid arteries and the origins of the anterior and middle cerebral arteries, accompanied by the formation of an abnormal vascular network at the base of the brain. ¹ The incidence of intracranial aneurysms in adults with MMD ranges from 3% to 14%, with aneurysms frequently occurring in the main vessels and peripheral arteries of the circle of Willis. ²

In this case, the patient presented with cerebral artery stenosis as the chief complaint. The initial symptoms were limited to transient limb weakness without specific neurological deficits, which closely overlap with the clinical manifestations of isolated cerebral infarction or arterial stenosis, making differentiation of associated pathologies difficult based on symptoms alone. Moreover, early-stage MMD progresses slowly, and initial abnormal vascular network formation is often asymptomatic. Unruptured aneurysms likewise typically remain symptom-free, resulting in prolonged concealment of multiple lesions during the disease course. Consequently, comprehensive identification using routine MRA alone is challenging. The first MRA in September 2024 revealed only multiple arterial stenoses, without detecting aneurysms or MMD characteristics. In July 2025, cranial MRA revealed new cerebral infarction and more extensive stenosis; however, it failed to confirm MMD diagnosis. This indicates that conventional MRA lacks sufficient sensitivity for detecting microaneurysms (diameter <3 mm) and early-stage MMD, potentially leading to misdiagnosis. Subsequent CTP revealed bilateral multi-regional cerebral perfusion abnormalities and delayed time to peak (TTP), providing crucial clues for MMD diagnosis but failing to directly confirm vascular occlusion or abnormal vascular networks. Ultimately, DSA confirmed the complete lesion spectrum: bilateral chronic middle cerebral artery occlusion, severe right internal carotid artery stenosis at the C6 segment, and right posterior communicating artery aneurysm. Previous studies have indicated that DSA remains the gold standard for diagnosing MMD. ³ This diagnostic process underscores the critical importance of multimodal imaging techniques. The patient presented with a complex pathological combination of MMD, aneurysm, and multi-site arterial stenosis, characterized by a right posterior communicating artery aneurysm (2.6 × 2.8 mm, cystic) superimposed on the underlying MMD, along with severe stenosis of the right internal carotid artery at the C6 segment and chronic occlusion of both middle cerebral arteries. The cerebral hemodynamic disturbance caused by MMD may contribute to aneurysm formation. Concurrently, arterial stenosis further exacerbates cerebral hypoperfusion, compelling collateral vessels to bear higher pressures. This creates a vicious cycle of stenosis, hypoperfusion, compensation, and increased aneurysm risk, revealing a multifaceted and interrelated complexity in the pathological mechanism. MMD with aneurysms is clinically uncommon, with a complex pathogenesis influenced by multiple factors, including hemodynamic alterations and pathological vascular architecture. These pathologic and anatomical changes render the treatment of MMD-associated aneurysms challenging. ⁴ Given the patient’s complex condition, including a cerebral aneurysm at risk of rupture, arterial stenosis, and cerebral hypoperfusion due to MMD, a multidisciplinary team—involving experts from neurosurgery, neurology, interventional radiology, and radiology departments—developed a staged treatment plan: “First, address the aneurysm and stenosis and then treat moyamoya disease.” This approach mitigates the risk of aneurysm rupture while improving cerebral perfusion, thereby creating favorable conditions for subsequent MMD treatment. Endovascular embolization has been demonstrated to be safe and effective for patients with MMD complicated by intracranial aneurysms. ⁵ This procedure pioneered the use of ANSWER technology, transforming the traditional dual approaches for treating stenosis and aneurysms. The intraoperative Fastunnel delivery balloon–expandable stent–graft system enabled a “four-in-one” treatment for combined aneurysm and stenotic lesions: pre-expansion, temporary balloon support, balloon protection, and stent placement. Following catheter expansion, the stent can be deployed without catheter withdrawal. This approach simultaneously achieves auxiliary aneurysm filling and treatment of stenotic vessels, streamlining procedures by eliminating separate steps for stenosis dilation and auxiliary stent placement. It reduces complications, enhances surgical efficiency, and provides an additional safety layer for patients by enabling balloon occlusion to halt bleeding in the event of acute aneurysm rupture. Although the patient was discharged in stable condition following interventional therapy, follow-up treatment for MMD remains necessary. Failure to strictly control risk factors, such as hypertension and smoking, may lead to recurrence or progression of the disease. Long-term monitoring is also required for risks including stent thrombosis after discontinuation of dual antiplatelet therapy and new vascular lesions caused by disease progression. Prognosis assessment must incorporate short-term complications. In summary, cerebral aneurysms with arterial stenosis and MMD present significant complexity in etiology, diagnosis, treatment implementation, and management. For patients with intracranial aneurysms and MMD, endovascular treatment options should be carefully selected based on the location and size of the aneurysm, ⁵ achieving favorable outcomes. Effective improvement in patient prognosis relies on multidisciplinary collaboration, precise imaging diagnosis, and individualized treatment strategies.